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St. Jude’s CEO is still betting on EnligHTN IV Study Renal Denervation System, despite Medtronic’s setback related to SYMPLICITY Phase IV

 

UPDATED on 1/14/2014

This is in continuation to our 1/9/2014 article:

Market Impact on Global Suppliers of Renal Denervation Systems by Pivotal US Trial: Metronics’ Symplicity Renal Denervation System FAILURE at Efficacy Endpoint

https://pharmaceuticalintelligence.com/2014/01/09/market-impact-on-global-suppliers-of-renal-denervation-systems-by-pivotal-us-trial-metronics-symplicity-renal-denervation-system-failure-at-efficacy-endpoint/

In the short term, the company, St. Jude suspended enrollment in three other related trials and announced plans to gather an independent panel of experts to plot a future course. 

St. Jude Medical won a CE mark for its next-gen EnligHTN IV renal denervation system over the summer, but halted its own U.S. trial in December. Minnesota-based St. Jude said it had struggled to recruit viable candidates for the 590-patient trial, and was concerned that Medtronic’s Symplicity might siphon off viable patients needed for its own study. At the time, St. Jude said it would work to develop a new protocol to address trial enrollment challenges.

According to Mark Hollmer:

Symplicity’s setbacks may make that job much easier for St. Jude. They also create new opportunities for other rivals focused on developing similar technology, such as Boston Scientific ($BSX) and Covidien ($COV).

Curator of this article has expressed a different view in 

https://pharmaceuticalintelligence.com/2014/01/09/market-impact-on-global-suppliers-of-renal-denervation-systems-by-pivotal-us-trial-metronics-symplicity-renal-denervation-system-failure-at-efficacy-endpoint/

St. Jude’s CEO is still betting on renal denervation, despite Medtronic’s setback

By Mark Hollmer

Medtronic’s Symplicity renal denervation device

If Medtronic’s ($MDT) recent U.S. clinical trial failure for its Symplicity renal denervation device throws the door wide open for its competitors, St. Jude Medical ($STJ) will likely waste no time walking through.

As MassDevice reported, St. Jude CEO Daniel Starks told an audience at the JPMorgan Healthcare conference in San Francisco that the company plans to keep plowing ahead with the development of its own technology.

“The fact that we had and that there have been favorable early clinical results in numerous other experiences is still valid,” MassDevice quoted Starks as saying. “There is open surgical data dating back several decades that was favorable to the impact of surgical renal denervation to treat hypertension.

That said, he also expressed genuine surprise about Medtronic’s trial setback.

“This was unexpected for us, to have a negative result from Medtronic’s trial, and it’s too soon for us to know what to make of that,” Starks said in the story.

Medtronic’s Symplicity device, which has a CE mark and is a market leader, had done well in previous trials in patients with different forms of hypertension and was on track to win FDA approval in 2015–potentially the first renal denervation device to reach that point.

The Minnesota device giant announced a few days ago that Symplicity proved safe in a 535-patient trial but failed to significantly lower blood pressure for drug-resistant hypertension.

This was a trial that mattered, designed to help fuel FDA approval.

Related Articles:

Medtronic’s flunked trial throws its hypertension program into doubt

St. Jude Medical will try again another day for a U.S. renal denervation study

St. Jude bags EU approval for next-gen renal denervation

 SOURCE

From: FierceMedicalDevices <editors@fiercemedicaldevices.com>
Date: Tue, 14 Jan 2014 18:14:06 +0000 (GMT)
To: <avivalev-ari@alum.berkeley.edu>

Renal Denervation: EnligHTN IV Study Called Off and Potential Novel Indications – Diastolic Heart Failure

Reporter: Aviva Lev-Ari, PhD, RN

This Open Access Scientific Journal has covered all the major developments reported on Renal Denervation since its inception

The Archive for Renal denervation

https://pharmaceuticalintelligence.com/category/cardiac-and-cardiovascular-surgical-procedures/renal-denervation/

Search Results for Renal Denervation

https://pharmaceuticalintelligence.com/?s=Renal+denervation

Heartwire Reported on December 09, 2013

EnligHTN IV Renal Denervation Study Called Off

ST PAUL, MN – The EnligHTN IV study (St Jude Medical, St Paul, MN), testing the multielectrode renal-denervation system in patients with resistant hypertension, has been stopped almost before it even began. The trial, which was announced in June and began enrolling a small number of patients this fall, was canceled because of concerns about slow enrollment.

To heartwire ,

Denise Perkins-Landry, a spokesperson for St Jude Medical, said the decision to discontinue the study was based on “anticipated recruitment challenges” and is not the result of any safety or efficacy issues with the device. “A US clinical trial for EnligHTN remains a very high priority for St Jude Medical, and we will be working with the FDA to develop a new protocol that will address anticipated enrollment challenges,” she stated in an email.

The full results of the SYMPLICITY HTN-3 trial, a study similar to the EnligHTN IV study, which is sponsored by Medtronic (Minneapolis, MN), are expected in early 2014. While neither device is approved for clinical use in the US, it is expected that the Medtronic renal-denervation system will be first. As a result, it might be difficult to enroll patients to a sham procedure if there is another commercially available system for treating resistant hypertension, according to St Jude.

EnligHTN IV was to be a randomized, single-blind, controlled study with patients randomized from as many as 80 clinical centers in the US and Canada. It was intended to show the safety and effectiveness of the renal-denervation system in the reduction of systolic blood pressure in 590 patients with an office blood pressure >160 mm Hg despite taking three or more antihypertensive medications, including a diuretic.

Abrupt Decision to Stop the Study

Dr William White (University of Connecticut Medical Center, Farmington), one of the cochairs of the EnligHTN IV steering committee, told heartwire the decision to cancel the study was made just last week. In fact, there were clinical centers already up and running in terms of enrollment, although these were pilot centers where any “bugs could be worked out.” The meeting for training investigators participating in the trial was scheduled for Saturday in Chicago, IL, although that is now off.

“In the grander scheme of things, I can tell you that the decision was not made because of any problem with the catheter or any safety issues,” said White. “Outside the US, the development is continuing as planned, but the biggest concern is that it might be very difficult, if not impossible, to continue doing a sham-controlled study a year from now if there were a commercially available renal-denervation catheter in the US, which there very well could be with Medtronic.”

Still, White said that it’s not even known if the SYMPLICITY HTN-3 study is positive or if the FDA will be satisfied with the trial and its outcomes. He said a lot of assumptions are being made by St Jude Medical in stopping the trial, and it could turn out to be a bad decision. In addition, reimbursement remains an open question.

“Commercially available doesn’t mean there’s going to be a payer,” White told heartwire . “If that happens, it will be doubly unfortunate for the patients that are out there because they might be willing and able to go into a clinical trial but they won’t have that opportunity.”

As a scientist, White said that he would have preferred the trial be pursued, regardless of what happens with Medtronic. He believes the EnligHTN catheter is “outstanding,” as it has multiple electrodes to enable physicians to thoroughly ablate the renal arteries within a couple of minutes. “The clinical scientist in me would have preferred that we go ahead as planned,” he said. “I think we would have gained a great deal of knowledge. And just because one study shows a p value of 0.05 doesn’t mean a second study will.”

The Medtronic SYMPLICITY renal-denervation system was launched in 2010 and is available in parts of Europe, Asia, Africa, and South America. The first-generation EnligHTN device has had CE Mark approval in Europe since 2012 while the updated second-generation system with multiple electrodes received European approval this past summer.

News of the halting of EnligHTN IV was first reported by Wells Fargo analyst Larry Biegelsen.

SOURCE

http://www.medscape.com/viewarticle/817482?nlid=41903_2105&src=wnl_edit_medp_card&uac=93761AJ&spon=2

On December 06, 2013 Marlene Busko reported to Heartwire on

Renal Denervation’s Structural, Functional Heart Benefits May Be Independent of BP

HAMBURG, GERMANY — In a small study of patients undergoing renal denervation for resistant hypertension, left-ventricular hypertrophy and diastolic function improved independently of changes in blood pressure and heart rate [1].

“The novelty of our findings is the independence of morphologic improvements [regression of LV hypertrophy] from hemodynamic changes (reduction of blood pressure and heart rate),” Dr Stephan H Schirmer (University of Saarland, Hamburg, Germany) told heartwire in an email. “If this is confirmed in larger trials, it might open up novel indications for the use of renal denervation, for example, in [diastolic] heart-failure patients, independent of blood pressure.”

Dr Deepak L Bhatt (Harvard Medical School, Boston, MA) told heartwire that the study observations are “provocative” and “exciting” but stressed that they need to be confirmed in a blinded, larger, multicenter study before they could be accepted into clinical practice. Bhatt and Dr George Bakris (University of Chicago, IL) are co–principal investigators for the ongoing SYMPLICITY HTN-3 trial of bilateral renal denervation in patients with uncontrolled hypertension.

The study was published online December 4, 2013 in the Journal of the American College of Cardiology.

Are Renal Denervation Effects Always Tied to BP Change?

Renal denervation reduces heart rate and blood pressure in patients with resistant hypertension, and as reported by heartwire , a recent small study suggested that the procedure also reduces left-ventricular mass and improves diastolic function in such patients, Schirmer and colleagues write.

They hypothesized that renal denervation might affect cardiac structure and function, independent of the effect on blood pressure.

They enrolled 66 consecutive patients who underwent renal denervation using the Flex catheter system (Medtronic) at their center during 2010 and 2011 for treatment of resistant hypertension (office systolic blood pressure >140 mm Hg). Patients had a mean age of 64 years, and 55% were men. They were on a mean of 4.3 antihypertensive drugs. All were taking a diuretic, 89% were taking a beta-blocker, and 55% were taking an angiotensin-receptor blocker.

Six months after renal denervation,

  • Mean blood pressure decreased from 172.9/92.5 to 151.3/85.5 mm Hg, confirmed by 24-hour ambulatory monitoring, if available (n=50).
  • Mean heart rate decreased from 67.7 to 60.5 bpm.
  • Mean left-ventricular mass index decreased from 61.5 to 53.4 g/m2.
  • Measures of diastolic function also improved.

The changes in cardiac function and ventricular size were not tied to the magnitude of the blood-pressure reduction, which “suggest[s] a direct effect of the sympathetic nervous system on myocardial morphology and function,” Schirmer and colleagues write. They call for further research to investigate functional cardiovascular benefits of renal denervation beyond blood-pressure reduction.

Promising Early Benefit, Needs Confirmation

In an accompanying editorial [2], Bakris and Dr Sandeep Nathan (University of Chicago) commend Schirmer and colleagues “for providing promising early benefit of catheter-based renal denervation and for highlighting a possible blood-pressure–independent facet of this technique.” However, they caution that although the findings are “intriguing,” the study’s limitations include that it was

  • relatively small,
  • conducted at a single center,
  • lacked a sham control, and
  • relied on echocardiography rather than magnetic resonance imaging.

Therefore, “these observations need confirmation before acceptance in clinical practice . . . and can only be applied to those with inclusion criteria used in their study,” the editorialists conclude.

“It’s an exciting, provocative result, and there’s a good chance that it will stand the test of time, but I still think in general, it’s best to be cautious about new technologies and relatively small studies, because time typically shows that they provide an overestimate of what the true effects will be,” Bhatt commented when interviewed.

“Whether the reduction in left-ventricular mass is beyond what would be anticipated with blood-pressure and heart-rate reduction—certainly this analysis suggests that is a possibility—needs to be confirmed in larger studies,” he added, echoing the authors and editorialists.

Potentially referring physicians, in the United States where the procedure is investigational, and even in Europe where it’s approved, appear to be waiting for the results of SYMPLICITY HTN-3, Bhatt said. This blinded, randomized, multicenter trial will provide a clearer picture of what sort of blood-pressure reductions are achievable in patients with resistant hypertension who undergo renal denervation. Results are expected by mid-2014.

References

  1. Schirmer SH, Sayed M, Reil J-C, et al. Improvements of left-ventricular hypertrophy and diastolic function following renal denervation – Effects beyond blood pressure and heart rate reduction. J Am Coll Cardiol 2013; DOI:10.1016/j.jacc.2013.10.073. Abstract
  2. Bakris G, Nathan S. Renal denervation and left ventricular mass regression: A benefit beyond blood pressure reduction? J Am Coll Cardiol 2013; DOI:10.1016/j.jacc.2013.11.015. Editorial

SOURCE

This Open Access Scientific Journal has covered all the major developments reported on Renal Denervation since its inception

The Archive for Renal denervation

https://pharmaceuticalintelligence.com/category/cardiac-and-cardiovascular-surgical-procedures/renal-denervation/

Search Results for Renal Denervation

https://pharmaceuticalintelligence.com/?s=Renal+denervation

For the ORIGINAL work on 

Renal Sympathetic Denervation: Updates on the State of Medicine

the Readers is called to go to the ORIGINAL SOURCES listed below:

Intravascular Stimulation of Autonomics: A Letter from Dr. Michael Scherlag

https://pharmaceuticalintelligence.com/2012/09/02/intravascular-stimulation-of-autonomics-a-letter-from-dr-michael-scherlag/

Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

https://pharmaceuticalintelligence.com/2012/09/02/imbalance-of-autonomic-tone-the-promise-of-intravascular-stimulation-of-autonomics/

Interaction of Nitric Oxide and Prostacyclin in Vascular Endothelium

https://pharmaceuticalintelligence.com/2012/09/14/interaction-of-nitric-oxide-and-prostacyclin-in-vascular-endothelium/

Absorb™ Bioresorbable Vascular Scaffold: An International Launch by Abbott Laboratories

https://pharmaceuticalintelligence.com/2012/09/29/absorb-bioresorbable-vascular-scaffold-an-international-launch-by-abbott-laboratories/

The Molecular Biology of Renal Disorders: Nitric Oxide – Part III

https://pharmaceuticalintelligence.com/2012/11/26/the-molecular-biology-of-renal-disorders/

Treatment of Refractory Hypertension via Percutaneous Renal Denervation

https://pharmaceuticalintelligence.com/2012/06/13/treatment-of-refractory-hypertension-via-percutaneous-renal-denervation/

Renal Denervation Technology of Vessix Vascular, Inc. been acquired by Boston Scientific Corporation (BSX) to pay up to $425 Million

https://pharmaceuticalintelligence.com/2012/11/08/renal-denervation-technology-of-vessix-vascular-inc-been-acquired-by-boston-scientific-corporation-bsx-to-pay-up-to-425-million/

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Myocardial Infarction: The New Definition After Revascularization

Reporter: Aviva Lev-Ari, PhD, RN

 

UPDATED on 7/31/2014

Myocardial Ischemia Symptoms

Reporter: Aviva Lev-Ari, PhD, RN

https://pharmaceuticalintelligence.com/2014/07/29/myocardial-ischemia-symptoms/

 

VIEW VIDEO

Gregg Stone, MD

Co-DIrector, Medical Research & Education Division Cardiovascular Research Foundation

http://www.medpagetoday.com/Cardiology/MyocardialInfarction/42256?xid=nl_mpt_DHE_2013-10-15&goback=%2Egmr_4346921%2Egde_4346921_member_5795830612724035588#%21

Primary source: Journal of the American College of Cardiology
Source reference: Moussa I, et al “Consideration of a new definition of clinically relevant myocardial infarction after coronary revascularization: an expert consensus document from the Society for Cardiovascular Angiography and Interventions (SCAI)” J Am Coll Cardiol2013; 62: 1563-1570.

Additional source: Journal of the American College of Cardiology
Source reference:White H “Avatar of the universal definition of periprocedural myocardial infarction” J Am Coll Cardiol 2013; 62: 1571-1574.

Moussa reported that he had no conflicts of interest.

Stone is a consultant for Boston Scientific, Eli Lilly, Daiichi Sankyo, and AstraZeneca. The other authors reported relationships with Guerbet, The Medicines Company, Bristol-Myers Squibb/Sanofi, Merck, Maya Medical, AstraZeneca, Abbott Vascular, Regado Biosciences, Janssen Pharma, Lilly/Daiichi Sankyo, St. Jude Medical, Medtronic, Terumo, Bridgepoint/Boston Scientific, Gilead, Boston Scientific, Eli Lilly, and Daiichi Sankyo.

White is co-chairman for the Task Force for the Universal Definiton of Myocardial Infarction; has received research grants from sanofi-aventis, Eli Lilly, The Medicines Company, the NIH, Pfizer, Roche, Johnson & Johnson, Schering-Plough, Merck Sharpe & Dohme, AstraZeneca, GlaxoSmithKline, Daiichi Sankyo Pharma Development, and Bristol-Myers Squibb; and has served on advisory boards for AstraZeneca, Merck Sharpe & Dohme, Roche, and Regado Biosciences.

WASHINGTON, DC — A “clinically meaningful” definition of MI following PCI or CABG is urgently needed to replace the arbitrarily chosen “universal definition” proposed in recent years that has no relevance to patients and may be muddying clinical-trial results. Those are the conclusions of a new expert consensus document released Monday by the Society of Cardiovascular Angiography and Interventions (SCAI)[1].

The notion of a “universal definition of MI” was first proposed in 2000 and updated in 2007 and 2012. The 2012 document defines a PCI-related MI as an increase in cardiac troponin (cTn) of more than five times the upper limit of normal (ULN) during the first 48 hours postprocedure plus specific clinical or ECG features. Post-CABG, the definition is a cTn increase of >10 times the ULN, plus different clinical or ECG features.

The problem, lead author Dr Issam Moussa (Mayo Clinic, Jacksonville, FL) told heartwire , is that these cutoffs were arbitrarily chosen and not based on any hard evidence that these biomarker levels spelled a poor prognosis. Moreover, “overnight, the rate of MI went from 5% following these procedures to 20% to 30%!” he said.

The SCAI committee, in its new document, focuses on post-PCI procedures and highlights the importance of acquiring baseline cardiac biomarkers and differentiating between patients with elevated baseline CK-MB (or cTn) in whom biomarker levels are stable or falling, as well as those in whom it hasn’t been established whether biomarkers are changing.

SCAI’s Proposed Clinically Meaningful MI Definitions

Group Definition
Normal baseline CK-MB CK-MB rise of >10x ULN or >5x ULN with new pathologic Q-waves in at least 2 contiguous leads or new persistent left bundle branch block
OR
In the absence of baseline CK-MB, a cTn rise of >70x ULN or a rise of>35 ULN plus new pathologic Q-waves in at least 2 contiguous leads or new persistent left bundle branch block
Elevated baseline biomarkers that are stable or falling A CK-MB or cTn rise that is equal (by an absolute increment) to the definitions described for patients with normal CK-MB at baseline.
Elevated baseline biomarkers that have not been shown to be stable or falling A CK-MB or cTn rise that is equal (by an absolute increment) to the definitions described for patients with normal CK-MB at baseline
Plus
New ST-segment elevation or depression
Plus
New-onset or worsening heart failure or sustained hypotension or other signs of a clinically relevant MI.

Moussa is quick to emphasize that these new clinically meaningful definitions have limited evidence to support them—and most of what exists supports CK-MB definitions, not cTn—but that the new document is based on the best scientific evidence available.

“We don’t want to come out with a definitive statement” saying this is the final word on MI definitions,” he stressed. “There is more science that needs to be done and there remains more uncertainty. We framed this to be inclusive and also to open the field for discussion.”

His hope is that this will lead to important changes in how patients are managed and money is spent. Currently, patients with clinically meaningless biomarker elevations may become unnecessarily panicked over news that they’ve had a “heart attack,” while hospital stays may be extended and further tests ordered on the basis of these results.

Moussa et al’s proposal also has important implications for clinical trials, he continued. Currently, for studies that include periprocedural MIs as an individual end point or as part of a composite end point, the very high number of biomarker-defined “MIs” collected in the trial could potentially overwhelm the true impact of any given therapy. “You are really using an end point that is truly not relevant to patients. . . . This could really affect the whole hypothesis.”

He’s expecting some push-back from cardiologists and academics, particularly those who championed the need for the universal definition in the first place, but believes most people will welcome a clinically meaningful definition.

“I think many in the medical community will accept this because they have not really been using the universal definition in their day-to-day practice anyhow.” What’s more, the National Cardiovascular Data Registry (NCDR) does not include the reporting of MI postangiography, in part because of concerns that the universal definition of MI overestimates the true incidence of this problem. “I think many in the community will look at this definition as more reflective of the true incidence of MI after angioplasty, and if it’s accepted, they are more likely to report it to databases like NCDR and use it to reflect quality-of-care processes.”

http://www.medscape.com/viewarticle/812533?nlid=35983_2105&src=wnl_edit_medp_card&uac=93761AJ&spon=2

  • ESC/ACCF/AHA/WHF Expert Consensus Document

Circulation.2012; 126: 2020-2035  Published online before print August 24, 2012,doi: 10.1161/​CIR.0b013e31826e1058

Third Universal Definition of Myocardial Infarction

  1. Kristian Thygesen;
  2. Joseph S. Alpert;
  3. Allan S. Jaffe;
  4. Maarten L. Simoons;
  5. Bernard R. Chaitman;
  6. Harvey D. White
  7. the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction
  1. *Corresponding authors/co-chairpersons: Professor Kristian Thygesen, Department of Cardiology, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark. Tel: +45 7846-7614; fax: +45 7846-7619: E-mail: kristhyg@rm.dk. Professor Joseph S. Alpert, Department of Medicine, Univ. of Arizona College of Medicine, 1501 N. Campbell Ave., P.O. Box 245037, Tucson AZ 85724, USA, Tel: +1 520 626 2763, Fax: +1 520 626 0967, E-mail: jalpert@email.arizona.edu. Professor Harvey D. White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, 1030 Auckland, New Zealand. Tel: +64 9 630 9992, Fax: +64 9 630 9915, E-mail: harveyw@adhb.govt.nz.

Table of Contents

  • Abbreviations and Acronyms. . . . . . . . . . . . . . . . . . . .2021

  • Definition of Myocardial Infarction. . . . . . . . . . . . . . .2022

  • Criteria for Acute Myocardial Infarction. . . . . . . . . . . .2022

  • Criteria for Prior Myocardial Infarction. . . . . . . . . . . .2022

  • Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2022

  • Pathological Characteristics of Myocardial Ischaemia and Infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2023

  • Biomarker Detection of Myocardial Injury With Necrosis. . .2023

  • Clinical Features of Myocardial Ischaemia and Infarction. . .2024

  • Clinical Classification of Myocardial Infarction. . . .2024
    • Spontaneous Myocardial Infarction (MI Type 1). . . .2024

    • Myocardial Infarction Secondary to an Ischaemic Imbalance (MI Type 2). . . . . . . . . . . . . . . . . . . . . . . .2024

    • Cardiac Death Due to Myocardial Infarction (MI Type 3). .2025

    • Myocardial Infarction Associated With Revascularization Procedures (MI Types 4 and 5). . . . . . . . . . . . . . . . . . …

New Definition for MI After Revascularization

Published: Oct 14, 2013 | Updated: Oct 15, 2013

By Todd Neale, Senior Staff Writer, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

The Society for Cardiovascular Angiography and Interventions (SCAI) has released a new definition for myocardial infarction (MI) following coronary revascularization aimed at identifying only those events likely to be related to poorer patient outcomes.

In the new criteria — published as an expert consensus document inCatheterization and Cardiovascular Interventions and the Journal of the American College of Cardiology — creatine kinase-myocardial band (CK-MB) is the preferred cardiac biomarker over troponin, and much greater elevations are required to define a clinically relevant MI compared with the universal definition of MI proposed in 2007 and revised in 2012.

Also, the new definition uses the same biomarker elevation thresholds to identify MIs following both percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), whereas the universal definition has different thresholds for events following the two procedures.

“What we’ve really tried to emphasize in this classification scheme is the primary link between biomarker elevations and prognosis,” according to Gregg Stone, MD, of Columbia University Medical Center and the Cardiovascular Research Foundation in New York City, one of the authors of the document.

“In the universal definition of MI, they even acknowledged that their criteria were arbitrary,” Stone said in an interview. “We’ve tried to reduce the arbitrariness of the cutoff values that we selected so that the researcher, academician, clinician, hospital administrator, etc., can be confident that these levels that we’re recommending are the ones that are associated with a worse prognosis for patients suffering periprocedural complications.”

The Change

The existing universal definition for MI defines events following PCI according to an increase in cardiac troponin to greater than five times the 99th percentile upper reference limit (URL) within 48 hours when baseline levels are normal, with confirmation by electrocardiogram (ECG), imaging, or symptoms.

For CABG-related MI, the increase must be more than 10 times the 99th percentile URL within 48 hours when baseline levels are normal, with confirmation by ECG, angiography, or imaging.

But, Stone and colleagues wrote, the relationship between that degree of troponin elevation after a revascularization procedure and prognosis is not as strong as the association between a CK-MB elevation and patient outcomes.

Using a small elevation in troponin to define a post-procedure MI could find myocardial necrosis that is unlikely to be associated with poor clinical outcomes, which could have far-reaching implications, they wrote.

“Widespread adoption of an MI definition not clearly linked to subsequent adverse events such as mortality or heart failure may have serious consequences for the appropriate assessment of devices and therapies, may affect clinical care pathways, and may result in misinterpretation of physician competence,” they wrote.

To address that issue, the expert panel convened by SCAI sought to define clinically relevant MI after PCI or CABG.

A clinically relevant MI is defined in the new document based on an increase of at least 10 times the upper limit of normal in the level of CK-MB within 48 hours after a revascularization procedure when baseline levels are normal.

When the CK-MB level is not available, then an increase in troponin I or T of at least 70 times the upper limit of normal can be used to define a clinically relevant MI, according to the authors.

However, if an ECG shows new pathologic Q-waves in at least two contiguous leads or a new persistent left bundle branch block, then the thresholds can be lowered to at least five times and at least 35 times the upper limit of normal for CK-MB and troponin, respectively.

Further guidance is provided for identifying clinically relevant post-procedure MIs when the cardiac biomarker levels are elevated at baseline.

Dueling Definitions

Co-chairman of the Task Force for the Universal Definition of Myocardial Infarction, Harvey White, DSc, of Auckland City Hospital in Auckland, New Zealand, noted some limitations of the new definition, including the lack of a requirement for ischemic symptoms.

“Ischemic symptoms have always been a basic tenet of the diagnosis of MI, and it should be no different for a [PCI-related] MI,” he wrote in an accompanying editorial.

In addition, with the use of such large elevations in biomarker levels in the new definition, “there will be very few PCI-related events identified, and an opportunity to improve patient outcomes may be lost,” he wrote.

Troponin should remain the preferred biomarker over CK-MB, White argued, pointing to variability in and analytical issues with CK-MB assays, the need for sex-specific cutoffs for CK-MB levels, the need for higher thresholds of CK-MB to determine abnormalities because all individuals have circulating levels of the biomarker, and the reduced sensitivity and specificity of CK-MB.

Also, he said, CK-MB is becoming increasingly unavailable at medical centers.

“With CK-MB becoming obsolete, troponin will become the gold standard, and CK-MB will no longer have a role in defining PCI injury and infarction in clinical practice,” White wrote.

Stone admitted that troponin ultimately might be preferable to CK-MB because of its greater specificity, although the evidence does not yet support it.

“I think there’s a general desirability to move to troponins, although when you look at the data that’s out there it’s much stronger correlating CK-MB elevations to subsequent prognosis,” he said. “I think a lot of the troponin elevations are just noise or troponins are just too sensitive.”

Room for Both?

White noted in his editorial that “the rationale for the SCAI definition has been well articulated by its authors and may be appropriate in an individual trial, but it should not supplant the universal definition of MI,” he wrote.

When asked whether the new definition would replace the universal definition, Stone said there is a place for both sets of criteria.

“We would propose the clinically relevant definition be the one that is used to make most substantial decisions right now, [such as] trade-offs between efficacy and safety for new drugs and devices, in judging hospital systems and physicians, etc.,” he said. “But I do think there’s value in both, and they will both continue to evolve over time as new data becomes evident.”

http://www.medpagetoday.com/Cardiology/MyocardialInfarction/42256?xid=nl_mpt_DHE_2013-10-15&goback=%2Egmr_4346921%2Egde_4346921_member_5795830612724035588#%21 

Articles citing 

Third Universal Definition of Myocardial Infarction

  • Improved long-term clinical outcomes in patients with ST-elevation myocardial infarction undergoing remote ischaemic conditioning as an adjunct to primary percutaneous coronary interventionEur Heart J. 2013;0:eht369v1-eht369

  • The role of myeloperoxidase (MPO) for prognostic evaluation in sensitive cardiac troponin I negative chest pain patients in the emergency departmentEuropean Heart Journal: Acute Cardiovascular Care. 2013;2:203-210,
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Read Full Post »


Pacemakers, Implantable Cardioverter Defibrillators (ICD) and Cardiac Resynchronization Therapy (CRT)

Curators: Justin D Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN

Updated on 2/16/2015

Mild, non-ischemic heart failure might be more deadly than thought, an Austrian group found, calling for broader ICD use.

SOURCE

http://www.medpagetoday.com/Cardiology/Strokes/50048?isalert=1&uun=g99985d3527R5099207u&utm_source=breaking-news&utm_medium=email&utm_campaign=breaking-news&xid=NL_breakingnews_2015-02-16

 

The voice of our Series A Content Consultant: Justin D Pearlman, MD, PhD, FACC

Pacemakers place one or more wires into heart muscle to trigger electro-mechanically coupled contraction. A single wire to the right atrium is called an AAI pacemaker (atrial sensing, atrial triggering, inhibit triggering if sensed). A single wire to the right ventricle is called a VVI pacemaker (ventricular sensing, ventricular triggering, inhibit if sensed). With two wires to the heart more combinations are possible, including atrial-ventricular sequential activation, a closer mimic to normal function (DDDR pacemaker: dual sensing, dual triggering, dual functions, and rate-responsive to mimic exercise adjustment of heart rate). Three wires are used for synchronization: one to the right atrium, one to the right ventricle apex, and a third lead into a distal branch of the coronary sinus to activate the far side of the left ventricle. Resynchronization is used to compensate for a dilated ventricle, especially one with conduction delays, where the timing of activation is so unbalanced that the heart contraction approaches a wobbling motion rather than a well coordinated contraction. Adjusting timing of activation of the right ventricle and left ventricle can offset dysynchrony (unbalanced timing) and thereby increase the amount of blood ejected by each heart beat contraction (ejection fraction). Patients with dilated cardiomyopathy and significant conduction delays can improve the ejection fraction by 10 or more percentage points, which offers a significant improvement in exertion tolerance and heart failure symptoms.

Patients with ejection fraction below 35%, among others, have an elevated risk of life-ending arrhythmias such as ventricular tachycardia. Ventricular tachycardia is an extreme example of a wobbling heart in which the electrical activation sequence circles around the heart sequentially activating a portion and blocking its ability to respond until the electric signal comes around again. Whenever a portion of the heart is activated, ions shift location, and further activation of that region is not possible until sufficient time passes so that the compartmentalized ion concentrations can be restored (repolarization). Pacing can interrupt ventricular tachycardia by depolarizing a region that supported the circular activation pattern. Failing that, an electric shock can stop an ineffective rhythm. After all regions stop activation, they will generally reactivate in the normal pulsatile synchronous manner. An implanted cardiac defibrillator is a device designed to apply an internal electric shock to pause all activation and thereby interrupt ventricular tachycardia.
UPDATED on 12/31/2013

Published on Friday, 27 December 2013

S-ICD – Subcutaneous Implantable Cardioverter Defibrillator – Boston Scientific

Boston Scientific Subcutaneous Implantable Cardiodefibrillator Device S-ICD

S-ICD – Subcutaneous Implantable Cardioverter Defibrillator – Boston Scientific

Boston Scientific Subcutaneous Implantable Cardiodefibrillator Device S-ICD

‘Regular’ Pacemaker/ICD with Leads and a ‘Can’
When we think of Pacemakers and ICD’s we naturally think of a ‘Can’ and Leads that track down into the heart. Whilst these devices work fantastically well and will continue to do so. Unfortunately the ‘lead’ part of the device opens the door for a few complications to possibly arise. Those who have a Pacemaker or ICD will probably be familiar with concerns over;
  1. Systemic Infection – Infections travelling down the Leads into the Heart
  2. Lead Displacement – The Lead moving away from the heart tissue and thus becoming pretty useless.
  3. Vascular/Organ Injury – Damage to the blood vessels being used for access or perforation of heart wall.
  4. Pneumothorax (damage to the lining around the Lung), Haemothorax (build up of blood in the chest cavity), and air embolism (air bubble trapped in a blood vessel).
These complications are one of the key motivations behind developing ‘leadless’ devices the first of which the St Jude Nanostim, a small VVI Pacemaker that fits directly into the heart.
Another device to address these issues is the Boston Scientific S-ICD

What is the Boston Scientific S-ICD?

The S-ICD is what is sometimes referred to as a ‘shock box’ it does not have the pacemaker functionality that many other ICD’s do have. It is ONLY there to terminate dangerous Arrhythmias.
*It does not have the pacing functionality of traditional ICD‘s because it DOES NOT HAVE A LEAD THAT ENTERS THE HEART.*
It is not a Pacemaker!
 
Without the lead(s) ENTERING the heart via a blood vessel there is a reduction in the risks mentioned previously that are associated traditional device. Another of the benefits is that the S-ICD is positioned and implanted using anatomical landmarks (visible parts of your body) and not Fluoroscopy (video X-Ray) which reduces radiation exposure to the patient.

Positioning of the S-ICD.

Boston Scientific Subcutaneous Implantable Cardiodefibrillator Device S-ICD

The ‘Can‘ (metal box that contains all the circuitry and battery), is buried under the skin on the outside of the ribs. Put your arms down by your sides, the device would go where your ribs meet the middle of your bicep. A lead is then run under the skin to the centre of your chest where its is anchored and then north, under the skin again until the tip of the lead is roughly at the top of the sternum.
For you physicians out there the ‘can’ is positioned at the mid-axillary line between the 5th and 6th intercostal spaces, the lead is then tunnelled to a small Xiphoid incision and then tunnelled north to a superior incision.

How is an S-ICD Implanted?

VIEW VIDEO
Having spoken to Boston Scientific it is becoming more apparent that the superior incision (cut at the top of the chest) may actually be removed from the procedure guidance as simply tunnelling the lead and ‘wedging’ the tip at that point is satisfactory – THIS IS NOT CONFIRMED AT THE MOMENT AND IS THEREFORE NOT PROCEDURE ADVICE.
Boston Scientific Subcutaneous Implantable Cardiodefibrillator Device S-ICD
Image Courtesy of
http://www.bostonscientific.com/

How does the S-ICD Work?

A ‘Shock Box’ basically needs to do 2 things. Firstly be able to SENSE if the heart has entered a Dangerous Arrhythmia and Secondly, be able to treat it.
The treatment part of the functionality is the easy bit – it delivers an electric shock across a ‘circuit’ that involves a large amount of the tissue in the heart. The lead has two ‘electrodes’ and the ‘Can’ is a third electrode allowing you different shocking ‘vectors’. By vectors we mean directions and area through which the electricity travels during a shock. This gives us extra options when implanting a device as some vectors will work better than others for the treatment of dangerous arrhythmias.

Shocking Vectors?

This is a concept you are familiar with without even thinking about it… when you are watching ER or another TV program and they Defibrillate the patient using the metal paddles, where do they position them? One either side of the heart? Precisely!! this is creating a ‘vector’ across the heart to involve the cardiac tissue. The paddles would be a lot less effective if you put one on the knee and one on the foot!

Boston Scientific Subcutaneous Implantable Cardiodefibrillator Device S-ICD

Now because the ‘Vectors’ used by the S-ICD are over a larger area than those with a traditional device – more energy has to be delivered to have the same desired affect. The upshot of this is that a larger battery is required to deliver the 80J! Bigger Battery = Bigger Box. This image shows a demo device but this is the exact size compared to a One Pound Coin! Now yes it is big but because of the extra room where they place the device it is pretty discrete and hidden in even slender patients.
STAT ATTACK!
The S-ICD System delivers up to 5 shocks per episode at 80 J with up to 128 seconds of ECG storage per episode and storage of up to 45 episodes.
The heart rate that the S-ICD is told to deliver therapy is programable between 170 and 250 bpm. Quite cleverly the device is able to also deliver a small amount of ‘pacing’ after a shock, when the heart can often run slowly. This is external pacing and will be felt!! It can run for 30s.

Sensing in an S-ICD.

 
The S-ICD uses its electrodes to produce an ECG similar to a surface ECG. 
 
Now the Sensing functionality is the devices ability to determine what Rhythm the heart is in! Without a lead in the heart to give us really accurate information the device is using a large area of heart, ribs and muscle. This means there is more potential for ‘artefact’. Artefact is the electrical interference and confusion – that could potentially lead to a patient being shocked when they do not require it – or not being shocked when they do…
Boston Scientific have come up with a very clever software/algorithm called ‘Insight’. Insight uses 3 separate methods to determine the nature of a heart rhythm.
  • Normal Sinus Rhythm Template (Do your heart beats look as they should)
  • Dynamic Morphology Analysis (A live comparison of heart beat to previous heart beat, do they all look the same or do they keep changing?)
  • QRS Width analysis (Are the tall ‘peaks’ on your ECG, the QRS’, wider than they normally are?)
These questions (with some very complex maths) and the rate of a rhythm are used to decide whether to ‘shock’ or not.
Insight Algorithm S-ICD

Image Courtesy of  http://www.bostonscientific.com/

How does Insight and the S-ICD compare to other ICD Devices?

The statistics for treatment success and inappropriate shocks (an electrocuted patient that did not need to be) actually compare very similarly if not favourably compared to other devices on the market – these two studies are well worth a read if you have the time 🙂
1. Burke M, et al. Safety and Efficacy of a Subcutaneous Implantable-Debrillator (S-ICD System US IDE Study). Late-Breaking Abstract Session. HRS 2012.
2. Lambiase PD, et al. International Experience with a Subcutaneous ICD; Preliminary Results of the EFFORTLESS S-ICD Registry. Cardiostim 2012.
3. Gold MR, et al. Head-to-head comparison of arrhythmia discrimination performance of subcutaneous and transvenous ICD arrhythmia detection algorithms: the START study. J Cardiovasc Electrophysiol. 2012;23;4:359-366.
Who qualifies?
Template S-ICD Eligibility

Template used to assess eligibility!
Image Courtesy of
http://www.bostonscientific.com/
Well essentially anyone who qualifies for a normal ‘shock box’ ICD but with one other requirement. The Insight Software requires that a person has certain characteristics on their ECG. This is essentially showing that they have tall enough and narrow enough complexes to allow the algorithm to perform effectively. A simple 12 lead ECG Laying and Standing will be obtained and then a ‘Stencil’ is passed over the Print out – If the complexes fit within the boundaries marked on the ‘stencil’ then you potentially qualify. If your ECG does not meet requirements then it will not be recommended for you to have the S-ICD.

There you have it a quick overview of the Boston Scientific S-ICD.

Thanks for Reading

Cardiac Technician

SOURCE

http://www.thepad.pm/2013/12/boston-scientific-s-icd.html#!

UPDATED on 10/15/2013

Frequency and Determinants of Implantable Cardioverter Defibrillator Deployment Among Primary Prevention Candidates With Subsequent Sudden Cardiac Arrest in the Community

  1. Kumar Narayanan, MD;
  2. Kyndaron Reinier, PhD;
  3. Audrey Uy-Evanado, MD;
  4. Carmen Teodorescu, MD, PhD;
  5. Harpriya Chugh, BS;
  6. Eloi Marijon, MD;
  7. Karen Gunson, MD;
  8. Jonathan Jui, MD, MPH;
  9. Sumeet S. Chugh, MD

+Author Affiliations


  1. From The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (K.N., K.R., A.U.-E., C.T., H.C., E.M., S.S.C.); and Departments of Pathology (K.G.) and Emergency Medicine (J.J.), Oregon Health and Science University, Portland, OR.
  1. Correspondence to Sumeet S. Chugh, MD, Cedars-Sinai Medical Center, The Heart Institute, AHSP Suite A3100, 127 S. San Vicente Blvd., Los Angeles, CA 90048, Los Angeles, CA 90048. E-mail sumeet.chugh@cshs.org

Abstract

Background—The prevalence rates and influencing factors for deployment of primary prevention implantable cardioverter defibrillators (ICDs) among subjects who eventually experience sudden cardiac arrest in the general population have not been evaluated.

Methods and Results—Cases of adult sudden cardiac arrest with echocardiographic evaluation before the event were identified from the ongoing Oregon Sudden Unexpected Death Study (population approximately 1 million). Eligibility for primary ICD implantation was determined from medical records based on established guidelines. The frequency of prior primary ICD implantation in eligible subjects was evaluated, and ICD nonrecipients were characterized. Of 2093 cases (2003–2012), 448 had appropriate pre– sudden cardiac arrest left ventricular ejection fraction information available. Of these, 92 (20.5%) were eligible for primary ICD implantation, 304 (67.9%) were ineligible because of left ventricular ejection fraction >35%, and the remainder (52, 11.6%) had left ventricular ejection fraction ≤35% but were ineligible on the basis of clinical guideline criteria. Among eligible subjects, only 12 (13.0%; 95% confidence interval, 6.1%–19.9%) received a primary ICD. Compared with recipients, primary ICD nonrecipients were older (age at ejection fraction assessment, 67.1±13.6 versus 58.5±14.8 years, P=0.05), with 20% aged ≥80 years (versus 0% among recipients, P=0.11). Additionally, a subgroup (26%) had either a clinical history of dementia or were undergoing chronic dialysis.

Conclusions—Only one fifth of the sudden cardiac arrest cases in the community were eligible for a primary prevention ICD before the event, but among these, a small proportion (13%) were actually implanted. Although older age and comorbidity may explain nondeployment in a subgroup of these cases, other determinants such as socioeconomic factors, health insurance, patient preference, and clinical practice patterns warrant further detailed investigation.

Key Words:

  • Received March 11, 2013.
  • Accepted August 21, 2013

http://circ.ahajournals.org/content/128/16/1733.abstract

UPDATED on 9/15/2013

based on 9/6/2013 Trials and Fibrillations — The Heart.org

http://www.theheart.org/columns/trials-and-fibrillations-with-dr-john-mandrola/new-post-39.do#!

Echo-CRT trial: Most important study released at ESC 2013

Cardiac resynchronization therapy (CRT) is a multilead pacing device that can extend lives and improve the quality of life of selected patients who suffer from reduced performance of the heart due to adverse timing of contraction (wobbling motion from conduction delays that cause asynchrony or  delayed activation of one portion of the left ventricle compared to others reducing net blood ejection).

The degree of benefit in CRT responders depends not only on the degree of asynchrony, but also on the delayed activity location in relation to the available locations for lead placement. CRT is an adjustment in the timing of muscle activiation to improve the concerted impact on blood ejection. Only patients likely to improve should be exposed to the risks and costs of CRT.

The Echo-CRT trial, presented September 3, 2013 at the European Society of Cardiology (ESC) 2013 Congressand simultaneously published in the New England Journal of Medicine, helps identify which patients may benefit from CRT devices. (See Steve Stiles’ report on heartwire),

Echo-CRT trial summary

Background is important

Previous CRT studies enrolled patients with QRS duration >120 or >130 ms for synchronizing biventricular pacing. Additional work confirmed the greatest benefit occurred in patients with QRS durations >150 ms and typical left bundle branch block (LBBB). Conflicting observational and small randomized trials were less clear for patients with shorter QRS durations—the majority of heart-failure patients. What’s more, most cardiologists have seen patients with “modest” QRS durations respond to CRT. In theory, wide QRS is only expected if the axis of significant delay projects onto the standard ECG views, whereas significant opportunity for benefit can be missed if the axis of significant delay is not wide in the standard views. CRT implanters have heard of patients with normal-duration QRS where echo shows marked dyssynchrony. This raised the  question: Are there CHF patients with mechanical dyssynchrony (determined by echo) but no electrical delay (as measured by the ECG) benefit from CRT?Unfortunately, echo does not resolve the issue either. Thus there is the residual question of who should be evaluated by a true 3D syncrhony assessment by cardiac MRI.

Echocardiographic techniques held promise to identify mechanical dyssynchrony, but like the standard 12 lead ECG, they also utilize limited orientations of views of the heart and hence the directions in which delays can be detected. Cardiac MRI Research (not limited in view angle) by JDPearlman showed that the axis of maximal delay in patients with asynchrony is within 30 degrees of the ECG and echo views in a majority of patients with asynchrony, but it can be 70-110 degrees away from the views used by echocardiography and by ECG in 20% of cases. Hence some patients who may benefit can be missed by ECG or Echo criteria.

Methodology

Echo-CRT was an industry-sponsored (Biotronik) investigator-initiated prospective international randomized controlled trial. All patients had mechanical dyssynchrony by echo, QRS <130 ms, and an ICD indication. CRT-D devices were implanted in all patients. Blinded randomization to CRT-on (404 patients) vs CRT-off (405 patients) was performed after implantation. Programming in the CRT-off group was set to minimize RV pacing. The primary outcome was a composite of all-cause mortality or hospitalization.

Six key findings

1. Although entry criteria for the trial was a QRS duration <130 ms, the mean QRS duration of both groups was 105 ms.

2. The data safety monitoring board terminated the trial prematurely because of an increased death rate in the CRT group.

3. No differences were noted in the primary outcome.

4. More patients died in the CRT group (hazard ratio=1.8).

5. The higher death rate in the CRT group was driven by cardiovascular death.

6. More patients in the CRT group were hospitalized, due primarily to device-related issues.

These findings send clear and simple messages to all involved with treating patients with heart failure. My interpretation of Echo-CRT is as follows:

Do not implant CRT devices in patients with “narrow” QRS complexes.

The signal of increased death was strong. A hazard ratio of 1.8 translates to an almost doubling of the risk of death. This finding is unlikely to be a statistical anomaly, as it was driven by CV death. The risks of CRT in nonresponders are well-known and include: increased RV pacing, possible proarrhythmia from LV pacing, and the need for more device-related surgery. Patients who do not respond to CRT get none of the benefits but all the potential harms—an unfavorable ratio indeed.

Echo is not useful for assessing dyssynchrony in patients with narrow QRS complexes.

Dr Samuel Asirvatham explains the concept of electropathy in a review article in the Journal of Cardiovascular Electrophysiology. He teaches us that the later the LV lateral wall is activated relative to the RV, the more the benefit of preexciting the lateral wall with an LV lead. That’s why the benefit from CRT in many cases increases with QRS duration, because—in a majority—a wide QRS means late activation of the lateral LV.

Simple triumphs over complicated—CRT response best estimated with the old-fashioned ECG.

In a right bundle branch block, the left ventricle is activated first; in LBBB, the LV lateral wall is last, and with a nonspecific ICD, there’s delayed conduction in either the His-Purkinje system or in ventricular muscle. What does a normal QRS say? It says the wave front of activation as projected onto the electric views obtained activates the LV and RV simultaneously. If those views capture the worst delay then they can eliminate the  need for resynchrony.

CRT benefit with mild-moderate QRS prolongation still not settled

Dr Robert Myerburg (here and here) teaches us to make a distinction between trial entry criteria and the actual values of the cohort.

Consider how this applies to QRS duration:  COMPANION and CARE-HF are clinical trials that showed definitive CRT benefit. Entry required a QRS duration >120 ms (130 ms in CARE-HF). But the actual mean QRS duration of enrolled patients was 160 ms. A meta-analysis of CRT trials confirmed benefit at longer QRS durations and questioned it below 150 ms. CRT guideline recommendations incorporate study entry criteria, not the mean values of actual patients in the trial. Patients enrolled in Echo-CRT had very narrow QRS complexes (105 ms). What to recommend in the common situation when a patient with a typical LBBB has a QRS duration straddling 130 ms is not entirely clear. The results of Echo-CRT might have been different had the actual QRS duration values been closer to 130 ms.

Conclusion

Echo-CRT study reinforces expectations based on cardiac physiology. In the practice of medicine, it’s quite useful to know when not to do something.

The trial should not dampen enthusiasm for CRT. Rather, it should focus our attention to patient selection—and the value of the 12-lead ECG.

 References

Rethinking QRS Duration as an Indication for CRT

SMITA MEHTA M.D.1 and SAMUEL J. ASIRVATHAM M.D., F.A.C.C.2,3

Author Information

  1. Department of Pediatric Cardiology, Cleveland Clinic, Cleveland, Ohio, USA
  2. Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
  3. Department of Pediatrics and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota, USA

*Samuel J. Asirvatham, M.D., Division of Cardiovascular Diseases, Department of Internal Medicine and Division of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. E-mail: asirvatham.samuel@mayo.edu

J Cardiovasc Electrophysiol, Vol. 23, pp. 169-171, February 2012.

http://onlinelibrary.wiley.com/doi/10.1111/j.1540-8167.2011.02163.x/full

Indications for Implantable Cardioverter-Defibrillators Based on Evidence and Judgment FREE

Robert J. Myerburg, MD; Vivek Reddy, MD; Agustin Castellanos, MD
J Am Coll Cardiol. 2009;54(9):747-763. doi:10.1016/j.jacc.2009.03.078

Implantable Cardioverter–Defibrillators after Myocardial Infarction

Robert J. Myerburg, M.D.

Division of Cardiology, University of Miami Miller School of Medicine, Miami.

N Engl J Med 2008; 359:2245-2253 November 20, 2008DOI: 10.1056/NEJMra0803409

END OF UPDATE

Electrical conduction of the Human Heart

  • Physiology and
  • Genetics

were explained by us in the following articles:

Genetics of Conduction Disease: Atrioventricular (AV) Conduction Disease (block): Gene Mutations – Transcription, Excitability, and Energy Homeostasis

On Devices and On Algorithms: Prediction of Arrhythmia after Cardiac Surgery and ECG Prediction of an Onset of Paroxysmal Atrial Fibrillation

Dilated Cardiomyopathy: Decisions on implantable cardioverter-defibrillators (ICDs) using left ventricular ejection fraction (LVEF)

Reduction in Inappropriate Therapy and Mortality through ICD Programming

Below, we present the following complementary topics:

Options for Cardiac Resynchronization Therapy (CRT) to Arrhythmias:

  • Implantable Pacemaker
  • Insertable Programmable Cardioverter Defibrillator (ICD)

UPDATED 8/6/2013

Medtronic Pacemaker Recall

 

17/07/2013

Australia’s regulatory authority, the Therapeutic Goods Administration (TGA) has issued a hazard alert pertaining to one of Medtronic’s pacing devices, the Consulta® Cardiac Resynchronization Therapy Pacemaker (CRT-P). The alert coincides somewhat with Medtronic’s own issuance of a field safety notice concerning Consulta and Syncra® CRT-P devices.

Background

Consulta and Syncra CRT-Ps are implantable medical devices used to treat heart failure. The devices provide pacing to help coordinate the heart’s pumping action and improve blood flow.

The two devices are the subject of a global manufacturer recall after Medtronic had identified an issue with a subset of both during production, although as yet there had been no reported or confirmed device failures. However, because of the potential for malfunction, Medtronic is requiring the return of non-implanted devices manufactured between April 1 and May 13, 2013 for re-inspection.

Seemingly this manufacturing issue could compromise the sealing of the device. Should an out-of-spec weld fail this could result in body fluids entering the device, which could cause it to malfunction leading to loss of pacing output. This could potentially see the return of symptoms including

  • fainting or lightheadedness,
  • dyspnoea (shortness of breath),
  • fatigue and
  • oedema.

Medtronic’s recall is thought to relate to 265 devices, 44 of which have been implanted in the US.

The Australian warning letter, issued by the TGA states that only one “at risk” Consulta CRT-P device has been implanted in the country and there have been no reports of device failures or patient injuries relating to this issue.

Neither Medtronic nor the TGA are suggesting any specific patient management measures other than routine follow-up in accordance with labelling instructions.

Pacemaker/Implantable Cardioverter Defibrillator (ICD) Insertion

Procedure Overview

What is a pacemaker/implantable cardioverter defibrillator (ICD) insertion?

A pacemaker/implantable cardioverter defibrillator (ICD) insertion is a procedure in which a pacemaker and/or an ICD is inserted to assist in regulating problems with the heart rate (pacemaker) or heart rhythm (ICD).

Pacemaker

When a problem develops with the heart’s rhythm, such as a slow rhythm, a pacemaker may be selected for treatment. A pacemaker is a small electronic device composed of three parts: a generator, one or more leads, and an electrode on each lead. A pacemaker signals the heart to beat when the heartbeat is too slow.

Illustration of a single-chamber pacemaker
Click Image to Enlarge

A generator is the “brain” of the pacemaker device. It is a small metal case that contains electronic circuitry and a battery. The lead (or leads) is an insulated wire that is connected to the generator on one end, with the other end placed inside one of the heart’s chambers.

The electrode on the end of the lead touches the heart wall. In most pacemakers, the lead senses the heart’s electrical activity. This information is relayed to the generator by the lead.

If the heart’s rate is slower than the programmed limit, an electrical impulse is sent through the lead to the electrode and the pacemaker’s electrical impulse causes the heart to beat at a faster rate.

When the heart is beating at a rate faster than the programmed limit, the pacemaker will monitor the heart rate, but will not pace. No electrical impulses will be sent to the heart unless the heart’s natural rate falls below the pacemaker’s low limit.

Pacemaker leads may be positioned in the atrium or ventricle or both, depending on the condition requiring the pacemaker to be inserted. An atrial dysrhythmia/arrhythmia (an abnormal heart rhythm caused by a dysfunction of the sinus node or the development of another atrial pacemaker within the heart tissue that takes over the function of the sinus node) may be treated with an atrial pacemaker.

Illustration of a dual-chamber pacemaker
Click Image to Enlarge

A ventricular dysrhythmia/arrhythmia (an abnormal heart rhythm caused by a dysfunction of the sinus node, an interruption in the conduction pathways, or the development of another pacemaker within the heart tissue that takes over the function of the sinus node) may be treated with a ventricular pacemaker whose lead wire is located in the ventricle.

It is possible to have both atrial and ventricular dysrhythmias, and there are pacemakers that have lead wires positioned in both the atrium and the ventricle. There may be one lead wire for each chamber, or one lead wire may be capable of sensing and pacing both chambers.

A new type of pacemaker, called a biventricular pacemaker, is currently used in the treatment of congestive heart failure. Sometimes in heart failure, the two ventricles (lower heart chambers) do not pump together in a normal manner. When this happens, less blood is pumped by the heart.

A biventricular pacemaker paces both ventricles at the same time, increasing the amount of blood pumped by the heart. This type of treatment is called cardiac resynchronization therapy.

Implantable cardioverter defibrillator (ICD)

An implantable cardioverter defibrillator (ICD) looks very similar to a pacemaker, except that it is slightly larger. It has a generator, one or more leads, and an electrode for each lead. These components work very much like a pacemaker. However, the ICD is designed to deliver an electrical shock to the heart when the heart rate becomes dangerously fast, or €œfibrillates.”

An ICD senses when the heart is beating too fast and delivers an electrical shock to convert the fast rhythm to a normal rhythm. Some devices combine a pacemaker and ICD in one unit for persons who need both functions.

The ICD has another type of treatment for certain fast rhythms called anti-tachycardia pacing (ATP). When ATP is used, a fast pacing impulse is sent to correct the rhythm. After the shock is delivered, a “back-up” pacing mode is used if needed for a short while.

The procedure for inserting a pacemaker or an ICD is the same. The procedure generally is performed in an electrophysiology (EP) lab or a cardiac catheterization lab.

Other related procedures that may be used to assess the heart include resting and exercise electrocardiogram (ECG), Holter monitor, signal-averaged ECG, cardiac catheterization, chest x-ray, computed tomography (CT scan) of the chest, echocardiography, electrophysiology studies, magnetic resonance imaging (MRI) of the heart, myocardial perfusion scans, radionuclide angiography, and ultrafast CT scan.

The heart’s electrical conduction system

Illustration of the anatomy of the heart, view of the electrical system
Click Image to Enlarge

The heart is, in the simplest terms, a pump made up of muscle tissue. Like all pumps, the heart requires a source of energy in order to function. The heart’s pumping energy comes from an indwelling electrical conduction system.

An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node), which is a small mass of specialized tissue located in the right atrium (right upper chamber) of the heart.

The sinus node generates an electrical stimulus regularly at 60 to 100 times per minute under normal conditions. This electrical stimulus travels down through the conduction pathways (similar to the way electricity flows through power lines from the power plant to your house) and causes the heart’s chambers to contract and pump out blood.

The right and left atria (the two upper chambers of the heart) are stimulated first and contract a short period of time before the right and left ventricles (the two lower chambers of the heart).

The electrical impulse travels from the sinus node to the atrioventricular (AV) node, where it stops for a very short period, then continues down the conduction pathways via the “bundle of His” into the ventricles. The bundle of His divides into right and left pathways to provide electrical stimulation to both ventricles.

What is an ECG?

This electrical activity of the heart is measured by an electrocardiogram (ECG or EKG). By placing electrodes at specific locations on the body (chest, arms, and legs), a tracing of the electrical activity can be obtained. Changes in an ECG from the normal tracing can indicate one or more of several heart-related conditions.

Dysrhythmias/arrhythmias (abnormal heart rhythms) are diagnosed by methods such as EKG, Holter monitoring, signal-average EKG, or electrophysiological studies. These symptoms may be treated with medication or procedures such as a cardiac ablation (removal of a location in the heart that is causing a dysrhythmia by freezing or radiofrequency).

Reasons for the Procedure

A pacemaker may be inserted in order to provide stimulation for a faster heart rate when the heart is beating too slowly, and when other treatment methods, such as medication, have not improved the heart rate.

An ICD may be inserted in order to provide fast pacing (ATP), cardioversion (small shock), or defibrillation (larger shock) when the heart beats too fast.

Problems with the heart rhythm may cause difficulties because the heart is unable to pump an adequate amount of blood to the body. If the heart rate is too slow, the blood is pumped too slowly.

If the heart rate is too fast or too irregular, the heart chambers are unable to fill up with enough blood to pump out with each beat. When the body does not receive enough blood, symptoms such as fatigue, dizziness, fainting, and/or chest pain may occur.

Some examples of rhythm problems for which a pacemaker or ICD might be inserted include:

  • atrial fibrillation – occurs when the atria beat irregularly and too fast
  • ventricular fibrillation – occurs when the ventricles beat irregularly and too fast
  • bradycardia – occurs when the heart beats too slow
  • tachycardia – occurs when the heart beats too fast
  • heart block – occurs when the electrical signal is delayed after leaving the SA node; there are several types of heart blocks, and each one has a distinctive ECG tracing

There may be other reasons for your physician to recommend a pacemaker or ICD insertion.

Risks of the Procedure

Possible risks of pacemaker or ICD insertion include, but are not limited to, the following:

  • bleeding from the incision or catheter insertion site
  • damage to the vessel at the catheter insertion site
  • infection of the incision or catheter site
  • pneumothorax – air becomes trapped in the pleural space causing the lung to collapse

If you are pregnant or suspect that you may be pregnant, you should notify your physician. If you are lactating, or breastfeeding, you should notify your physician.

Patients who are allergic to or sensitive to medications or latex should notify their physician.

For some patients, having to lie still on the procedure table for the length of the procedure may cause some discomfort or pain.

There may be other risks depending upon your specific medical condition. Be sure to discuss any concerns with your physician prior to the procedure.

Before the Procedure

  • Your physician will explain the procedure to you and offer you the opportunity to ask any questions that you might have about the procedure.
  • You will be asked to sign a consent form that gives your permission to do the test. Read the form carefully and ask questions if something is not clear.
  • You will need to fast for a certain period of time prior to the procedure. Your physician will notify you how long to fast, usually overnight.
  • If you are pregnant or suspect that you are pregnant, you should notify your physician.
  • Notify your physician if you are sensitive to or are allergic to any medications, iodine, latex, tape, or anesthetic agents (local and general).
  • Notify your physician of all medications (prescription and over-the-counter) and herbal supplements that you are taking.
  • Notify your physician if you have heart valve disease, as you may need to receive an antibiotic prior to the procedure.
  • Notify your physician if you have a history of bleeding disorders or if you are taking any anticoagulant (blood-thinning) medications, aspirin, or other medications that affect blood clotting. It may be necessary for you to stop some of these medications prior to the procedure.
  • Your physician may request a blood test prior to the procedure to determine how long it takes your blood to clot. Other blood tests may be done as well.
  • You may receive a sedative prior to the procedure to help you relax. If a sedative is given, you will need someone to drive you home afterwards.
  • The upper chest may be shaved or clipped prior to the procedure.
  • Based upon your medical condition, your physician may request other specific preparation.

During the Procedure

Picture of a chest X-ray, showing a single-chamber implanted pacemaker
Chest X-ray with Implanted Pacemaker

A pacemaker or implanted cardioverter defibrillator may be performed on an outpatient basis or as part of your stay in a hospital. Procedures may vary depending on your condition and your physician’s practices.

Generally, a pacemaker or ICD insertion follows this process:

  1. You will be asked to remove any jewelry or other objects that may interfere with the procedure.
  2. You will be asked to remove your clothing and will be given a gown to wear.
  3. You will be asked to empty your bladder prior to the procedure.
  4. An intravenous (IV) line will be started in your hand or arm prior to the procedure for injection of medication and to administer IV fluids, if needed.
  5. You will be placed in a supine (on your back) position on the procedure table.
  6. You will be connected to an electrocardiogram (ECG or EKG) monitor that records the electrical activity of the heart and monitors the heart during the procedure using small, adhesive electrodes. Your vital signs (heart rate, blood pressure, breathing rate, and oxygenation level) will be monitored during the procedure.
  7. Large electrode pads will be placed on the front and back of the chest.
  8. You will receive a sedative medication in your IV before the procedure to help you relax. However, you will likely remain awake during the procedure.
  9. The pacemaker or ICD insertion site will be cleansed with antiseptic soap.
  10. Sterile towels and a sheet will be placed around this area.
  11. A local anesthetic will be injected into the skin at the insertion site.
  12. Once the anesthetic has taken effect, the physician will make a small incision at the insertion site.
  13. A sheath, or introducer, is inserted into a blood vessel, usually under the collarbone. The sheath is a plastic tube through which the pacer/ICD lead wire will be inserted into the blood vessel and advanced into the heart.
  14. It will be very important for you to remain still during the procedure so that the catheter placement will not be disturbed and to prevent damage to the insertion site.
  15. The lead wire will be inserted through the introducer into the blood vessel. The physician will advance the lead wire through the blood vessel into the heart.
  16. Once the lead wire is inside the heart, it will be tested to verify proper location and that it works. There may be one, two, or three lead wires inserted, depending on the type of device your physician has chosen for your condition. Fluoroscopy, (a special type of x-ray that will be displayed on a TV monitor), may be used to assist in testing the location of the leads.
  17. Once the lead wire has been tested, an incision will be made close to the location of the catheter insertion (just under the collarbone). You will receive local anesthetic medication before the incision is made.
  18. The pacemaker/ICD generator will be slipped under the skin through the incision after the lead wire is attached to the generator. Generally, the generator will be placed on the non-dominant side. (If you are right-handed, the device will be placed in your upper left chest. If you are left-handed, the device will be placed in your upper right chest).
  19. The ECG will be observed to ensure that the pacer is working correctly.
  20. The skin incision will be closed with sutures, adhesive strips, or a special glue.
  21. A sterile bandage/dressing will be applied.

After the Procedure

In the hospital

After the procedure, you may be taken to the recovery room for observation or returned to your hospital room. A nurse will monitor your vital signs for a specified period of time.

You should immediately inform your nurse if you feel any chest pain or tightness, or any other pain at the incision site.

After the specified period of bed rest has been completed, you may get out of bed. The nurse will assist you the first time you get up, and will check your blood pressure while you are lying in bed, sitting, and standing. You should move slowly when getting up from the bed to avoid any dizziness from the period of bedrest.

You will be able to eat or drink once you are completely awake.

The insertion site may be sore or painful, but pain medication may be administered if needed.

Your physician will visit with you in your room while you are recovering. The physician will give you specific instructions and answer any questions you may have.

Once your blood pressure, pulse, and breathing are stable and you are alert, you will be taken to your hospital room or discharged home.

If the procedure is performed on an outpatient basis, you may be allowed to leave after you have completed the recovery process. However, if there are concerns or problems with your ECG, you may stay in the hospital for an additional day (or longer) for monitoring of the ECG.

You should arrange to have someone drive you home from the hospital following your procedure.

At home

You should be able to return to your daily routine within a few days. Your physician will tell you if you will need to take more time in returning to your normal activities. In addition, you should not do any lifting or pulling on anything for a few weeks. You may be instructed not to lift your arms above your head for a period of time.

You will most likely be able to resume your usual diet, unless your physician instructs you differently.

It will be important to keep the insertion site clean and dry. Your physician will give you specific bathing instructions.

Your physician will give you specific instructions about driving. If you had an ICD, you will not be able to drive until your physician gives you approval. Your physician will explain these limitations to you, if they are applicable to your situation.

You will be given specific instructions about what to do if your ICD discharges a shock. For example, you may be instructed to dial 911 or go to the nearest emergency room in the event of a shock from the ICD.

Ask your physician when you will be able to return to work. The nature of your occupation, your overall health status, and your progress will determine how soon you may return to work.

Notify your physician to report any of the following:

  • fever and/or chills
  • increased pain, redness, swelling, or bleeding or other drainage from the insertion site
  • chest pain/pressure, nausea and/or vomiting, profuse sweating, dizziness and/or fainting
  • palpitations

Your physician may give you additional or alternate instructions after the procedure, depending on your particular situation.

Pacemaker/ICD precautions

The following precautions should always be considered. Discuss the following in detail with your physician, or call the company that made your device:

  • Always carry an ID card that states you are wearing a pacemaker or an ICD. In addition, you should wear a medical identification bracelet that states you have a pacemaker or ICD.
  • Use caution when going through airport security detectors. Check with your physician about the safety of going through such detectors with your type of pacemaker. In particular, you may need to avoid being screened by hand-held detector devices, as these devices may affect your pacemaker.
  • You may not have a magnetic resonance imaging (MRI) procedure. You should also avoid large magnetic fields.
  • Abstain from diathermy (the use of heat in physical therapy to treat muscles).
  • Turn off large motors, such as cars or boats, when working on them (they may temporarily €œconfuse” your device).
  • Avoid certain high-voltage or radar machinery, such as radio or television transmitters, electric arc welders, high-tension wires, radar installations, or smelting furnaces.
  • If you are having a surgical procedure performed by a surgeon or dentist, tell your surgeon or dentist that you have a pacemaker or ICD, so that electrocautery will not be used to control bleeding (the electrocautery device can change the pacemaker settings).
  • You may have to take antibiotic medication before any medically invasive procedure to prevent infections that may affect the pacemaker.
  • Always consult your physician if you have any questions concerning the use of certain equipment near your pacemaker.
  • When involved in a physical, recreational, or sporting activity, you should avoid receiving a blow to the skin over the pacemaker or ICD. A blow to the chest near the pacemaker or ICD can affect its functioning. If you do receive a blow to that area, see your physician.
  • Always consult your physician when you feel ill after an activity, or when you have questions about beginning a new activity.

SOURCE

http://stanfordhospital.org/healthLib/greystone/heartCenter/heartProcedures/pacemakerImplantableCardioverterDefibrillatorICDInsertion.html

In Summary: Who Needs a Pacemaker?

Doctors recommend pacemakers for many reasons. The most common reasons are bradycardia and heart block.

Bradycardia is a heartbeat that is slower than normal. Heart block is a disorder that occurs if an electrical signal is slowed or disrupted as it moves through the heart.

Heart block can happen as a result of aging, damage to the heart from a heart attack, or other conditions that disrupt the heart’s electrical activity. Some nerve and muscle disorders also can cause heart block, including muscular dystrophy.

Your doctor also may recommend a pacemaker if:

  • Aging or heart disease damages your sinus node’s ability to set the correct pace for your heartbeat. Such damage can cause slower than normal heartbeats or long pauses between heartbeats. The damage also can cause your heart to switch between slow and fast rhythms. This condition is called sick sinus syndrome.
  • You’ve had a medical procedure to treat an arrhythmia called atrial fibrillation. A pacemaker can help regulate your heartbeat after the procedure.
  • You need to take certain heart medicines, such as beta blockers. These medicines can slow your heartbeat too much.
  • You faint or have other symptoms of a slow heartbeat. For example, this may happen if the main artery in your neck that supplies your brain with blood is sensitive to pressure. Just quickly turning your neck can cause your heart to beat slower than normal. As a result, your brain might not get enough blood flow, causing you to feel faint or collapse.
  • You have heart muscle problems that cause electrical signals to travel too slowly through your heart muscle. Your pacemaker may provide cardiac resynchronization therapy (CRT) for this problem. CRT devices coordinate electrical signaling between the heart’s lower chambers.
  • You have long QT syndrome, which puts you at risk for dangerous arrhythmias.

Doctors also may recommend pacemakers for people who have certain types ofcongenital heart disease or for people who have had heart transplants. Children, teens, and adults can use pacemakers.

Before recommending a pacemaker, your doctor will consider any arrhythmia symptoms you have, such as dizziness, unexplained fainting, or shortness of breath. He or she also will consider whether you have a history of heart disease, what medicines you’re currently taking, and the results of heart tests.

Diagnostic Tests

Many tests are used to detect arrhythmias. You may have one or more of the following tests.

EKG (Electrocardiogram)

An EKG is a simple, painless test that detects and records the heart’s electrical activity. The test shows how fast your heart is beating and its rhythm (steady or irregular).

An EKG also records the strength and timing of electrical signals as they pass through your heart. The test can help diagnose bradycardia and heart block (the most common reasons for needing a pacemaker).

A standard EKG only records the heartbeat for a few seconds. It won’t detect arrhythmias that don’t happen during the test.

To diagnose heart rhythm problems that come and go, your doctor may have you wear a portable EKG monitor. The two most common types of portable EKGs are Holter and event monitors.

Holter and Event Monitors

A Holter monitor records the heart’s electrical activity for a full 24- or 48-hour period. You wear one while you do your normal daily activities. This allows the monitor to record your heart for a longer time than a standard EKG.

An event monitor is similar to a Holter monitor. You wear an event monitor while doing your normal activities. However, an event monitor only records your heart’s electrical activity at certain times while you’re wearing it.

For many event monitors, you push a button to start the monitor when you feel symptoms. Other event monitors start automatically when they sense abnormal heart rhythms.

You can wear an event monitor for weeks or until symptoms occur.

Echocardiography

Echocardiography (echo) uses sound waves to create a moving picture of your heart. The test shows the size and shape of your heart and how well your heart chambers and valves are working.

Echo also can show areas of poor blood flow to the heart, areas of heart muscle that aren’t contracting normally, and injury to the heart muscle caused by poor blood flow.

Electrophysiology Study

For this test, a thin, flexible wire is passed through a vein in your groin (upper thigh) or arm to your heart. The wire records the heart’s electrical signals.

Your doctor uses the wire to electrically stimulate your heart. This allows him or her to see how your heart’s electrical system responds. This test helps pinpoint where the heart’s electrical system is damaged.

Stress Test

Some heart problems are easier to diagnose when your heart is working hard and beating fast.

During stress testing, you exercise to make your heart work hard and beat fast while heart tests, such as an EKG or echo, are done. If you can’t exercise, you may be given medicine to raise your heart rate.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/whoneeds.html

What Are the Risks of Pacemaker Surgery?

Pacemaker surgery generally is safe. If problems do occur, they may include:

  • Swelling, bleeding, bruising, or infection in the area where the pacemaker was placed
  • Blood vessel or nerve damage
  • A collapsed lung
  • A bad reaction to the medicine used during the procedure

Talk with your doctor about the benefits and risks of pacemaker surgery.

How Does a Pacemaker Work?

A pacemaker consists of a battery, a computerized generator, and wires with sensors at their tips. (The sensors are called electrodes.) The battery powers the generator, and both are surrounded by a thin metal box. The wires connect the generator to the heart.

A pacemaker helps monitor and control your heartbeat. The electrodes detect your heart’s electrical activity and send data through the wires to the computer in the generator.

If your heart rhythm is abnormal, the computer will direct the generator to send electrical pulses to your heart. The pulses travel through the wires to reach your heart.

Newer pacemakers can monitor your blood temperature, breathing, and other factors. They also can adjust your heart rate to changes in your activity.

The pacemaker’s computer also records your heart’s electrical activity and heart rhythm. Your doctor will use these recordings to adjust your pacemaker so it works better for you.

Your doctor can program the pacemaker’s computer with an external device. He or she doesn’t have to use needles or have direct contact with the pacemaker.

Pacemakers have one to three wires that are each placed in different chambers of the heart.

  • The wires in a single-chamber pacemaker usually carry pulses from the generator to the right ventricle (the lower right chamber of your heart).
  • The wires in a dual-chamber pacemaker carry pulses from the generator to the right atrium (the upper right chamber of your heart) and the right ventricle. The pulses help coordinate the timing of these two chambers’ contractions.
  • The wires in a biventricular pacemaker carry pulses from the generator to an atrium and both ventricles. The pulses help coordinate electrical signaling between the two ventricles. This type of pacemaker also is called a cardiac resynchronization therapy (CRT) device.

Cross-Section of a Chest With a Pacemaker

The image shows a cross-section of a chest with a pacemaker. Figure A shows the location and general size of a double-lead, or dual-chamber, pacemaker in the upper chest. The wires with electrodes are inserted into the heart's right atrium and ventricle through a vein in the upper chest. Figure B shows an electrode electrically stimulating the heart muscle. Figure C shows the location and general size of a single-lead, or single-chamber, pacemaker in the upper chest.

The image shows a cross-section of a chest with a pacemaker. Figure A shows the location and general size of a double-lead, or dual-chamber, pacemaker in the upper chest. The wires with electrodes are inserted into the heart’s right atrium and ventricle through a vein in the upper chest. Figure B shows an electrode electrically stimulating the heart muscle. Figure C shows the location and general size of a single-lead, or single-chamber, pacemaker in the upper chest.

Types of Pacemaker Programming

The two main types of programming for pacemakers are

  • demand pacing and
  • rate-responsive pacing.

A demand pacemaker monitors your heart rhythm. It only sends electrical pulses to your heart if your heart is beating too slow or if it misses a beat.

A rate-responsive pacemaker will speed up or slow down your heart rate depending on how active you are. To do this, the device monitors your

  • sinus node rate,
  • breathing,
  • blood temperature, and
  • other factors to determine your activity level.

Your doctor will work with you to decide which type of pacemaker is best for you.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/howdoes.html

What To Expect During Pacemaker Surgery

Placing a pacemaker requires minor surgery. The surgery usually is done in a hospital or special heart treatment laboratory.

Before the surgery, an intravenous (IV) line will be inserted into one of your veins. You will receive medicine through the IV line to help you relax. The medicine also might make you sleepy.

Your doctor will numb the area where he or she will put the pacemaker so you don’t feel any pain. Your doctor also may give you antibiotics to prevent infection.

First, your doctor will insert a needle into a large vein, usually near the shoulder opposite your dominant hand. Your doctor will then use the needle to thread the pacemaker wires into the vein and to correctly place them in your heart.

An x-ray “movie” of the wires as they pass through your vein and into your heart will help your doctor place them. Once the wires are in place, your doctor will make a small cut into the skin of your chest or abdomen.

He or she will slip the pacemaker’s small metal box through the cut, place it just under your skin, and connect it to the wires that lead to your heart. The box contains the pacemaker’s battery and generator.

Once the pacemaker is in place, your doctor will test it to make sure it works properly. He or she will then sew up the cut. The entire surgery takes a few hours.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/during.html

What To Expect After Pacemaker Surgery

Expect to stay in the hospital overnight so your health care team can check your heartbeat and make sure your pacemaker is working well. You’ll likely have to arrange for a ride to and from the hospital because your doctor may not want you to drive yourself.

For a few days to weeks after surgery, you may have pain, swelling, or tenderness in the area where your pacemaker was placed. The pain usually is mild; over-the-counter medicines often can relieve it. Talk to your doctor before taking any pain medicines.

Your doctor may ask you to avoid vigorous activities and heavy lifting for about a month after pacemaker surgery. Most people return to their normal activities within a few days of having the surgery.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/after.html

How Will a Pacemaker Affect My Lifestyle?

Once you have a pacemaker, you have to avoid close or prolonged contact with electrical devices or devices that have strong magnetic fields. Devices that can interfere with a pacemaker include:

  • Cell phones and MP3 players (for example, iPods)
  • Household appliances, such as microwave ovens
  • High-tension wires
  • Metal detectors
  • Industrial welders
  • Electrical generators

These devices can disrupt the electrical signaling of your pacemaker and stop it from working properly. You may not be able to tell whether your pacemaker has been affected.

How likely a device is to disrupt your pacemaker depends on how long you’re exposed to it and how close it is to your pacemaker.

To be safe, some experts recommend not putting your cell phone or MP3 player in a shirt pocket over your pacemaker (if the devices are turned on).

You may want to hold your cell phone up to the ear that’s opposite the site where your pacemaker is implanted. If you strap your MP3 player to your arm while listening to it, put it on the arm that’s farther from your pacemaker.

You can still use household appliances, but avoid close and prolonged exposure, as it may interfere with your pacemaker.

You can walk through security system metal detectors at your normal pace. Security staff can check you with a metal detector wand as long as it isn’t held for too long over your pacemaker site. You should avoid sitting or standing close to a security system metal detector. Notify security staff if you have a pacemaker.

Also, stay at least 2 feet away from industrial welders and electrical generators.

Some medical procedures can disrupt your pacemaker. These procedures include:

  • Magnetic resonance imaging, or MRI
  • Shock-wave lithotripsy to get rid of kidney stones
  • Electrocauterization to stop bleeding during surgery

Let all of your doctors, dentists, and medical technicians know that you have a pacemaker. Your doctor can give you a card that states what kind of pacemaker you have. Carry this card in your wallet. You may want to wear a medical ID bracelet or necklace that states that you have a pacemaker.

Physical Activity

In most cases, having a pacemaker won’t limit you from doing sports and exercise, including strenuous activities.

You may need to avoid full-contact sports, such as football. Such contact could damage your pacemaker or shake loose the wires in your heart. Ask your doctor how much and what kinds of physical activity are safe for you.

Ongoing Care

Your doctor will want to check your pacemaker regularly (about every 3 months). Over time, a pacemaker can stop working properly because:

  • Its wires get dislodged or broken
  • Its battery gets weak or fails
  • Your heart disease progresses
  • Other devices have disrupted its electrical signaling

To check your pacemaker, your doctor may ask you to come in for an office visit several times a year. Some pacemaker functions can be checked remotely using a phone or the Internet.

Your doctor also may ask you to have an EKG (electrocardiogram) to check for changes in your heart’s electrical activity.

Battery Replacement

Pacemaker batteries last between 5 and 15 years (average 6 to 7 years), depending on how active the pacemaker is. Your doctor will replace the generator along with the battery before the battery starts to run down.

Replacing the generator and battery is less-involved surgery than the original surgery to implant the pacemaker. Your pacemaker wires also may need to be replaced eventually.

Your doctor can tell you whether your pacemaker or its wires need to be replaced when you see him or her for followup visits.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/lifestyle.html

Clinical Trial on Pace Makers

clinical trials related to pacemakers, talk with your doctor. You also can visit the following Web sites to learn more about clinical research and to search for clinical trials:

For more information about clinical trials for children, visit the NHLBI’s Children and Clinical Studies Web page.

SOURCE

http://www.nhlbi.nih.gov/health/health-topics/topics/pace/trials.html

RESOUCES on PaceMakers

Links to Other Information About Pacemakers

NHLBI Resources

Non-NHLBI Resources

Clinical Trials

SOURCE

 

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Reporter: Aviva Lev-Ari, PhD, RN

 

In this Journal Stent technology was researched thoroughly, the reader is advised to enrich his/hers knowledge on Re-vascularization technology by reviewing the following articles and the bibliography in each of them:

Coronary Artery Disease – Medical Devices Solutions: From First-In-Man Stent Implantation, via Medical Ethical Dilemmas to Drug Eluting Stents

Aviva Lev-Ari, PhD, RN 8/13/2012

Drug Eluting Stents: On MIT’s Edelman Lab’s Contributions to Vascular Biology and its Pioneering Research on DES

Larry H Bernstein, MD, FACP, Author and  Aviva Lev-Ari, PhD, RN, Curator 4/25/2013

Vascular Repair: Stents and Biologically Active Implants

Larry H Bernstein, MD, FACP, Author and  Aviva Lev-Ari, PhD, RN, Curator 5/4/2013

Biomaterials Technology: Models of Tissue Engineering for Reperfusion and Implantable Devices for Revascularization 5/5/2013

Revascularization: PCI, Prior History of PCI vs CABG

Aviva Lev-Ari, PhD, RN 4/25/2013

To Stent or Not? A Critical Decision

Aviva Lev-Ari, PhD, RN 10/23/2012

New Drug-Eluting Stent Works Well in STEMI

Aviva Lev-Ari, PhD, RN 8/22/2012

OrbusNeich seizes Boston Scientific stents in Germany as part of patent infringement proceedings

May 21, 2013

OrbusNeich seizes Boston Scientific stents in Germany as part of patent infringement proceedings

WIESBADEN, Germany, May 21, 2013 /PRNewswire/ — Medical device manufacturer OrbusNeich Medical Inc. and its subsidiary, OrbusNeich Medical GmbH (collectively “OrbusNeich”) today announced that it has enforced the seizure of over 190 stent systems from Boston Scientific Corporation (NYSE: BSX) in connection with its patent infringement proceedings in the Dusseldorf Regional Court. The products were found on May 15, 2013, at the premises of Boston Scientific Medizintechnik GmbH in Ratingen (Germany), the German subsidiary of Boston Scientific Corporation (collectively “Boston Scientific”).

In violation of the Court’s April 30, 2013 Preliminary Injunction, Boston Scientific initially denied access to search its premises – the court’s decision grants OrbusNeich the right to seize stents in the possession of Boston Scientific that have been commercially distributed but not yet used. Boston Scientific claimed that none of the concerned stent systems were in its possession at the location in Ratingen. Only after the Police were called did Boston Scientific allow the bailiff to search the building and seize the products.

The April 30, 2013, ruling, which Boston Scientific has appealed, allows OrbusNeich to prevent Boston Scientific from marketing and selling the affected stent lines in Germany, which include the Small Vessel, Small Workhorse and Workhorse Stents of Boston Scientific’s PROMUS Element™, PROMUS Element Plus™, OMEGA™, TAXUS Element™, SYNERGY™ and Promus PREMIER™ product lines. In this decision, the Regional Court found that the geometric pattern of these stents infringe OrbusNeich’s patent EP 1 341 482.

On May 13, 2013, OrbusNeich obtained a second Preliminary Injunction against Boston Scientific following Boston Scientific’s attempt to circumvent the first Injunction by transferring the German distribution of the affected products to Boston Scientific (UK) Ltd. and Boston Scientific Ltd. Boston Scientific may appeal this decision.

In addition to the Preliminary Injunctions, OrbusNeich’s principal patent infringement proceedings are also before the Dusseldorf Regional Court. In these proceedings, OrbusNeich is seeking damages, a permanent injunction and other relief for alleged infringement of the German parts of the EP 1 341 412 and ‘482 patents by the affected stent lines. A hearing in this main proceeding is scheduled for May 2014.

Similar infringement proceedings have also been filed in The Netherlands and Ireland.

The proceedings follow a favorable ruling for OrbusNeich by the European Patent Office (EPO) on February 11, 2013, in connection with the ‘482 patent. The EPO decision, which has been appealed, upheld the claim of the ‘482 patent, as amended, against an opposition by Boston Scientific and Terumo, claiming the patent was invalid.

About OrbusNeich

OrbusNeich is a global company that designs, develops, manufactures and markets innovative medical devices for the treatment of vascular diseases. Current products are the world’s first pro-healing stent, the Genous™ Stent, as well as other stents and balloons marketed under the names of Azule™, R stent™, Scoreflex™, Sapphire™, Sapphire II™ and Sapphire NC™. Development stage products include the COMBO Dual Therapy Stent™, the world’s first dual therapy stent. OrbusNeich is headquartered in Hong Kong and has operations in Shenzhen, China; Fort Lauderdale, Fla.; Hoevelaken, The Netherlands; and Tokyo, Japan. OrbusNeich supplies medical devices to interventional cardiologists in more than 60 countries. For more information, visit http://www.OrbusNeich.com.

Media Contact:
Jed Repko – Bryan Darrow – Taylor Ingraham
Joele Frank , Wilkinson Brimmer Katcher
212-355-4449

SOURCE: OrbusNeich Medical Inc.

Read more: OrbusNeich seizes Boston Scientific stents in Germany as part of patent infringement proceedings – FierceMedicalDevices http://www.fiercemedicaldevices.com/press-releases/orbusneich-seizes-boston-scientific-stents-germany-part-patent-infringement#ixzz2TwxCAgth

http://www.fiercemedicaldevices.com/press-releases/orbusneich-seizes-boston-scientific-stents-germany-part-patent-infringement?utm_medium=nl&utm_source=internal

 

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Reporter: Aviva Lev-Ari, PhD, RN

UPDATED on 5/29, 2013

Renal Denervation Safe in Real-World Setting

By Todd Neale, Senior Staff Writer, MedPage Today

Published: May 25, 2013

Reviewed by F. Perry Wilson, MD, MSCE; Instructor of Medicine, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Action Points:

PARIS — May 21-24, 2013

Out in everyday practice, renal denervation with the Symplicity device safely lowers blood pressure in patients with hypertension, preliminary results from the Global SYMPLICITY registry showed.

The Global SYMPLICITY registry is part of the clinical program evaluating the Symplicity device. It has been approved for use in Europe and elsewhere but remains restricted to investigational use in the U.S. Medtronic, which makes the Symplicity device, announced on Thursday that it has completed enrollment in Symplicity HTN-3, the pivotal U.S. trial.

The registry has a targeted enrollment of about 5,000 patients from about 200 centers worldwide; 149 sites spread throughout Canada, Mexico, South America, Europe, Africa, the Middle East, Asia, and Australia have already started collecting data.

Any patient who receives renal denervation can be included in the registry, and thus the study will include patients with hypertension and other conditions associated with increased sympathetic activity, including heart failure, insulin resistance, atrial fibrillation, sleep apnea, and chronic kidney disease.

European Society of Cardiology‘s recently published consensus paper on renal denervation, which recommended treatment in patients with a systolic blood pressure of 160 mm Hg or higher (or at least 150 mm Hg for type 2 diabetics) who were taking at least three antihypertensive medications, including a diuretic.

SOURCE:

Expert consensus document from the European Society of Cardiology on catheter-based renal denervation

http://eurheartj.oxfordjournals.org/content/early/2013/04/25/eurheartj.eht154.extract

Most of the first 617 patients included the registry (60%) were treated in accordance with the European Society of Cardiology’s recently published consensus paper on renal denervation, above.

About one-fifth of the patients (22%) started with a systolic blood pressure of at least 180 mm Hg, which was the average baseline blood pressure in the Symplicity HTN-1 and HTN-2 trials.

The average starting blood pressure overall was 164/89 mm Hg, and patients were taking an average of 4.35 medications. Common comorbidities included diabetes (38.2%), renal disease (30.1%), sleep apnea (16.3%), a history of cardiac disease (49%), heart failure (9.3%), and atrial fibrillation (11.9%).

The registry data showed significant drops in blood pressure measured both in the office and with 24-hour ambulatory monitoring, although the reductions were smaller than those seen in the clinical trials.

That’s not surprising, according to Mahfoud, because out in everyday practice blood pressure is not recorded as appropriately as in a clinical trial setting and poor compliance to medication becomes more of an issue. In fact, he said, a recent study showed that 47% of patients with resistant hypertension were not adherent to their medication regimens.

Also contributing to the smaller reductions in the real-world population is the fact that the average starting blood pressure was lower than in the clinical trials, Mahfoud said, adding that it is known that renal denervation induces greater reductions in blood pressure among those with the highest readings initially.

Mahfoud reported receiving institutional grant/research support from Medtronic, St. Jude, Recor, and serving as a consultant for St. Jude, Medtronic, Boston Scientific, and Cordis. Medtronic makes the Symplicity renal denervation device.

 Primary source: European Association of Percutaneous Cardiovascular Interventions

SOURCE REFERENCE:

Mahfoud F, et al “Early results following renal denervation for treatment of hypertension in a real-world population: the Global SYMPLICITY registry” EuroPCR 2013.

Adverse Events:
Of the first 617 patients included in the registry, only two had vascular complications related to access during the procedure, and none had serious events stemming from delivery of the radiofrequency energy to the renal artery; the rate of vasospasm was 9%, according to Felix Mahfoud, MD, of Saarland University Medical Center in Homburg/Saar, Germany.Through 6 months of follow-up, there were two hospitalizations for hypertensive crisis, two myocardial infarctions, one new case of end-stage renal disease from nephrotoxic overdose, and one death that was not considered to be related to the procedure, he reported at the EuroPCR meeting here.The procedure was not only safe, but also effective at lowering blood pressure, with reductions in office-based readings ranging from 13/6 mm Hg among patients with a baseline systolic blood pressure of 140 mm Hg or higher to 28/18 mm Hg among those with a baseline systolic pressure of 180 mm Hg or higher at 3 months. The findings were similar at 6 months.

“The take-home message will be hopefully … that renal denervation is a safe procedure providing blood pressure lowering in patients with high blood pressure at baseline and that that procedure might have an impact on clinical outcomes,” Mahfoud said in an interview.

Positive Effects of Renal Denervation Ablation for Hypertension in Controlled Randomized SYMPLICITY HTN-2 Trial

Renal Nerve Ablation Effects on BP Lasting

Download Complimentary Source PDF 

By Chris Kaiser, Cardiology Editor, MedPage Today

Published: January 08, 2013
Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Late-term results from a study of the safety and effectiveness of renal denervation to reduce hypertension mirrored positive results seen earlier in the randomized SYMPLICITY HTN-2 trial, researchers found.

The mean reduction in systolic blood pressure at 1 year post procedure was a significant 28.1 mmHg (P<0.001), similar to the mean 31.7 mmHg drop at 6 months (P=0.16 for the comparison), according to Murray Esler, MD, of the Baker IDI Heart and Diabetes Institute in Melbourne, Australia, and colleagues.

Those in the control group who crossed over to the intervention at 6 months also had a significant fall in systolic blood pressure from a mean 190 to 166 mmHg (P<0.001), researchers reported in the January issue of Circulation: Journal of the American Heart Association.

The increasing prevalence of hypertension is a worldwide phenomenon, with an estimated 1.56 billion predicted to be affected in 2025, the authors noted. Yet, many of these patients cannot control their blood pressure (with control being defined as a pressure <140/90 mmHg) even when taking three or more antihypertensive medications.

Esler and colleagues cited a 2005 study that found a range of 47% to 87% of people in North America and Europe whose blood pressure is not under control (Lancet 2005; 365: 217-223).

Renal denervation has shown promise in these patients who are refractory to medication. The percutaneous procedure uses energy such as radiofrequency waves to scar the renal artery in an attempt to disrupt the sympathetic nerves, thereby affecting blood pressure.

Three-year data from the nonrandomized SYMPLICITY HTN-1 study were in line with 2- and 1-year results, showing a mean drop of 33/19 mmHg associated with the intervention.

In the current study, researchers from the multi-center randomized controlled SYMPLICITY HTN-2 trial enrolled 106 patients with essential hypertension (systolic blood pressure ≥160 mmHg, or ≥150 mmHg for diabetics). Patients were taking at least three antihypertensive medications.

The initial 1-year data from the SYMPLICITY HTN-2 trial were reported at the 2012 American College of Cardiology meeting. The primary endpoint was a change in systolic blood pressure at 6 months. Also at the 6-month mark, patients in the control group were allowed to cross over and receive the treatment; they were then followed for 6 more months.

The 6-month data were based on 101 patients (49 in the treatment group versus 51 controls). The 1-year data were based on 47 patients in the primary treatment group and 35 per-protocol controls who crossed over. The crossover patients also had to have a systolic blood pressure of ≥160 mmHg.

The significant decrease of 28.1 mmHg in systolic blood pressure in the treatment arm at 1 year was matched by significant drops in diastolic blood pressure at 6 and 12 months, as well as in the crossover group at 6 months (P<0.001 for all).

The authors reported that 84% of initial denervation patients had a decrease of at least 10 mmHg at 6 months; at 1 year, the number was 79%. In the crossover group, that rate was 63% at 6 months.

Interestingly, there was no significant difference in the changes in medication — reduced dosage or fewer drugs — between the treatment arm and controls, despite the reduction in blood pressure for the treatment arm.

“These data further substantiate the safety of renal sympathetic denervation via delivery of controlled radiofrequency energy bursts,” Esler and colleagues concluded.

They also noted that renal function remained unchanged at both 6 and 12 months. A pilot study by the Melbourne group looking specifically at patients with chronic kidney disease found renal denervation to be safe in this population.

The limitations to the current study include the lack of 24-hour blood pressure monitoring and the lack of blinding among the staff measuring blood pressure. The investigators noted that the ongoing SYMPLICITY HTN-3 trial addresses these limitations.

This study was funded by Medtronic Ardian.

Esler and three co-authors reported receiving research support from Medtronic Ardian. During the conduct of the trial, senior author Sobotka was chief medical officer of Ardian, and was a medical adviser to Medtronic.

From the American Heart Association:

 SOURCE:

Other articles on this topic on this Open Access Online Scientific Journal:

Lev-Ari, A. (2012aa). Renal Sympathetic Denervation: Updates on the State of Medicine

https://pharmaceuticalintelligence.com/2012/12/31/renal-sympathetic-denervation-updates-on-the-state-of-medicine/

 

Lev-Ari, A. (2012U). Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

https://pharmaceuticalintelligence.com/2012/09/02/imbalance-of-autonomic-tone-the-promise-of-intravascular-stimulation-of-autonomics/

Lev-Ari, A. (2012C). Treatment of Refractory Hypertension via Percutaneous Renal Denervation

https://pharmaceuticalintelligence.com/2012/06/13/treatment-of-refractory-hypertension-via-percutaneous-renal-denervation/

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Renal Denervation Technology of Vessix Vascular, Inc. been acquired by Boston Scientific Corporation (BSX) to pay up to $425 Million

Reporter: Aviva Lev-Ari, PhD, RN

For a detailed study of available technologies and who are the KEY Manufacturers for Renal Denervation Technology

go to 

Treatment of Refractory Hypertension via Percutaneous Renal Denervation

https://pharmaceuticalintelligence.com/2012/06/13/treatment-of-refractory-hypertension-via-percutaneous-renal-denervation/

Boston Scientific Corporation (BSX) Paying Up to $425 Million for Vessix Vascular, Inc.

11/8/2012 7:05:44 AM

NATICK, Mass., Nov. 8, 2012 /PRNewswire/ — Boston Scientific Corporation (NYSE: BSX) is extending its reach into the strategically critical renal denervation market by signing a definitive agreement to acquire Vessix Vascular, Inc., a privately held company based in Laguna Hills, California. Vessix Vascular has developed a catheter-based renal denervation system for the treatment of uncontrolled hypertension. The acquisition is expected to close by the end of November 2012.

“Hypertension is a major global healthcare challenge, affecting more than one billion people worldwide,” said Mike Mahoney, president and chief executive officer at Boston Scientific. “Renal denervation represents a potential breakthrough therapy for the treatment of uncontrolled hypertension and is an important part of the Boston Scientific growth strategy. The acquisition of Vessix Vascular adds a second generation, highly differentiated technology to our hypertension strategy while accelerating our entry into what we expect to be a multi-billion dollar market by 2020.”

Hypertension is the leading attributable cause of death worldwide. Despite the widespread availability of antihypertensive medications, the blood pressure of many patients remains high and uncontrolled. Renal denervation is an emerging, catheter-based therapy for medication-resistant hypertension that uses radiofrequency energy to disrupt the renal sympathetic nerves whose hyperactivity leads to uncontrolled high blood pressure. Renal denervation has been demonstrated in published clinical studies to significantly reduce systolic blood pressure.

The Vessix Vascular V2 Renal Denervation System has received CE Mark in Europe and TGA approval in Australia. Vessix Vascular has initiated the REDUCE-HTN post-market surveillance study and expects to initiate a full launch of the product in CE Mark countries in 2013.

A high-resolution image of the Vessix Vascular V2 Renal Denervation System is available for download at:http://bostonscientific.mediaroom.com/image-gallery?mode=gallery&cat=1762.

“The Vessix System offers the potential for a significant step forward in the treatment of uncontrolled hypertension,” said Prof. Horst Sievert, M.D., Ph.D., Director of the CardioVascular Center Frankfurt, Sankt Katharinen Hospital, in Frankfurt, Germany. “In my experience, the system offers ease of use, faster treatment times with decreased patient discomfort and an intuitive approach to renal denervation that leverages the expertise of the interventionalist with balloon catheter technology.”

“We expect that hypertension therapies will be a key growth driver for Boston Scientific going forward,” said Jeff Mirviss, president of the Peripheral Interventions business for Boston Scientific. “We believe the Vessix Vascular Renal Denervation System will position us for leadership in this important market. We look forward to offering this technology to help patients better control their blood pressure, which also may lead to reduced healthcare costs associated with uncontrolled hypertension.”

Upon completion of the acquisition, Vessix Vascular will become part of the Peripheral Interventions business at Boston Scientific. The portfolio of this business includes products that treat vascular system blockages in areas such as the carotid and renal arteries and the lower extremities.

“Physician response to the V2 Renal Denervation System has been outstanding,” said Raymond W. Cohen, chief executive officer at Vessix Vascular. “We are confident that the combination of the Vessix Vascular renal denervation technology with the Boston Scientific broad global clinical and commercial scale will result in a new standard for the treatment of uncontrolled hypertension.”

The agreement calls for an upfront payment of $125 million, plus additional clinical- and sales-based milestones aggregating a maximum of $300 million over the period between 2013 and 2017. Boston Scientific currently expects the net impact of this transaction on adjusted earnings per share to be immaterial for years 2013 and 2014 and break-even to accretive thereafter, and more dilutive on a GAAP basis as a result of acquisition-related net charges and amortization, which will be determined during the fourth quarter.

The V2 Renal Denervation System is an investigational device and not available for use or sale in the United States.

About Vessix Vascular
Founded in 2003, Vessix is a private company developing novel RF balloon catheter and bipolar RF generator technology. The company has operations in the United States and in Europe, and is backed by world-class European and U.S. venture capital firms including NeoMed Management, Edmond de Rothschild Investment Partners, OrbiMed Advisors LLC and Christopher Weil & Company.

About Boston Scientific
Boston Scientific is a worldwide developer, manufacturer and marketer of medical devices that are used in a broad range of interventional medical specialties. For more information, please visit: http://www.bostonscientific.com/.

Cautionary Statement Regarding Forward-Looking Statements
This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Forward-looking statements may be identified by words like “anticipate,” “expect,” “project,” “believe,” “plan,” “estimate,” “intend” and similar words. These forward-looking statements are based on our beliefs, assumptions and estimates using information available to us at the time and are not intended to be guarantees of future events or performance. These forward-looking statements include, among other things, statements regarding our business plans, our growth strategy and drivers, markets for our products and our position in those markets, timing of closing the transaction and expected accretion/dilution, product launches, and product performance and importance. If our underlying assumptions turn out to be incorrect, or if certain risks or uncertainties materialize, actual results could vary materially from the expectations and projections expressed or implied by our forward-looking statements. These factors, in some cases, have affected and in the future (together with other factors) could affect our ability to implement our business strategy and may cause actual results to differ materially from those contemplated by the statements expressed in this press release. As a result, readers are cautioned not to place undue reliance on any of our forward-looking statements.

Factors that may cause such differences include, among other things: future economic, competitive, reimbursement and regulatory conditions; new product introductions; demographic trends; intellectual property; litigation; financial market conditions; and future business decisions made by us and our competitors. All of these factors are difficult or impossible to predict accurately and many of them are beyond our control. For a further list and description of these and other important risks and uncertainties that may affect our future operations, see Part I, Item 1A Risk Factors in our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, which we may update in Part II, Item 1A Risk Factors in Quarterly Reports on Form 10-Q we have filed or will file hereafter. We disclaim any intention or obligation to publicly update or revise any forward-looking statements to reflect any change in our expectations or in events, conditions or circumstances on which those expectations may be based, or that may affect the likelihood that actual results will differ from those contained in the forward-looking statements. This cautionary statement is applicable to all forward-looking statements contained in this document.

CONTACT:
Steven Campanini
508-652-5740 (office)
Media Relations
Boston Scientific Corporation
steven.campanini@bsci.com

Michael Campbell
508-650-8023 (office)
Investor Relations
Boston Scientific Corporation
investor_relations@bsci.com

SOURCE: Boston Scientific Corporation, 11/8/2012

Additional coverage of the Vascular and Cardiac Repair Medical Devices Market 

go to:

Cardiovascular Medical Devices

 

Lev-Ari, A. (2012U). Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

https://pharmaceuticalintelligence.com/2012/09/02/imbalance-of-autonomic-tone-the-promise-of-intravascular-stimulation-of-autonomics/

Lev-Ari, A. (2012R). Coronary Artery Disease – Medical Devices Solutions: From First-In-Man Stent Implantation, via Medical Ethical Dilemmas to Drug Eluting Stents https://pharmaceuticalintelligence.com/2012/08/13/coronary-artery-disease-medical-devices-solutions-from-first-in-man-stent-implantation-via-medical-ethical-dilemmas-to-drug-eluting-stents/

 

Lev-Ari, A. (2012K). Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

https://pharmaceuticalintelligence.com/2012/07/18/percutaneous-endocardial-ablation-of-scar-related-ventricular-tachycardia/

 

Lev-Ari, A. (2012C). Treatment of Refractory Hypertension via Percutaneous Renal Denervation

https://pharmaceuticalintelligence.com/2012/06/13/treatment-of-refractory-hypertension-via-percutaneous-renal-denervation/

Lev-Ari, A. (2012D). Competition in the Ecosystem of Medical Devices in Cardiac and Vascular Repair: Heart Valves, Stents, Catheterization Tools and Kits for Open Heart and Minimally Invasive Surgery (MIS)

https://pharmaceuticalintelligence.com/2012/06/22/competition-in-the-ecosystem-of-medical-devices-in-cardiac-and-vascular-repair-heart-valves-stents-catheterization-tools-and-kits-for-open-heart-and-minimally-invasive-surgery-mis/

Lev-Ari, A. (2012E). Executive Compensation and Comparator Group Definition in the Cardiac and Vascular Medical Devices Sector: A Bright Future for Edwards Lifesciences Corporation in the Transcatheter Heart Valve Replacement Market

https://pharmaceuticalintelligence.com/2012/06/19/executive-compensation-and-comparator-group-definition-in-the-cardiac-and-vascular-medical-devices-sector-a-bright-future-for-edwards-lifesciences-corporation-in-the-transcatheter-heart-valve-replace/

 

Lev-Ari, A. (2012F). Global Supplier Strategy for Market Penetration & Partnership Options (Niche Suppliers vs. National Leaders) in the Massachusetts Cardiology & Vascular Surgery Tools and Devices Market for Cardiac Operating Rooms and Angioplasty Suites

https://pharmaceuticalintelligence.com/2012/06/22/global-supplier-strategy-for-market-penetration-partnership-options-niche-suppliers-vs-national-leaders-in-the-massachusetts-cardiology-vascular-surgery-tools-and-devices-market-for-car/

 

Lev-Ari, A. (2012G).  Heart Remodeling by Design: Implantable Synchronized Cardiac Assist Device: Abiomed’s Symphony

https://pharmaceuticalintelligence.com/2012/07/23/heart-remodeling-by-design-implantable-synchronized-cardiac-assist-device-abiomeds-symphony/

 

Lev-Ari, A. (2006S). First-In-Man Stent Implantation Clinical Trials & Medical Ethical Dilemmas. Bouve College of Health Sciences, Northeastern University, Boston, MA 02115

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FDA Approval for Under-Skin Defibrillator goes to Boston Scientific Corporation

Reporter: Aviva Lev-Ari, PhD, RN

 

Boston Scientific Corporation (BSX) Wins FDA Approval for Under-Skin Defibrillator

 

10/1/2012 7:09:13 AM

 

NATICK, Mass., Sept. 28, 2012 /PRNewswire/ — The U.S. Food and Drug Administration has granted Boston Scientific Corporation (NYSE: BSX) regulatory approval for its S-ICD® System, the world’s first and only commercially available subcutaneous implantable defibrillator (S-ICD) for the treatment of patients at risk for sudden cardiac arrest (SCA). The S-ICD System sits entirely just below the skin without the need for thin, insulated wires — known as electrodes or ‘leads’ — to be placed into the heart. This leaves the heart and blood vessels untouched, offering patients an alternative to transvenous implantable cardioverter defibrillators (ICDs), which require leads to be placed in the heart itself.

 

“The S-ICD System establishes the first new category of cardiac rhythm management devices since the introduction of cardiac resynchronization therapy,” said Raul Weiss, M.D., Associate Professor-Clinical, Cardiovascular Medicine at The Ohio State University. “Doctors now have a breakthrough treatment option that provides protection from sudden cardiac arrest without touching the heart.”

Approval of the S-ICD System was based on data from a 330-patient, prospective, non-randomized, multicenter clinical study, which evaluated the safety and effectiveness of the system in patients at risk of SCA. The S-ICD System met the primary endpoints of the study, and results were presented earlier this year at the Heart Rhythm Society 33rd Annual Scientific Sessions. The study results support that the S-ICD System is an important new treatment option for a wide range of primary and secondary prevention patients.

“With the addition of the S-ICD System, we believe Boston Scientific has a compelling and highly differentiated portfolio that will help fuel our growth strategy,” said Hank Kucheman, chief executive officer, Boston Scientific. “We are the only company to offer an FDA-approved subcutaneous implantable defibrillator and expect this to be the case for several years. The S-ICD System, coupled with our numerous recent regulatory approvals and our other innovative products, such as the WATCHMAN® Left Atrial Appendage Closure Device and Alair® Bronchial Thermoplasty System for the treatment of severe asthma, demonstrates our continued commitment to developing and bringing to market innovative products for physicians and their patients.”

Sudden cardiac arrest is an abrupt loss of heart function. Most episodes are caused by the rapid and/or chaotic activity of the heart known as ventricular tachycardia or ventricular fibrillation. Recent estimates show that approximately 850,000 people in the United States are at risk of SCA and indicated for an ICD device, but remain unprotected.

“Each year, thousands of patients indicated for an ICD are not referred to a specialist and remain untreated,” said William T. Abraham, MD, FACC, Director, Division of Cardiovascular Medicine at The Ohio State University Heart Center. “The S-ICD System is an important new treatment option that has the potential to improve patient acceptance of ICD therapy.”

The S-ICD System is designed to provide the same protection from sudden cardiac arrest as transvenous ICDs. The system has two main components: (1) the pulse generator, which powers the system, monitors heart activity, and delivers a shock if needed, and (2) the electrode, which enables the device to sense the cardiac rhythm and deliver shocks when necessary. Both components are implanted just under the skinthe generator at the side of the chest, and the electrode beside the breastbone. Unlike transvenous ICDs, the heart and blood vessels remain untouched. Implantation with the S-ICD System is straightforward using anatomical landmarks, without the need for fluoroscopy (an x-ray procedure that makes it possible to see internal organs in motion). Fluoroscopy is required for implanting the leads attached to transvenous ICD systems.

Boston Scientific expects to begin a phased launch of the S-ICD System that will expand over time as medical professionals are trained on the safe and effective use of the system. The company acquired the S-ICD System earlier this year when it completed the acquisition of Cameron Health, Inc. The S-ICD System received CE Mark in 2009 and is commercially available in many countries in Europe as well as in New Zealand. To date, more than 1,400 devices have been implanted in patients around the world. To download a high-resolution image of the S-ICD System go to: http://bostonscientific.mediaroom.com/home.

The S-ICD System is intended to provide defibrillation therapy for the treatment of life-threatening ventricular tachyarrhythmias in patients who do not have symptomatic bradycardia, incessant ventricular tachycardia, or spontaneous, frequently recurring ventricular tachycardia that is reliably terminated with anti-tachycardia pacing.

The WATCHMAN device is an investigational device in the United States. It is limited by applicable law to investigational use and not available for sale.

About Boston Scientific
Boston Scientific is a worldwide developer, manufacturer and marketer of medical devices that are used in a broad range of interventional medical specialties. For more information, please visit: www.bostonscientific.com.

Cautionary Statement Regarding Forward-Looking Statements
This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Forward-looking statements may be identified by words like “anticipate,” “expect,” “project,” “believe,” “plan,” “estimate,” “intend” and similar words. These forward-looking statements are based on our beliefs, assumptions and estimates using information available to us at the time and are not intended to be guarantees of future events or performance. These forward-looking statements include, among other things, statements regarding our business plans and growth strategy, markets for our products, regulatory approvals, the importance of the S-ICD System, our technology, clinical trials, product launches, product performance and competitive offerings. If our underlying assumptions turn out to be incorrect, or if certain risks or uncertainties materialize, actual results could vary materially from the expectations and projections expressed or implied by our forward-looking statements. These factors, in some cases, have affected and in the future (together with other factors) could affect our ability to implement our business strategy and may cause actual results to differ materially from those contemplated by the statements expressed in this press release. As a result, readers are cautioned not to place undue reliance on any of our forward-looking statements.

Factors that may cause such differences include, among other things: future economic, competitive, reimbursement, legal and regulatory conditions; clinical trials and outcomes; new product introductions; product performance; demographic trends; intellectual property; litigation; financial market conditions; and future business decisions made by us and our competitors. Such factors are difficult or impossible to predict accurately and many of them are beyond our control. For a further list and description of these and other important risks and uncertainties that may affect our future operations, see Part I, Item 1A Risk Factors in our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, which we may update in Part II, Item 1A Risk Factors in Quarterly Reports on Form 10-Q we have filed or will file hereafter. We disclaim any intention or obligation to publicly update or revise any forward-looking statements to reflect any change in our expectations or in events, conditions or circumstances on which those expectations may be based, or that may affect the likelihood that actual results will differ from those contained in the forward-looking statements. This cautionary statement is applicable to all forward-looking statements contained in this document.

CONTACT: Denise Kaigler
508-650-8330 (office)
Media Relations
Boston Scientific Corporation
denise.kaigler@bsci.com
Michael Campbell
508-650-8023 (office)
Investor Relations
Boston Scientific Corporation
investor_relations@bsci.com

SOURCE Boston Scientific Corporation

www.bostonscientific.com

 

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Treatment of Refractory Hypertension via Percutaneous Renal Denervation 

Curator: Aviva Lev-Ari, PhD, RN

UPDATED  8/5/2013

VIEW VIDEO – Editorial the Heart.org

Renal denervation: Clinical lessons from around the world

Renal Denervation treatment represents a medical subfield, it has its roots in surgical sympathectomy techniques dating back to the 1930s. This radical approach to blood pressure control, which did not specifically target renal nerves, was ultimately abandoned due to associated perioperative complications. However, experience in renal transplantation, a procedure in which the renal nerves are selectively severed, suggests that the denervated kidney can maintain volume and electrolyte homeostasis.

http://ajpregu.physiology.org/content/298/2/R245.full

http://www.ncbi.nlm.nih.gov/pubmed/3326559?dopt=Abstract

Potential effects of renal denervation are on improved glucose control, sleep apnea, and treatment of heart failure syndromes and renal dysfunction – all consequences of sustained hypersympathetic activity.

Based on these observations, the specific targeting of renal nerves as a major operative in the pathophysiology of hypertension and other conditions associated with increased sympathetic activity (renal dysfunction and heart failure) appears to be an attractive therapeutic approach.

http://bmctoday.net/evtoday/2012/02/article.asp?f=renal-artery-denervation-a-brave-new-frontier

A new therapeutic paradigm of percutaneous renal artery denervation using the application of radiofrequency (RF) energy (Symplicity renal denervation system [Ardian, acquired by Medtronic, Inc., Minneapolis, MN]) has recently been demonstrated to be safe, effective, and durable in significantly reducing systolic blood pressure in patients with resistant hypertension.

This new technology represents the first time that physicians have been able to target renal nerves specifically via a catheter-based intervention. This endovascular approach opens the door to better understanding the relationship between sympathetic hyperactivity and hypertension.

Current therapeutic strategies center on lifestyle changes and pharmacologic interventions; however, the rates of blood pressure control and therapeutic efforts to reduce the rate of progression of hypertensive end-organ damage (resulting in myocardial infarction, stroke, and renal dysfunction) remain a neglected priority.

http://rd.springer.com/article/10.1007/s11906-010-0119-1

Renal denervation is used to treat uncontrolled hypertension, or high blood pressure, by the ablation of the nerves that line the renal arteries using a catheter. The Cleveland Clinic called renal denervation the No. 1 healthcare innovation of 2012. More than 12 million patients worldwide whose blood pressure remains uncontrolled despite taking three or more anti-hypertensive medications representing a global market opportunity for renal denervation that could ultimately grow to $30 billion. The Millennium Research Group estimates that the hypertension-treating devices could generate $4.4 billion per year, Bloomberg reported. That number could swell if the FDA indicates the systems for simple hypertension and not just the drug-resistant sort. As Bloomberg notes, a boom in hypertension devices would be a welcome development for the device industry, which has struggled over the past four years with recalls, litigation and regulatory woes, leading to a 7% decline in Standard & Poor’s Healthcare Equipment Index.

“At least 23 companies, mainly smaller, private companies are developing products,” Wang said, based on information she gathered at the American College of Cardiology Conference in Chicago in March.

http://medcitynews.com/2012/04/medtronic-aside-a-whole-host-of-firms-chasing-hypertension-market/

http://www.fiercemedicaldevices.com/story/bloomberg-hypertension-devices-could-pay-big-us/2012-05-25?utm_medium=nl&utm_source=internal

According to the American Heart Association, a 5 mm Hg (millimeters of mercury) reduction in systolic blood pressure results in a 14 percent decrease in stroke, a 9 percent decrease in heart disease, and a 7 percent decrease in overall mortality. Renal denervation has shown in clinical studies to be safe, durable and effective in reducing systolic blood pressure by as much as 20 percent.

Numerous analysts suggest that there are more than 12 million patients worldwide whose blood pressure remains uncontrolled, despite taking three or more anti-hypertensive medications. This represents a global market opportunity for renal denervation approaching $30 billion.

Procedure Benefits

Hypertension, though often asymptomatic, is the number one risk factor for premature death worldwide.1 Renal Denervation (RDN) treatment aims to address this condition at its source to provide a substantial and durable reduction in blood pressure. After the procedure, people can often return to their normal activities quickly. The benefit is often achieved after several weeks to months.

Benefits and New Indications for Usage of Intravascular Stimulation/Ablation of Autonomics

1. Reduction in Heart Rate and Heart Rate Variability

Dr. Scherlag experiments noted changes in heart rate which have also been reported in SYMPLICITY HTN-1 and SYMPLICITY HTN-2 (8-9).  The SYMPLICITY HTN-2 study demonstrated profound bradycardia in 13% of patients that was treated with atropine.

The intra-procedure effect on heart rate during renal artery denervation documented in the  SYMPLICITY trials is also manifest long term by measuring heart rate variability (10). Indeed, cardiac effects would be expected with autonomic modulation.  Besides the two example above showing that cardiac sympathetic denervation effects heart rate, there are many more that are just beginning to be reported in the literature.

These articles shows the effects of renal denervation on heart rate.

http://www.ncbi.nlm.nih.gov/pubmed/1735574
http://www.ncbi.nlm.nih.gov/pubmed/8777835

A Cleveland Clinic review article states: “Additionally, the resting heart rate was lower and heart rate recovery after exercise improved after the procedure, particularly in patients without diabetes.”
http://www.ccjm.org/content/79/7/501.full

2. Renal Sympathetic Denervation lowers Atrial Fibrillation

This article discusses the effect of renal sympathetic denervation on atrial fibrillation.

http://www.ncbi.nlm.nih.gov/pubmed/22585944

3. Regression of Left Ventricular Hypertrophy, Increase in Ejection Fraction (EF) and improved Diastolic Dysfunction

“Brandt reported regression of left ventricular hypertrophy and significantly improved cardiac functional parameters, including increase in ejection fraction and improved diastolic dysfunction, in a study of 46 patients who underwent renal denervation. This findings suggests a potential beneficial effect on cardiac remodeling.” (Brandt MC, Mahfoud F, Reda S, et al. Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension. J Am Coll Cardiol 2012; 59:901–909)

4. Reduction in Ventricular Tachyarrhythmias (VT)

“Ukena reported reduction in ventricular tachyarrhythmias in two patients with congestive heart failure who had therapy-resistant electrical storm.” (Ukena C, Bauer A, Mahfoud F, et al. Renal sympathetic denervation for treatment of electrical storm: first-inman experience. Clin Res Cardiol 2012; 101:63–67)

5. Intravascular Stimulation of Autonomics Effects on Heart Failure

The most recent data from Europe shows the following effects on heart failure:

http://www.eurekalert.org/pub_releases/2012-08/esoc-rdg082712.php
http://www.theheart.org/article/1364267.do

Dr. Scherlag, writes, [N]early ten examples of the effects of “CARDIAC SYMPATHETIC DENERVATION” and what are the effects on the kidney?

No change in GFR.  No change in creatinine.

https://pharmaceuticalintelligence.com/2012/09/02/imbalance-of-autonomic-tone-the-promise-of-intravascular-stimulation-of-autonomics/

Procedure Risks

Although major complications are uncommon, RDN treatment carries many of the same risks as an angioplasty procedure for the treatment of artery disease. The catheter insertion site could become infected, become bruised or bleed heavily. Other possible complications include heart attack, stroke, kidney damage or malfunction, heart rhythm disturbances, arterial damage, hypotension, sudden cardiac death, burns and pain. Imaging agents, pain medications and anti-spasm agents are commonly used during the procedure and carry known risks.

1. Mathers, C., et al. World Health Organization; 2009

http://www.ardian.com/ous/patients/benefits-risks.shtml

Medical Debate on the Procedure – The candidates are hypertensive patients receiving blood-pressure-lowering medication that are truly “resistant.”

The Symplicity system (Medtronic) is the far-and-away front runner, having demonstrated average office-based BP drops of 32/12 mm Hg at six months in the SYMPLICITY HTN 2 trial, as reported by heartwire, with 84% of patients having had a >10-mm-Hg drop in systolic blood pressure from baseline.

Upwards of 20 other companies, according to Dr Ron Waksman (Washington Hospital, DC), are busy developing competing systems, some of which were featured in a EuroPCR session devoted to emerging technologies in May 2012 in Paris.

Leading this pack is St Jude’s EnligHTN system, which received CE Mark on the opening day of the meeting. Dr Stephen Worthley (Royal Adelaide Hospital, Australia) presented 30-day results in 47 resistant-hypertension patients treated with the multielectrode, RF-ablation-based system. Mean office BP changes at one month in EnligHTN 1 were -28 systolic and -10 diastolic (p<0.0001 from baseline), with 78% of patients having systolic BP drops of >10 mm Hg.

https://www.massdevice.com/news/europcr-st-judes-enlightn-lowers-blood-pressure-faster-rival-systems

In terms of safety, no serious complications were seen in the renal artery or at the access site in the EnligHTN study; minor procedure-related events included four hematomas, three vasovagal responses to sheath removal, and two postprocedure transient bradycardias.

Other devices featured in the session included a second RF-energy system and two ultrasound systems, see below technology description by supplier.

The risk of cardiovascular death doubles with every 20 point increase in systolic blood pressure, so an average blood pressure reduction of 28 points is quite significant and demonstrates just how effective the technology is. Principal investigator Prof. Stephen Worthley said in prepared remarks. “From other clinical trials studying the impact of renal denervation we have learned that blood pressure continues to be reduced over time, so I would not be surprised to see this trend continue and see an even greater benefit for patients.” St. Jude’s study included 47 patients with high blood pressure that wasn’t managed with drug therapy. Participants had an average of 176/96 mmHg baseline blood pressure, despite taking multiple medications, before the denervation procedure and an average of 148/87 mmHg after. More than 40% had systolic rates below 140 mmHg.

http://investors.sjm.com/phoenix.zhtml?c=73836&p=irol-newsArticle&ID=1695802

Interventionalists who spoke with heartwire were unvaryingly excited about the potential of renal denervation, with some caveats.

“You need enthusiasm to develop new things, and in hypertension we haven’t seen an innovation in decades,” Dr Thomas Lüscher (University Hospital Zürich, Switzerland) told heartwire. “So just the possibility that you would be able to have a persistent treatment effect by a procedure that helps severe hypertension patients and maybe in the future even the option to cure hypertension is very exciting indeed. But I agree it’s a dream at this point. I think we need the SYMPLICITY HTN 3 trial, which hopefully will confirm what the other studies have shown.”

Now enrolling at as many as 90 US centers, SYMPLICITY HTN 3, Lüscher pointed out, has design characteristics addressing two concerns with the earlier trials, namely a sham procedure for the control group and ambulatory blood-pressure monitoring in all patients.

During the same emerging-technologies session, Lüscher explored the albeit-scant data supporting a role for renal denervation in other conditions: everything from metabolic syndrome and obstructive sleep apnea to heart failure, atrial fibrillation, and polycystic-ovary syndrome.

But his counterpoint, Dr Jean Renkin (UCL St Luc University Hospital, Brussels, Belgium), was skeptical, pointing to the myriad unanswered questions with the technology.

“Currently, reasonably solid data are available only for patients with hypertension resistant to pharmacotherapy, which cannot necessarily be extrapolated to other forms of hypertension or conditions referred to [by Dr Lüscher]. However, at this point in time, no clouds have appeared in the sky, so let us dream on.”

Dr Renkin had one staggering number for the audience to consider: of 5000 patients who have undergone renal denervation, only 250 were actually treated as part of clinical studies. While no device has US approval, five denervation systems already hold CE Mark in Europe and are being used with increasing frequency.

Treating the Truly Medication Treatment “Resistant”

For a comprehensive presentation of Triple Antihypertensive Combination Therapy Significantly Lowers Blood Pressure in Hard-to-Treat Patients with Hypertension and Diabetes, refer to

https://pharmaceuticalintelligence.com/2012/05/29/445/

Another talking point is the proportion of patients who are truly “resistant.” The number agreed on by Lüscher, Waksman, and session comoderator Dr Robert Whitbourn (St Vincent’s Hospital, Fitzroy, Australia) was that just 3% of all hypertensive patients receiving blood-pressure-lowering medication are truly “resistant.” Numbers as high as 30% have been suggested in other reports, he noted.

“Interestingly, when we’ve been involved in various trials, every cardiologist says they have hundreds of these patients, but when we actually go to get them, no one actually has any,” Whitbourn quipped. “I think it should be a sobering thought—the numbers are actually quite small.”

Dr William Wijns (Cardiovascular Center Aalst, Belgium), also speaking with heartwire, agreed that the subset was “small” but argued it was “still big numbers, millions of people,” and “a massive unmet need.”

Waksman, insisting he was “excited” by what he called “robust reductions in blood pressure,” nevertheless urged eager interventionalists to work with hypertension experts and resist the urge “to jump on patients before we truly verify that they are resistant to medical treatment.”

In the vast majority of people even for whom renal denervation is appropriate, it “won’t be a cure,” Waksman said. “Most of these patients will have to continue on medical treatment—this is not replacing medical treatment, it is just getting [patients] more in control.”

http://www.theheart.org/article/1402321/print.do

The Global Supplier Ecosystem for Renal Denervation Systems

US Campbell, CA Kona Medical is attempting to address these limitations. The system delivers energy from outside the patient to the renal nerves. Ultimately, the procedure will be a “no puncture,” noninvasive technique, compatible with technologies that will allow for temperature and lesion mapping. A noninvasive procedure will allow titration of the therapy— that is, the application of patient-specific dose fractions while monitoring therapeutic effect in between fractions. The basis of the technology is focused ultrasound, not high intensity (HIFU) as one might see and expect in the treatment of tumors, but low-intensity focused ultrasound (LIFU). The biologic underpinnings of this treatment are described in past literature for treating nerves using ultrasound. Kona noninvasive system. The system is depicted in a custom chair; another version of the system is compatible with a standard fluoroscopy or MRI table. Both ultrasound (through elastography and the evolution of temperature mapping and MRI) allow further imaging and analysis of the treatment area. The dose distribution surrounding the artery is that of an annular ring around the wall of the artery. Kona has shown in animal studies that a heat/vibratory cloud at one plane along the artery is highly effective at long-term inhibition of renal nerves with no visible effect on any portion of the artery at any time point.

US, Ronkonkoma, NY & Germany – Paradise  by ReCor Medical 6-F compatible catheter with a cylindrical transducer that emits ultrasound energy circumferentially, allowing for a more efficient renal denervation procedure First-in-human (15 patients at 3 months) BP drop, mm Hg -32/-16 at 3 mo. The ultrasound transducer lies within a low-pressure balloon that allows for self-centering of the transducer and gentle contact with the artery wall for uniform circumferential denervation. This means that nerves below the surface of the artery wall are damaged in 360° with a single emission. The balloon also enables cooled fluid to circulate during the energy delivery process, thereby cooling the endothelial wall and protecting it from any excessive heating that could be caused by other energy sources or designs. Preliminary F-I-M clinical data for PARADISE were reported previously at the “TRenD 2012” transcatheter renal denervation scientific meeting by cardiologist Thomas A. Mabin, M.D., Vergelegen Medi-Clinic, South Africa. The updated PARADISE data show that systolic blood pressure was reduced by a statistically significant average of 36 mm Hg in 8 patients at 90-days follow-up. The scientific literature demonstrates that only a 5 mm Hg reduction in BP results in a 14% decrease in stroke, a 9% decrease in heart disease, and a 7% decrease in mortality.

US, San Leandro, CA The Mercator Bullfrog by Mercator MedSystems, Inc. is a catheter-guided system designed to inject therapeutic agents directly, nonsystemically, and safely through blood vessel walls into adventitial tissues and has received US Food and Drug Administration 510(k) clearance. The Bullfrog catheter is tipped with a balloon-sheathed microneedle and is guided and inflated in a manner similar to an angioplasty catheter but with far lower expansion pressures (2 atm vs 6–20 atm) in vessels of 3 to 6 mm in diameter. It is compatible with 0.014-inch guidewires and 6-F introducer sheaths. When the desired injection site is reached, the balloon is inflated with saline and radiopaque contrast, securing the system for injection and sliding the microneedle through the vessel wall. Nonclinical studies have shown that the Bullfrog catheter is able to deliver up to 5 mL per injection into the renal artery adventitia with no apparent safety concerns. Guanethidine Ismelin) is delivered to the renal artery adventitia to accomplish sympathetic denervation. Given locally, guanethidine is known to induce an autonomic denervation directly and through an immune-mediated pathway. Mercator’s preclinical experiments have shown that guanethidine, injected at appropriate concentrations into the adventitial space around renal arteries, selectively ablates the nerves in the adventitia around the renal artery after a single, 20-minute procedure

J Neurosci. 1983;3:714-724

US – Laguna Hills, CA – V2 Radiofrequency Baloon by Vessix Vascular, Inc. Bipolar RF balloon catheter REDUCE-HTN pilot (10 patients)

BP drop, mm Hg -30/-11 at 1 mo V 2 catheter, a patented noncompliant balloon catheter with RF electrodes and thermistors mounted on the exterior of the balloon, and the proprietary V 2 bipolar RF generator. Once inserted into the renal artery, a 30-second inflation/treatment per renal artery delivers simultaneous RF therapy with independent temperature control to all electrode pairs. V 2 catheter is available in balloon diameters ranging from 4 to 7 mm, with a balloon length of 25 mm. Larger-diameter balloons have eight electrode pairs, and smaller-diameter balloons have four to six electrode pairs made of solid gold, which are biocompatible and facilitate good electrode contact with the renal arterial wall. In addition, the electrodes are radiopaque, allowing the V 2 catheter to be easily visualized under fluoroscopy. Beginning in the first quarter of 2012, the V 2 renal denervation system will be utilized in the company’s first international, multicenter clinical study: REDUCEHTN.

Israel, Tel Aviv – Tivus by Cardiosonic  A6-F transducer-tipped catheter, ultrasound energy (Animal data only) The solution for renal denervation is a high-intensity, nonfocused ultrasonic (US) catheter system named TIVUS (Therapeutic IntraVascular UltraSound) (Figure 3). By applying ultrasonic energy, the TIVUS technology enables remote, localized, controlled, and repeatable thermal modulation of the renal vessel wall tissue, resulting in safe renal nerve ablation. The remote thermal effect is located in the adventitia and perivascular region, with no thermal damage to the endothelium and media, therefore, preventing the development of vessel injury processes. Swine kidney tissue NE concentrations at 30- and 90-day follow-up have demonstrated successful renal denervation as witnessed by a 50% or more decline in tissue NE. Localized tissue thermal modulation/ablation, without damage to the blood vessel wall.

US, MN – SYMPLICITY HTN 2 by Medtronic   average office-based BP drops of BP drop, mm Hg 32/12 mm Hg at six months in the SYMPLICITY HTN 2 trial, as reported by heartwire, with 84% of patients having had a >10-mm-Hg drop in systolic blood pressure from baseline. 14 points in 30 days and 27 points after 1 year. Available in Europe. Medtronic is the furthest ahead in its development process, predicting it will get Symplicity on the American market by 2015. catheter in the renal artery near each kidney to deliver radiofrequency energy to ablate the nerves. A single electrode in contrast to St. Jude’s mutli-electrode approach, is already on the road to FDA review with clinical trials approved last summer in the U.S. Symplicity system has been safely used in nearly 5,000 patients since commercialization

US, MN – EnligHTN 1 by  St Jude radiofrequency (RF) energy to create lesions (tiny scars) along the renal sympathetic nerves Mean office BP changes at one month in BP drop, mm Hg 28 systolic and -10 diastolic after 1 month (p<0.0001 from baseline), with 78% of patients having systolic BP drops of >10 mm Hg. St. Jude Medical’s (St. Paul, MN) announcement in late 2011 of the first patient to be enrolled in their first-in-man ARSENAL trial 15 at the University of Adelaide

Ireland, Dublin – OneShot™ by Covidien acquisition of Maya Medical, Saratoga, CA New Irrigated RF Balloon Catheter secure first human use for the device in the third quarter of this year, followed by a CE mark for the drug-resistant hypertension treatment in 2013. Presumably, a filing with the FDA would follow that. the OneShot renal denervation system, was born out of the company’s extensive expertise in radiofrequency (RF) ablation and percutaneous coronary interventions (PCI), drawing upon the benefits and best practice standards of each distinct yet complementary clinical discipline. The result is a unique product platform that could further accelerate the paradigm shift in the management of resistant hypertension. consistent with Maya’s balloon-based approach is the ability to deliver predictable apposition of the RF electrode to the vessel wall for more controlled targeted delivery of the RF energy. By offering a more reliable single-treatment approach coupled with enhanced ease of use and reduced procedure times, Maya Medical believes its OneShot renal denervation system has the potential to significantly expand clinical adoption

http://bmctoday.net/evtoday/2012/02/article.asp?f=renal-artery-denervation-a-brave-new-frontier

US, Natick, MA Boston Scientific lags behind in the race to cash in on hypertension-treating devices, incoming CEO Michael Mahoney said at a Monday conference that it has a plan for its RDN renal denervation system. As MassDevice reports, Mahoney said Boston Sci expects to secure first human use for the device in the third quarter of this year, followed by a CE mark for the drug-resistant hypertension treatment in 2013.

St Jude’s EnligHTN system

Said Frank Callaghan, president of the St. Jude Medical Cardiovascular Division “This launch is important because it represents a significant growth opportunity and exemplifies our commitment to advancing the practice of medicine. We’ve applied the decades of insight we’ve gained from developing successful ablation technologies that treat cardiac arrhythmias to establish an innovative solution for hypertension.” With the unique basket design, each placement of the ablation catheter allows a consistent and predictable pattern of four ablations in 90-second intervals. Compared to single electrode ablations, the multi-electrode EnligHTN system has the potential to improve consistency and procedural reliability, save time as well as result in workflow and cost efficiencies. Additionally, the minimal catheter repositioning may result in a reduction of contrast and fluoroscopic (x-ray) exposure. The technology includes a guiding catheter, ablation catheter and ablation generator. The generator uses a proprietary, temperature-controlled algorithm to deliver effective therapy.

http://investors.sjm.com/phoenix.zhtml?c=73836&p=irol-newsArticle&ID=1695802

http://medgadget.com/2012/05/st-jude-medical-launches-enlightn-renal-denervation-system.html

St Jude’s EnligHTN system – view video

http://www.sjmprofessional.com/Products/Intl/Renal-Ablation-Therapy/enlightn-renal-denervation-system.aspx

Covidien

Unveiled a Novel Renal Denervation System OneShot™ at EuroPCR congress in Paris on 5/16/2012. “Live” Cases with New Irrigated RF Balloon Catheter for Treatment of Medication-resistant Hypertension and poor outcomes of pharmacological agents. The OneShot system is an irrigated, radiofrequency (RF) based balloon catheter used to ablate the renal sympathetic nerves located in the outer wall of the renal arteries. The OneShot technology received CE mark clearance in February 2012.

The OneShot system was featured in “live” cases at the Covidien-sponsored “Tools & Techniques (TNT) Interventions” presentation and panel session for hypertension and renal denervation at the EuroPCR congress. Professor Dirk Scheinert performed two cases at Park Hospital in Leipzig, Germany, that were transmitted live at the Palais des Congrès de Paris. In addition, John Ormiston, MD, Medical Director for Mercy Angiography and President of the Asia-Pacific Society of Interventional Cardiology in New Zealand, presented first-in-human results of cases performed with the OneShot system in New Zealand. The OneShot system and Covidien’s other endovascular solutions was on display at the EuroPCR meeting.

Additional faculty in the TNT session is a distinguished group of speakers including:

Professor Karl-Heinz Kuck, MD, F.A.C.C. – Director, Cardiology Department
Allgemeines Krankenhaus St. Georg – Hamburg, Germany

Dr. Stephen R. Ramee, FACC, FSCAI
Ochsner Medical Center – New Orleans, Louisiana

Dr. John Ormiston, MBChB, FRACP – Medical Director
Mercy Hospital Angiography Unit – Auckland, New Zealand

Professor Marc Sapoval, MD, PhD – Department Head
Cardiovascular/Interventional Radiology – Hospital Pompidou University – Paris, France

Dr. Renu Virmani – Medical Director
CVPath Institute – Gaithersburg, Maryland

Covidien discloses that it purchased Maya Medical for $60 million in cash on April 20. If Maya Medical meets certain regulatory and sales milestones, it will receive up to an additional $170 million. Covidien notes that Maya Medical’s OneShot system received the CE Mark in February.

MedCity News was the first to report Covidien’s interest in Maya Medical on 5/8/2012.

In a note to investors Monday, analyst Bob Hopkins of Bank of America said that renal denervation “has the potential to be one of the largest new markets in medtech over the next 2-4 years and for [Covidien] this looks like another small deal with big potential.”

http://medcitynews.com/2012/05/covidien-discloses-60m-purchase-of-hypertension-treatment-firm/?edition=medical-devices

Clinical Trial for RAPID is ongoing

 Rapid Renal Sympathetic Denervation for Resistant Hypertension (RAPID)

This study is currently recruiting participants.

Verified June 2012 by Maya Medical

First Received on January 25, 2012.   Last Updated on June 4, 2012   History of Changes

Sponsor: Covidien (Maya Medical)
Collaborator: Meditrial Europe LTD
Information provided by (Responsible Party): Maya Medical
ClinicalTrials.gov Identifier: NCT01520506

  Purpose

Maya Medical OneShot™ Ablation System use is to deliver low-level radio frequency (RF) energy through the wall of the renal artery to denervate the human kidney.

Condition Intervention Phase
Hypertension, Resistant to Conventional Therapy Device: Maya Medical OneShot Phase 2
Study Type: Interventional
Study Design: Endpoint Classification: Safety/Efficacy StudyIntervention Model: Single Group AssignmentMasking: Open LabelPrimary Purpose: Treatment
Official Title: Rapid Renal Sympathetic Denervation for Resistant Hypertension Using the Maya Medical OneShot™ Ablation System

http://www.clinicaltrials.gov/ct2/results?term=Renal+Denervation&pg=2&show_flds=Y

Covidien into direct competition with Medtronic, whose Symplicity renal denervation system is approved in Europe. Currently, the system is being tested in the U.S. St. Jude Medical, Medtronic’s in-state rival, is also developing a therapy and that is expected to have a limited European market launch before the end of the year. But it is not only the larger players that Covidien will have to play against in Europe. A whole host of companies is developing products there, including ReCor Medical.

http://www.canada.com/entertainment/ReCor+Medical+discloses+data+from+clinical+study+PARADISE+ultrasound/6430884/story.html

Medtronic

Medical device giant Medtronic (NYSE: MDT), November 23, 2010 said it has agreed to pay $800 million upfront, plus commercial milestone payments through 2015, to acquire Mountain View, CA-based Ardian. Medtronic had previously built up an 11 percent ownership stake in Ardian, when it invested with its venture backers, which include Morgenthaler Ventures, Advanced Technology Ventures, Split Rock Partners, and Emergent Medical Partners. Ardian’s windfall comes about one week after it presented some eye-opening clinical trial results in The Lancet, and at the American Heart Association’s scientific meeting.

http://www.xconomy.com/san-francisco/2010/11/23/medtronic-buys-ardian-for-800m-upfront-grabs-novel-treatment-for-high-blood-pressure/

Clinical Trial for SYMPLICITY is ongoing.

Renal Denervation in Patients With Uncontrolled Hypertension (SYMPLICITY HTN-3)

This study is currently recruiting participants.

Verified June 2012 by Medtronic Vascular

First Received on August 15, 2011.   Last Updated on June 11, 2012   History of Changes

Sponsor: Medtronic Vascular
Information provided by (Responsible Party): Medtronic Vascular
ClinicalTrials.gov Identifier: NCT01418261

  Purpose

The Symplicity HTN-3 study is a, multi-center, prospective, single-blind, randomized, controlled study of the safety and effectiveness of renal denervation in subjects with uncontrolled hypertension. Bilateral renal denervation will be performed using the Symplicity Catheter – a percutaneous system that delivers radiofrequency (RF)energy through the luminal surface of the renal artery.

Condition Intervention Phase
Uncontrolled Hypertension Device: Renal denervation (Symplicity Catheter System) Phase 3
Study Type: Interventional
Study Design: Allocation: RandomizedEndpoint Classification: Safety/Efficacy StudyIntervention Model: Parallel AssignmentMasking: Single Blind (Subject)Primary Purpose: Treatment

http://clinicaltrials.gov/ct2/show/NCT01418261

 The Symplicity™ Renal Denervation System has two main components:

The elements are designed to work together as an integrated system to ensure consistent performance:

Symplicity™ Catheter – Low profile, endovascular energy delivery catheter

Symplicity™ Generator – Automated, portable RF generator

The Symplicity Renal Denervation System uses controlled, low-power radiofrequency (RF) energy to deactivate the renal nerves, thereby selectively reducing both the pathologic central sympathetic drive to the kidney and the renal contribution to central sympathetic hyperactivity. The outcome, we hope, will be a significant and sustained reduction in both blood pressure and the level of systemically damaging neurohormones. Since the endovascular procedure does not involve an implant, patients recover quickly and can soon return to their daily living. The device may usher in a new era in the treatment of hypertension, hopefully allowing a one-time procedure to offer patients a long-lasting benefit.

Medtronic Procedure – view video

http://www.ardian.com/ous/medical-professionals/procedure.shtml

Conclusions

The entire industry subsegment is awaiting the results of SYMPLICITY HTN-3. Forecasts of market share by supplier will be predicated on this Clinical Trial completion.

Shutting down overactive nerves around the kidneys as a strategy for fighting resistant hypertension is “one of the most exciting growth markets in medical devices,” Sean Salmon, vice president and general manager of Medtronic’s coronary and peripheral business, said in a statement.

I had a piece in these pages last week about what kind of difference the Ardian treatment was making. The most recent Ardian study showed the new treatment, in combination with standard drugs, was able to bring average blood pressure scores down from 178 over 97 to 146 over 85 after six months of follow-up, while those who just got standard treatments were essentially unchanged. The results were “a big achievement,” according to Murray Esler, the study’s principal investigator.

http://www.xconomy.com/san-francisco/2010/11/23/medtronic-buys-ardian-for-800m-upfront-grabs-novel-treatment-for-high-blood-pressure/

Resources

REFERENCES for Dr. Scherlag’s 1999 Patent and pioneering work on Intravascular Stimulation/Ablation of Autonomics

1. Schauerte P, Scherlag BJ, Scherlag MA, Goli S, Jackman WM, Lazzara R. Transvenous parasympathetic cardiac nerve stimulation: an approach for stable sinus rate control. J Electrophysiol. 1999 Nov;10(11):1517-24.

2. Schauerte P, Scherlag BJ, Scherlag MA, Goli S, Jackman WM, Lazzara R. Ventricular rate control during atrial fibrillation by cardiac parasympathetic nerve stimulation: a transvenous approach. J Am Coll Cardiol. 1999 Dec;34(7):2043-50.

3. Schauerte P, Scherlag BJ, Pitha J, Scherlag MA, Reynolds D, Lazzara R, Jackman WM. Catheter ablation of cardiac autonomic nerves for prevention of vagal atrial fibrillation. Circulation. 2000 Nov 28;102(22):2774-80.

4. Scherlag MA, Scherlag BJ, Yamanashi W, Schauerte P, Goli S, Jackman WM, Reynolds D, Lazzara R. Endovascular neural stimulation via a novel basket electrode catheter: comparison of electrode configurations. J Interv Card Electrophysiol. 2000 Apr;4(1):219-24.

5. Scherlag BJ, Yamanashi WS, Schauerte P, Scherlag M, Sun YX, Hou Y, Jackman WM, Lazzara R. Endovascular stimulation within the left pulmonary artery to induce slowing of heart rate and paroxysmal atrial fibrillation. Cardiovasc Res. 2002 May; 54(2):470-5.

6. Hasdemir C, Scherlag BJ, Yamanashi WS, Lazzara R, Jackman WM. Endovascular stimulation of autonomic neural elements in the superior vena cava using a flexible loop catheter. Jpn Heart J. 2003 May;44(3):417-27.

7. Webster W Jr, Scherlag BJ, Scherlag MA, Schauerte P. Method and apparatus for   transvascular treatment of tachycardia and fibrillation. US Patent 6,292,695. Filed June 17, 1999.

8. Krum H, Schlaich M, Whitbourn R, Sobotka PA, Sadowski J, Bartus K, Kapelak B, Walton A, Sievert H, Thambar S, Abraham WT, Esler M. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet. 2009;373(9671):1275-1281.

9. Symplicity HTN-2 Investigators. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet. 2010;376:1903-1909.

10. Frank Himmel MD, Joachim Weil MD, Michael Reppel MD, Kai Mortensen MD, Klaas Franzen, Leidinger Ansgar MD, Heribert Schunkert MD, Frank Bode MD.  Improved Heart Rate Dynamics in Patients Undergoing Percutaneous Renal Denervation. Letter to the Editor. JCH. 31 MAY 2012.1751-7176.

Sympathetic Hyperactivity & Hypertension

For more information on hypertension, please visit the medical professional hypertension portal at TheHeart.org .

Siddiqi L, Joles JA, Grassi G, Blankestijn PJ. Is kidney ischemia the central mechanism in parallel activation of the renin and sympathetic system? J Hypertens. 2009 Jul;27(7):1341-9.

Augustyniak RA, Tuncel M, Zhang W, Toto RD, Victor RG. Sympathetic overactivity as a cause of hypertension in chronic renal failure. J Hypertens. 2002;20(1):3-9.

DiBona GF. Sympathetic nervous system and the kidney in hypertension. Curr Opin Nephrol Hypertens. 2002;11(2):197-200.

Mancia G, Grassi G, Giannattasio C, Seravalle G. Sympathetic activation in the pathogenesis of hypertension and progression of organ damage. Hypertension. 1999;34(4 Pt 2):724-728.

References in Scientific Journals about Renal Denervation Treatment

Symplicity HTN-2 Investigators. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet. 2010;376:1903-1909.

Symplicity HTN-1 Investigators. Catheter-Based Renal Sympathetic Denervation for Resistant Hypertension – Durability of Blood Pressure Reduction Out to 24 Months. Hypertension. Volume 57, Number 5, May 2011.

Rippy, M. et al. Catheter-Based Renal Sympathetic Denervation: Chronic Preclinical Evidence for Renal Artery Safety. Clin Res Cardiol. 2011 Dec; 100(12): Pages 1095-1101.

Mahfoud, F. et al. Effect of Renal Sympathetic Denervation on Glucose Metabolism in Patients With Resistant Hypertension. Circulation. Volume 123, No. 18, May 10, 2011. Pages 1940-1946.

Witkowski A., et al. Effects of Renal Sympathetic Denervation on Blood Pressure, Sleep Apnea Course, and Glycemic Control in Patients with Resistant Hypertension and Sleep Apnea. Hypertension. Volume 58, Number 4, October 2011. Pages 559-565.

Krum H, Schlaich M, Whitbourn R, Sobotka PA, Sadowski J, Bartus K, Kapelak B, Walton A, Sievert H, Thambar S, Abraham WT, Esler M. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet. 2009;373(9671):1275-1281.

Schlaich MP, Sobotka PA, Krum H, Lambert E, Esler MD. Renal Sympathetic-Nerve Ablation for Uncontrolled Hypertension. N Engl J Med. 2009;361(9):932-934.

Schlaich MP, Sobotka PA, Krum H, Whitbourn R, Walton A, Esler MD. Renal Denervation as a Therapeutic Approach for Hypertension. Novel Implications for an Old Concept. Hypertension. 2009;54(6):1195-1201.

Esler M. The 2009 Carl Ludwig Lecture: pathophysiology of the human sympathetic nervous system in cardiovascular diseases: the transition from mechanisms to medical management. J Appl Physiol. 2010;108(2):227-237.

Dibona GF, Esler MD. Translational Medicine: the antihypertensive effect of renal denervation. Am J Physiol Regul Integr Comp Physiol. 2010;298(2):R245-253.

Katholi RE, Rocha-Singh KJ. The role of renal sympathetic nerves in hypertension: has percutaneous renal denervation refocused attention on their clinical significance? Prog Cardiovasc Dis. 2009;52(3):243-248.

Doumas M, Faselis C, Papademetriou V. Renal Sympathetic Denervation and Systemic Hypertension. Am J Cardiol. 2010;105(4):570-576.

Schlaich MP, Krum H, Sobotka PA. Renal sympathetic nerve ablation: the new frontier in the treatment of hypertension. Curr Hypertens Rep. 2010;12(1):39-46.

Katholi RE, Rocha-Singh KJ, Goswami NJ, Sobotka PA. Renal nerves in the maintenance of hypertension: A potential therapeutic target. Curr Hypertens Rep. 2010;12:196-204.

Esler MD, Lambert EA, Schlaich M, Navar LG. The Dominant Contributor to Systemic Hypertension: Chronic Activation of the Sympathetic Nervous System vs Activation of the Intrarenal Renin-Angiotensin System. J Appl Physiol. 2010.

Fisher JP, Fadel PJ. Therapeutic strategies for targeting excessive central sympathetic activation in human hypertension. Exp Physiol. 2010;95(5):572-580.

Malpas SC. Sympathetic nervous system overactivity and its role in the development of cardiovascular disease. Physiol Rev. 2010;90:513-557.

Lambert GW, Straznicky NE, Lambert EA, Dixon JB, Schlaich MP. Sympathetic nervous activation in obesity and the metabolic syndrome–causes, consequences and therapeutic implications. Pharmacol Ther. 2010;126:159-172.

Masuo K, Lambert GW, Esler MD, Rakugi H, Ogihara T, Schlaich MP. The role of sympathetic nervous activity in renal injury and end-stage renal disease. Hypertens Res. 2010;33:521-528.

Schlaich MP, Socratous F, Hennebry S, Eikelis N, Lambert EA, Straznicky N, Esler MD, Lambert GW. Sympathetic activation in chronic renal failure. J Am Soc Nephrol. 2009;20(5):933-939.

Bock JS, Gottlieb SS. Cardiorenal syndrome: New perspectives. Circulation. 2010;121:2592-2600.

Goldsmith SR, Sobotka PA, Bart BA. The sympathorenal axis in hypertension and heart failure. Journal of Cardiac Failure. 2010;16(5):369-373.

Grassi G. Assessment of sympathetic cardiovascular drive in human hypertension: achievements and perspectives. Hypertension. 2009;54(4):690-697.

Ritz E. New approaches to pathogenesis and management of hypertension. Clin J Am Soc Nephrol. 2009;4(12):1886-1891.

Ritz E, Rump LC. Control of sympathetic activity–new insights; new therapeutic targets? Nephrol Dial Transplant. 2010;25(4):1048-1050.

Joyner MJ, Charkoudian N, Wallin BG. Sympathetic nervous system and blood pressure in humans: Individualized patterns of regulation and their implications. Hypertension. 2010;56:10-16.

Mann JF. Whats new in hypertension 2009? Nephrol Dial Transplant. 2010;25(1):37-41.

Bravo EL, Rafey MA, Nally JV, Jr. Renal denervation for resistant hypertension. Am J Kidney Dis. 2009;54(5):795-797.

King A. Hypertension: RF ablation of renal nerves. Nature Reviews Nephrology. 2009;5:364.

Doumas M, Douma S. Interventional management of resistant hypertension. Lancet. 2009;373(9671):1228-1230.

Paulis L. Novel therapeutic targets for hypertension. Nat Rev Cardiol. 2010.

OBrien E. Renal sympathetic denervation for resistant hypertension. Lancet. 2009;373(9681):2109; author reply 2109-2110.

Titze S, Uder M, Schmieder R. Renal nerve ablation: innovative therapy for treatment of resistant hypertension. MMW Fortschr Med. 2009;151(42):52-53.

Katona PG. Biomedical engineering in heart-brain medicine: A review. Cleve Clin J Med. 2010;77 Suppl 3:S46-50.

Abstracts about Renal Denervation Treatment

Schlaich M, Krum H, Walton T, Whitbourn R, Sobotka P, Esler M. Two-year durability of blood pressure reduction with catheter-based renal sympathetic denervation. Journal of Hypertension. 2010;28:e446.

Esler M, Schlaich M, Sobotka P, Whitbourn R, Sadowski J, Bartus K, et al. Catheter-Based Renal Denervation Reduces Total Body and Renal Noradrenaline Spillover and Blood Pressure in Resistant Hypertension. Journal of Hypertension. 2009;27(suppl 4):s167.

Schlaich MP, Krum H, Whitbourn R, Walton T, Lambert GW, Sobotka PA, et al. Effects of Renal Sympathetic Denervation on Noradrenaline Spillover and Systemic Blood Pressure in Patients with Resistant Hypertension. Journal of Hypertension. 2009;27(suppl 4):s154.

Schlaich M, Krum H, Walton T, Lambert E, Lambert G, Sobotka P, et al. A Novel Catheter Based Approach to Denervate the Human Kidney Reduces Blood Pressure and Muscle Sympathetic Nerve Activity in a Patient with End Stage Renal Disease and Hypertension. Journal of Hypertension. 2009;27(suppl 4):s437.

 

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