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Posts Tagged ‘Atrial fibrillation’

Orthotopic Heart Transplant (OHT): Effects of Autonomic Innervation / Denervation on Atrial Fibrillation (AF) Genesis and Maintenance

Author and Curator: Larry H. Bernstein, MD, FCAP

and

Curator: Aviva Lev-Ari, PhD, RN

Sympathetic stimulation increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects.

Noheria A, Patel SM, Mirzoyev S, Madhavan M, Friedman PA, Packer DL, Daly RC, Kushwaha SS, Edwards BS, Asirvatham SJ.

Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, California.
Pacing Clin Electrophysiol. 2013 Jun;36(6):741-7. http://dx.doi.org/10.1111/pace.12102. Epub 2013 Feb 25.

http://www.cvphysiology.com/Blood%20Pressure/ANS-medulla.gif
ANS- autonomic innervation of heart

The medulla, located in the brainstem above the spinal cord, is the primary site in the brain for regulating sympathetic and parasympathetic (vagal) outflow to the heart and blood vessels. The nucleus tractus solitarius (NTS) of the medulla receives sensory input from different systemic and central receptors (e.g., baroreceptors and chemoreceptors).
The heart is innervated by vagal and sympathetic fibers. The right vagus nerve primarily innervates the SA node, whereas the left vagus innervates the AV node; however, there can be significant overlap in the anatomical distribution. Atrial muscle is also innervated by vagal efferents, whereas the ventricular myocardium is only sparsely innervated by vagal efferents. Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.
Cardiac function is altered by neural activation. Sympathetic stimulation increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects.  Sympathetic and parasympathetic effects on heart function are mediated by beta-adrenoceptors and muscarinic receptors, respectively.
The overall effect of sympathetic activation is to increase cardiac output, systemic vascular resistance (both arteries and veins), and arterial blood pressure. Enhanced sympathetic activity is particularly important during exercise, emotional stress, and during hemorrhagic shock.
The actions of autonomic nerves are mediated by the release of neurotransmitters that bind to specific cardiac receptors and vascular receptors. These receptors are coupled to signal transduction pathways that evoke changes in cellular function.

                                         Sympathetic                      Parasympathetic

Heart

Chronotropy (rate)

+ + +                                     − − −

Inotropy (contractility)

+ + +                                      − 1

 Lusitropy (relaxation)                              
                                             + + +                                     –  1 
Dromotropy (conduction velocity)

                                              + +                                       − − −

Vessels

Arterial constriction    + + +                                    0

Venous constriction      + + +                                    0

Relative magnitude of responses indicated by number of + or – signs.
1 More pronounced in atria than ventricles.

CV Physiology: Autonomic Innervation of the Heart and Vasculature
http://www.cvphysiology.com/Blood%20Pressure/BP008.htm

Ablation Therapy for Cardiac Arrhythmias

By Richard N. Fogoros, M.D., About.com Guide Updated November 18, 2011
The most common form of ablation is done during a specialized form of cardiac catheterization, performed by a type of doctor known as a cardiac electrophysiologist (heart rhythm specialist). These procedures are sometimes called “trans-catheter ablations.”
During trans-catheter ablation procedures, specialized electrode catheters are positioned inside the heart, and the cardiac electrical system is mapped, showing the abnormal electrical pathways that are often responsible for producing the rapid heart rate. If these abnormal pathways are identified, the tip of the catheter (a tube) is placed on the abnormal pathway and the pathway is ablated (eliminated). The ablation itself is accomplished by transmitting some form of energy through the catheter (heat energy, freezing energy, or microwave energy), in order to damage the tissue at the tip of the catheter.

Decreased postoperative atrial fibrillation following cardiac transplantation: the significance of autonomic denervation.

BACKGROUND:  Endocardial ablation approaches have been proposed to targeting the retroatrial cardiac ganglia to treat atrial fibrillation (AF) . The potential value using this approach is unknown. Disruption of the autonomic inputs with orthotropic heart transplant (OHT) provides a unique opportunity to study the effects of autonomic innervation on AF genesis and maintenance.
The investigators hypothesized that due to denervation, the risk of postoperative AF would be lower following OHT compared to surgical maze even though both groups get isolation of the pulmonary veins.
METHODS:  We reviewed 155 OHTs (mean age 52 ± 11 years, 72% males) and used 1:1 age-, sex-, and date-of-surgery-matched two control groups from patients undergoing surgical maze or only coronary artery bypass grafting (CABG). Using conditional logistic regression we compared the odds of AF within 2 weeks following OHT versus controls.
RESULTS: Postoperative AF occurred in 10/155 (6.5%) OHT patients.
  1. The conditional odds of postoperative AF were lower for OHT as compared to controls (vs maze: odds ratio [OR] 0.27 [95% confidence interval (CI) 0.13-0.57], vs CABG: OR 0.38 [0.17-0.81], P = 0.003; and
  2. on additional adjustment for left atrial enlargement, vs maze: OR 0.28 [0.13-0.60], vs CABG: OR 0.14 [0.04-0.47], P = 0.0009).
CONCLUSIONS:
Risk of postoperative AF is significantly lower with OHT as in comparison to surgical maze. As both surgeries entail isolation of the pulmonary veins but
  • only OHT causes disruption of autonomic innervation,
this observation supports a mechanistic role of autonomic nervous system in AF. The benefit of targeting the cardiac autonomic system to treat AF needs further investigation.

Other related articles published on this Open Access Online Scientific Journal, including the following:

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

Aviva Lev-Ari, PhD, RN

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

Renal Sympathetic Denervation: Updates on the State of Medicine

Aviva Lev-Ari, PhD, RN

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

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

Justin D Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2013/05/07/on-devices-and-on-algorithms-arrhythmia-after-cardiac-surgery-prediction-and-ecg-prediction-of-paroxysmal-atrial-fibrillation-onset/

Xarelto (Rivaroxaban): Anticoagulant Therapy gains FDA New Indications and Risk Reduction for: (DVT) and (PE), while in use for Atrial fibrillation increase in Gastrointestinal (GI) Bleeding Reported

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2012/11/04/xarelto-rivaroxaban-anticoagulant-therapy-gains-fda-new-indications-and-risk-reduction-for-dvt-and-pe-while-in-use-for-atrial-fibrillation-increase-in-gastrointestinal-gi-bleeding-reported/
Sustained Cardiac Atrial Fibrillation: Management Strategies by Director of the Arrhythmia Service and Electrophysiology Lab at The Johns Hopkins Hospital

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2012/10/16/sustained-cardiac-atrial-fibrillation-management-strategies-by-director-of-the-arrhythmia-service-and-electrophysiology-lab-at-the-johns-hopkins-hospital/
Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2012/08/16/stroke-and-bleeding-in-atrial-fibrillation-with-chronic-kidney-disease/
Atrial Fibrillation: The Latest Management Strategies

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2012/07/16/atrial-fibrillation-the-latest-management-strategies/
Genetics of Conduction Disease: Atrioventricular (AV) Conduction Disease (block): Gene Mutations – Transcription, Excitability, and Energy Homeostasis

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2013/04/28/genetics-of-conduction-disease-atrioventricular-av-conduction-disease-block-gene-mutations-transcription-excitability-and-energy-homeostasis/

Minimally Invasive Structural CVD Repairs: FDA grants 510(k) Clearance to Philips’ EchoNavigator – X-ray and 3-D Ultrasound Image Fused

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2013/03/21/minimally-invasive-structural-cvd-repairs-fda-grants-510k-to-philips-echonavigator-x-ray-and-3-d-ultrasound-image-fused/

Accurate Identification and Treatment of Emergent Cardiac Events

Larry Bernstein, MD, FCAP
http://pharmaceuticalintelligence.com/2013/03/15/accurate-identification-and-treatment-of-emergent-cardiac-events/

Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

Aviva Lev-Ari, PhD, RN

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

Sympathetic (red) and parasympathetic (blue) n...

Sympathetic (red) and parasympathetic (blue) nervous system Русский: Аанатомия иннервации вегетативной нервной системы. Системы: симпатическая (красным) и парасимпатическая (синим) Українська: Аанатомія іннервації вегетативної нервової системи. Симпатична (червоним) та парасимпатична (синім) гілки Polski: Układ autonomiczny: czerwony – sympatyczny, niebieski – parasympatyczny. (Photo credit: Wikipedia)

Scheme of atrial fibrillation (top) and sinus ...

Scheme of atrial fibrillation (top) and sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation. (Photo credit: Wikipedia)

English: A graphical representation of the Ele...

English: A graphical representation of the Electrical conduction system of the heart showing the Sinoatrial node, Atrioventricular node, Bundle of His, Purkinje fibers, and Bachmann’s bundle (Photo credit: Wikipedia)

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

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC

and

Article Curator: Aviva Lev-Ari, PhD, RN

Cleveland Clinic research spurs a device that could predict arrhythmia after cardiac surgery

April 30, 2013 9:03 am by  |

ECG

Heart doctors at the Cleveland Clinic  hope to give doctors a way to tell which patients might develop arrhythmia after cardiac surgery.

Atrial fibrillation (AFIB) is one of the most common complications of heart surgeries, and also occurs as a complication of elevated alcohol use, high blood pressure, valve disease or thyroid disease. Atrial fibrillation consists of the round parts of the Valentine heart (the atria) shivering chaotically instead of beating rhythmically. Atrial fibrillation is a common arrhythmia, eventually affecting 20% of adults. There are 3 varieties: paroxysmal (intermittent), persistent (continual) and permanent (unremitting).  When AFIB lasts longer than 24-48 hours the risk of forming a blood clot in the atria rises, which in turn can cause a stroke or a heart attack. AFIB often results in fast heart rates which may cause low blood pressure and its possible consequences (organ injury, heart attack). Also, prolonged fast rates weaken the heart (reversible rate-related cardiomyopathy), which can persist for months after regaining target ranges for the heart rates (target for rate control is 60-80/minute instead of the fast rates of 100-180/min that are common with untreated AFIB).

A scoring system (CHADS2) can predict who may suffer from a stroke due to AFIB that lasts >24-48 hours, and in particular, who may benefit from longterm anticoagulation (blood thinners to interfere with clot formation). A pill-in-the-pocket can stop AFIB within hours.  Amiodarone, a highly toxic medication (10% long-term uses face side effects of serious damage to liver, lung, thyroid or eyes), is often prescribed “off-label” (without FDA endorsement) because it is 70% effective in preventing AFIB recurrence, and it has less anticontractility (weakening of the strength of heart beats) than most other rhythm medications. Then next most effective medication for suppression of AFIB long-term is sotalol, which reduces the strength of heart contraction (may not be tolerated by patients with severe heart failure) and it prolongs QT interval of repolarization after each heartbeat, a risk factor for a deadly rhythm called torsades de pointes. Interventional cures (“AFIB ablation”) have been developed to prevent recurrences.

Predicting AFIB may have several benefits: (1) potentially, earlier use of pill-in-the-pocket could prevent episodes rather that wait for them to occur, get noticed, and then treated, as only ~50% of AFIB episodes are noticed by the patient, according to electrographic monitor reports; (2) surrogate endpoint (prediction of onset) may offer useful guidance as to sufficiency of a suppressive therapy to enable lower dosing of toxic treatments; (3)  surrogate endpoint (prediction of onset) may offer useful guidance as to sufficient lowering of alohol intake, sufficient control of blood pressure, sufficient control of thyroid abnormalities, and other prevention opportunities; (4) surrogate endpoints may facilitate AFIB ablation.

Work done in the lab of Dr. C. Allen Bashour indicated that most patients who experience atrial fibrillation after heart surgery show clues beforehand in the form of subtle changes in their ECG readings that aren’t detected with the way they’re monitored now.

Rindex Medical is commercializing a tool that would enable physicians to predict which patients will experience AF so they can receive prophylactic treatment before it occurs.

“Right now they basically guess, or treat everyone prophylactically,” said co-founder Alex Arrow. “Some clinicians say they have an intuition about who will get it, but it’s mostly guesswork.”

Rindex’s A-50 AF Prediction System uses algorithms developed at the Clinic to analyze a patient’s ECG signals through 17 steps and produce a score, from 1 to 100, of how likely that patient is to experience AF. Arrow said the final product will be a touch-screen monitor that displays a score and tracks the score over a nine-hour period.

The Redwood City, California, company has been issued the first of its patents for the device and the exclusive license from Cleveland Clinic to develop the technology. Self-funded by Arrow and co-founders Denis Hickey and Lucas Fairfield, Rindex has a working prototype and is making progress on preparations for its 510(k) application. Arrow said the company shouldn’t need to raise a series A until it’s ready for a clinical trial.

Many other research groups have explored ways to predict AF in its various forms from natriuretic peptides to ECG changes, but no method has been established as reliably for this purpose.

Read more: http://medcitynews.com/2013/04/cleveland-clinic-research-spurs-a-device-that-could-predict-arrhythmias-after-cardiac-surgery/#ixzz2ScbxIyW0

http://medcitynews.com/2013/04/cleveland-clinic-research-spurs-a-device-that-could-predict-arrhythmias-after-cardiac-surgery/?goback=%2Egde_1503357_member_237204073

Dec 13, 2012

ECG predicts atrial fibrillation onset

Atrial fibrillation (AF), the most common cardiac arrhythmia, is categorized by different forms. One sub-type is paroxysmal AF (PAF), which refers to episodes of arrhythmia that generally terminate spontaneously after no more than a few days. Although the underlying causes of PAF are still unknown, it’s clear that predicting the onset of PAF would be hugely beneficial, not least because it would enable the application of treatments to prevent the loss of sinus rhythm.

Many research groups are tackling the issue of predicting the onset of PAF. Now, however, researchers in Spain have developed a method that assesses the risk of PAF at least one hour before its onset. To date, the approach has not only successfully discriminated healthy individuals and PAF patients, but also distinguished patients far from and close to PAF onset (Physiol. Meas. 33 1959).

“The ability to assess the risk of arrhythmia at least one hour before its onset is clinically relevant,” Arturo Martinez from the University of Castilla-La Mancha told medicalphysicsweb. “Our method assesses the P-wave feature time course from single-lead long-term ECG recordings. Using a single ECG lead reduces the computational burden, paving the way for a real-time system in future.”

Analysing sinus rhythm

If the heart is beating normally, the sinus rhythm observed on an ECG will contain certain generic features, such as a P-wave that reflects the atrial depolarization and a large characteristic R peak flanked by two minima representing the depolarization of the heart’s right and left ventricles. If an irregular heart beat is suspected, an ECG will be used and typical findings include the absence of a P-wave.

“We hypothesized that different stages of AF could be identified when analysing long-term recordings extracted from patients prone to AF,” commented Martinez. “Our method differs to others in that we also use just one single lead to detect small differences in features from the P-wave time course.”

P for paroxysmal

Martinez and his collaborators, Raul Alcaraz and Jose Rieta, studied 24-hour Holter ECG recordings from 24 patients in whom PAF had been detected for the first time. For each patient, the longest sinus rhythm interval in the recording was selected, and the two hours preceding the onset of PAF were analysed. These readings were compared with those from 28 healthy individuals. In all cases, only the trace from the V1 ECG lead was considered.

A major challenge for the researchers was to extract the P-wave from the baseline noise. To overcome this, they used an automatic delineator algorithm based on a phasor transform that determines the precise time point relating to the onset, peak and offset of the P-wave. The authors described this algorithm in a previous research paper (Physiol. Meas. 31 1467).

“All of the recordings in our study were visually supervised by expert cardiologists who corrected the P-wave fiducial points when needed,” said Martinez. “Even in the presence of noise, which generated an incredible amount of P-wave distortion, our delineator provided location errors lower than 8 ms.”

In order to assess which time course features might be useful to predict the onset of PAF, the researchers analysed a number of variables. First, they examined factors representing the duration of the P-wave (Pdur), such as the distance between the P-wave onset and peak (Pini) and the distance between the P-wave peak and its offset (Pter). They then studied factors relating P- to R-waves, such as the distance between the two waves’ peaks (PRk) and, finally, beat-to-beat P-wave factors, such as the distance between two consecutive P-wave onset points (PPon).

“The most remarkable trends were provided by the features measuring P-wave duration,” report the authors in their paper. “Pduridentified appropriately 84.21% of all the analysed patients, obtaining a discriminant accuracy of 90.79% and 83.33% between healthy subjects and PAF patients far from PAF and close to PAF, respectively. The metrics related to the PR interval showed the most limited ability to identify patient groups.”

About the author

Jacqueline Hewett is a freelance science and technology journalist based in Bristol, UK.

http://medicalphysicsweb.org/cws/article/research/51820

Original Article

Physiol Meas. 2010 Nov;31(11):1467-85. doi: 10.1088/0967-3334/31/11/005. Epub 2010 Sep 24.

Application of the phasor transform for automatic delineation of single-lead ECG fiducial points.

Martínez AAlcaraz RRieta JJ.

Source

Innovation in Bioengineering Research Group, University of Castilla La Mancha, Spain. arturo.martinez@uclm.es

Abstract

This work introduces a new single-lead ECG delineator based on phasor transform. The method is characterized by its robustness, low computational cost and mathematical simplicity. It converts each instantaneous ECG sample into a phasor, and can precisely manage P and T waves, which are of notably lower amplitude than the QRS complex. The method has been validated making use of synthesized and real ECG sets, including the MIT-BIH arrhythmia, QT, European ST-T and TWA Challenge 2008 databases. Experiments with the synthesized recordings reported precise detection and delineation performances in a wide variety of ECGs, with signal-to-noise ratios of 10 dB and above. For real ECGs, the QRS detection was characterized by an average sensitivity of 99.81% and positive predictivity of 99.89%, for all the analyzed databases (more than one million beats). Regarding delineation, the maximum localization error between automatic and manual annotations was lower than 6 ms and its standard deviation was in agreement with the accepted tolerances for expert physicians in the onset and offset identification for QRS, P and T waves. Furthermore, after revising and reannotating some ECG recordings by expert cardiologists, the delineation error decreased notably, becoming lower than 3.5 ms, on average, and reducing by a half its standard deviation. This new proposed strategy outperforms the results provided by other well-known delineation algorithms and, moreover, presents a notably lower computational cost.

SOURCES:

Original Database

MIT-BIH Polysomnographic Database

This database is described in

Ichimaru Y, Moody GB. Development of the polysomnographic database on CD-ROM. Psychiatry and Clinical Neurosciences 53:175-177 (April 1999).

Please cite this publication when referencing this material, and also include the standard citation for PhysioNet:

Goldberger AL, Amaral LAN, Glass L, Hausdorff JM, Ivanov PCh, Mark RG, Mietus JE, Moody GB, Peng C-K, Stanley HE. PhysioBank, PhysioToolkit, and PhysioNet: Components of a New Research Resource for Complex Physiologic Signals. Circulation 101(23):e215-e220 [Circulation Electronic Pages; http://circ.ahajournals.org/cgi/content/full/101/23/e215]; 2000 (June 13).

The MIT-BIH Polysomnographic Database is a collection of recordings of multiple physiologic signals during sleep. Subjects were monitored in Boston’s Beth Israel Hospital Sleep Laboratory for evaluation of chronic obstructive sleep apnea syndrome, and to test the effects of constant positive airway pressure (CPAP), a standard therapeutic intervention that usually prevents or substantially reduces airway obstruction in these subjects. The database contains over 80 hours’ worth of four-, six-, and seven-channel polysomnographic recordings, each with an ECG signal annotated beat-by-beat, and EEG and respiration signals annotated with respect to sleep stages and apnea. For further information, see Signals and Annotations.

The database consists of 18 records, each of which includes 4 files:

Sleep/apneaannotations Beatannotations Signals Header View waveforms *
slp01a.st slp01a.ecg slp01a.dat slp01a.hea
slp01b.st slp01b.ecg slp01b.dat slp01b.hea
slp02a.st slp02a.ecg slp02a.dat slp02a.hea
slp02b.st slp02b.ecg slp02b.dat slp02b.hea
slp03.st slp03.ecg slp03.dat slp03.hea
slp04.st slp04.ecg slp04.dat slp04.hea
slp14.st slp14.ecg slp14.dat slp14.hea
slp16.st slp16.ecg slp16.dat slp16.hea
slp32.st slp32.ecg slp32.dat slp32.hea
slp37.st slp37.ecg slp37.dat slp37.hea
slp41.st slp41.ecg slp41.dat slp41.hea
slp45.st slp45.ecg slp45.dat slp45.hea
slp48.st slp48.ecg slp48.dat slp48.hea
slp59.st slp59.ecg slp59.dat slp59.hea
slp60.st slp60.ecg slp60.dat slp60.hea
slp61.st slp61.ecg slp61.dat slp61.hea
slp66.st slp66.ecg slp66.dat slp66.hea
slp67x.st slp67x.ecg slp67x.dat slp67x.hea

(*) You may follow these links to view the signals and st annotations using either WAVE (under Linux, SunOS, or Solaris) or WVIEW (under MS-Windows). To do so successfully, you must have configured your browser to use wavescript (for WAVE) or wvscript (for WVIEW) as a helper application, as described in the WAVE User’s Guide(see the section titled WAVE and the Web) and in Setting up WVSCRIPT.

Andrew Walsh observed that the calibration originally provided for the BP signal of record slp37 is incorrect (since it yielded negative BPs). slp37.hea now contains an estimated BP calibration that yields more plausible BPs; these should not be regarded as accurate, however, since there is no independent calibration standard available for this recording.

SOURCE:
Original Article
Proc Inst Mech Eng H. 2010;224(1):27-42.

Finding events of electrocardiogram and arterial blood pressure signals via discrete wavelet transform with modified scales.

Ghaffari AHomaeinezhad MRAkraminia MDavaeeha M.

Source

Cardiovascular Research Group, Department of Mechanical Engineering, K. N. Toosi University of Technology, Tehran, Iran.

Abstract

A robust electrocardiogram (ECG) wave detection-delineation algorithm that can be applied to all ECG leads is developed in this study on the basis of discrete wavelet transform (DWT). By applying a new simple approach to a selected scale obtained from DWT, this method is capable of detecting the QRS complex, P-wave, and T-wave as well as determining parameters such as start time, end time, and wave sign (upward or downward). In the proposed method, the selected scale is processed by a sliding rectangular window of length n and the curve length in each window is multiplied by the area under the absolute value of the curve. In the next step, an adaptive thresholding criterion is conducted on the resulted signal. The presented algorithm is applied to various databases including the MIT-BIH arrhythmia database, European ST-T database, QT database, CinC Challenge 2008 database as well as high-resolution Holter data gathered in the DAY Hospital. As a result, the average values of sensitivity and positive prediction Se = 99.84 per cent and P+ = 99.80 per cent were obtained for the detection of QRS complexes with an average maximum delineation error of 13.7, 11.3, and 14.0 ms for the P-wave, QRS complex, and T-wave respectively. The presented algorithm has considerable capability in cases of a low signal-to-noise ratio, high baseline wander, and in cases where QRS complexes and T-waves appear with abnormal morphologies. Especially, the high capability of the algorithm in the detection of the critical points of the ECG signal, i.e. the beginning and end of the T-wave and the end of the QRS complex was validated by the cardiologist and the maximum values of 16.4 and 15.9 ms were recognized as absolute offset error of localization respectively. Finally, in order to illustrate an alternative capability of the algorithm, it is applied to all 18 subjects of the MIT-BIH polysomnographic database and the end-systolic and end-diastolic points of the blood pressure waveform were extracted and values of sensitivity and positive prediction Se = 99.80 per cent and P+ = 99.86 per cent were obtained for the detection of end-systolic, end-diastolic pulses.

http://www.ncbi.nlm.nih.gov/pubmed/20225455

Original Article

A robust wavelet-based multi-lead electrocardiogram delineation algorithm

  • a Department of Mechanical Engineering, K.N. Toosi University of Technology, Tehran, Iran
  • b CardioVascular Research Group (CVRG), Iran
  • c Non-invasive Cardiac Electrophysiology Laboratory, DAY Hospital, Tehran, Iran

Abstract

A robust multi-lead ECG wave detection-delineation algorithm is developed in this study on the basis of discrete wavelet transform (DWT). By applying a new simple approach to a selected scale obtained from DWT, this method is capable of detecting QRS complex, P-wave and T-wave as well as determining parameters such as start time, end time, and wave sign (upward or downward). First, a window with a specific length is slid sample to sample on the selected scale and the curve length in each window is multiplied by the area under the absolute value of the curve. In the next step, a variable thresholding criterion is designed for the resulted signal. The presented algorithm is applied to various databases including MIT-BIH arrhythmia database, European ST-T Database, QT Database, CinC Challenge 2008 Database as well as high resolution Holter data of DAY Hospital. As a result, the average values of sensitivity and positive predictivity Se = 99.84% and P+ = 99.80% were obtained for the detection of QRS complexes, with the average maximum delineation error of 13.7 ms, 11.3 ms and 14.0 ms for P-wave, QRS complex and T-wave, respectively. The presented algorithm has considerable capability in cases of low signal-to-noise ratio, high baseline wander, and abnormal morphologies. Especially, the high capability of the algorithm in the detection of the critical points of the ECG signal, i.e. the beginning and end of T-wave and the end of the QRS complex was validated by cardiologists in DAY hospital and the maximum values of 16.4 ms and 15.9 ms were achieved as absolute offset error of localization, respectively.

Abbreviations

  • ACL, area-curve length;
  • ECG, electrocardiogram;
  • DWT, discrete wavelet transform;
  • QTDB, QT database;
  • MITDB, MIT-BIH arrhythmia database; 
  • TWADB, T-wave alternans database;
  • CSEDB, common standards for electrocardiography database;
  • EDB, European ST-T database;
  • P+, positive predictivity (%);
  • Se,sensitivity (%);
  • FIR, finite-duration impulse response;
  • LE, location error;
  • CHECK#0, procedure of evaluating obtained results using MIT annotation files;
  • CHECK#1, procedure of evaluating obtained results consulting with a control cardiologist;
  • CHECK#2, procedure of evaluating obtained results consulting with a control cardiologist and also at least with 3 residents

Keywords

  • ECG delineation;
  • Discrete wavelet transform;
  • Variable threshold;
  • Validation

Figures and tables from this article:

Full-size image (14 K)
Fig. 1. FIR filter-bank implementation to generate discrete wavelet transform based on à trous algorithm.
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Fig. 2. Graphical representation of the logic of the proposed simple transformation for detecting onset and offset edges. In case I, both area and curve length are minimum, (ACLI < ACLII ≤ ACLIII).
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Fig. 3. The flow-chart of the proposed wavelet-aided electrocardiogram delineation algorithm (rectangle: operation, ellipse: result).
Full-size image (113 K)
Fig. 4. An excerpted segment from a total delineated ECG. Delineated (a) P-waves, (b) QRS complexes and (c) T-waves. (Circles: edges of event, triangles: peak of events, Partition A: lead I, Partition B: lead II).
Full-size image (76 K)
Fig. 5. Procedure of detecting and delineating of P and T-waves using ACL signal between two successive QRS complexes. (a) Simultaneously depiction of ACL, original ECG and the corresponding selected DWT scale, (b) QRS delineation, and (c) P and T-waves delineation.
SOURCE:

Volume 31, Issue 10, December 2009, Pages 1219–1227

http://www.sciencedirect.com/science/article/pii/S1350453309001647

Other related articles published on this Open Access Online Scientific Journal include the following:

Sustained Cardiac Atrial Fibrillation: Management Strategies by Director of the Arrhythmia Service and Electrophysiology Lab at The Johns Hopkins Hospital   http://pharmaceuticalintelligence.com/2012/10/16/sustained-cardiac-atrial-fibrillation-management-strategies-by-director-of-the-arrhythmia-service-and-electrophysiology-lab-at-the-johns-hopkins-hospital/

Cardiac Arrhythmias: A Risk for Extreme Performance Athletes                                                                                                                                                       http://pharmaceuticalintelligence.com/2012/08/08/cardiac-arrhythmias-a-risk-for-extreme-performance-athletes/

Acute Chest Pain/ER Admission: Three Emerging Alternatives to Angiography and PCI    http://pharmaceuticalintelligence.com/2013/03/10/acute-chest-painer-admission-three-emerging-alternatives-to-angiography-and-pci/

Dilated Cardiomyopathy: Decisions on implantable cardioverter-defibrillators (ICDs) using left ventricular ejection fraction (LVEF) and Midwall Fibrosis: Decisions on Replacement using late gadolinium enhancement cardiovascular MR (LGE-CMR)
http://pharmaceuticalintelligence.com/2013/03/10/dilated-cardiomyopathy-decisions-on-implantable-cardioverter-defibrillators-icds-using-left-ventricular-ejection-fraction-lvef-and-midwall-fibrosis-decisions-on-replacement-using-late-gadolinium/

Ablation Devices Market to 2016 – Global Market Forecast and Trends Analysis by Technology, Devices & Applications
http://pharmaceuticalintelligence.com/2012/12/23/ablation-devices-market-to-2016-global-market-forecast-and-trends-analysis-by-technology-devices-applications/

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Importance of Omega-3 Fatty Acids in Reducing Cardiovascular Disease

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

UPDATED on 7/24/2018

Omega-3 fats Supplements Effect on Cardiovascular Health: EPA and DHA has little or no effect on Mortality or Cardiovascular Health

Reporter: Aviva Lev-Ari, PhD, RN

https://pharmaceuticalintelligence.com/2018/07/24/omega-3-fats-supplements-effect-on-cardiovascular-health-epa-and-dha-has-little-or-no-effect-on-mortality-or-cardiovascular-health/

 

The available evidence for cardiovascular effects of n-3 polyunsaturated fatty acid (PUFA) consumption has been reviewed here, focusing on long chain (seafood) n-3 PUFA, including their principal dietary sources, effects on physiological risk factors, potential molecular pathways and bioactive metabolites, effects on specific clinical endpoints, and existing dietary guidelines. Major dietary sources include fatty fish and other seafood. n-3 PUFA consumption lowers plasma triglycerides, resting heart rate, and blood pressure and might also improve myocardial filling and efficiency, lower inflammation, and improve vascular function. Experimental studies demonstrate direct anti-arrhythmic effects, which have been challenging to document in humans. n-3 PUFA affect a myriad of molecular pathways, including alteration of physical and chemical properties of cellular membranes, direct interaction with and modulation of membrane channels and proteins, regulation of gene expression via nuclear receptors and transcription factors, changes in eicosanoid profiles, and conversion of n-3 PUFA to bioactive metabolites. In prospective observational studies and adequately powered randomized clinical trials, benefits of n-3 PUFA seem most consistent for coronary heart disease mortality and sudden cardiac death. Potential effects on other cardiovascular outcomes are less-well-established, including conflicting evidence from observational studies and/or randomized trials for effects on nonfatal myocardial infarction, ischemic stroke, atrial fibrillation, recurrent ventricular arrhythmias, and heart failure. Research gaps include the relative importance of different physiological and molecular mechanisms, precise dose-responses of physiological and clinical effects, whether fish oil provides all the benefits of fish consumption, and clinical effects of plant-derived n-3 PUFA. Overall, current data provide strong concordant evidence that n-3 PUFA are bioactive compounds that reduce risk of cardiac death. National and international guidelines have converged on consistent recommendations for the general population to consume at least 250 mg/day of long-chain n-3 PUFA or at least 2 servings / week of oily fish.

Source References:

http://content.onlinejacc.org/article.aspx?articleid=1146941

http://www.ncbi.nlm.nih.gov/pubmed/17047219

http://www.ncbi.nlm.nih.gov/pubmed/18614744

http://www.ncbi.nlm.nih.gov/pubmed/19364995

http://www.ncbi.nlm.nih.gov/pubmed/16172267

Other articles related to this topic were published on this Open Access Online Scientific Journal, including the following:

Reversal of Cardiac mitochondrial dysfunction

Larry H Bernstein, MD, FACP, RN 04/14/2013

http://pharmaceuticalintelligence.com/2013/04/14/reversal-of-cardiac-mitochondrial-dysfunction/

Can resolvins suppress acute lung injury?

Larry H Bernstein, MD, FACB, RN 03/06/2013

http://pharmaceuticalintelligence.com/2013/03/06/can-resolvins-suppress-acute-lung-injury/

Calcium (Ca) supplementation (>1400 mg/day): Higher Death Rates from all Causes and Cardiovascular Disease in Women

Aviva Lev-Ari, PhD., RN 02/19/2013

http://pharmaceuticalintelligence.com/2013/02/19/calcium-ca-supplementation-1400-mgday-higher-death-rates-from-all-causes-and-cardiovascular-disease-in-women/

Endothelial Function and Cardiovascular Disease

Larry H Bernstein, MD, FCAP, Pathologist, Contributor, RN 10/25/2012

http://pharmaceuticalintelligence.com/2012/10/25/endothelial-function-and-cardiovascular-disease/

Mediterranean Diet is BEST for patients with established Heart Disorders

Aviva Lev-Ari, PhD, RN 10/15/2012

http://pharmaceuticalintelligence.com/2012/10/15/mediterranean-diet-is-best-for-patients-with-established-heart-disorders/

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Xarelto (Rivaroxaban): Anticoagulant Therapy gains FDA New Indications and Risk Reduction for: (DVT) and (PE), while in use for Atrial fibrillation increase in Gastrointestinal (GI) Bleeding Reported

Reporter: Aviva Lev-Ari, PhD, RN

 

UPDATED on 8/17/2018

NOAC’s Brain Bleed Risk Outside Afib May Be Dose-Dependent

Higher risk seen only with higher rivaroxaban doses in meta-analysis

by Ashley Lyles, MedPage Today Intern 

The findings indicate the following risk of intracranial hemorrhage versus aspirin:

  • 10 mg of rivaroxaban taken once per day or 5 mg taken two times a day (three trials, OR 1.43, 95% CI 0.93-2.21)
  • 5 mg of apixaban twice daily (one trial, OR 0.84, 95% CI 0.38-1.88)

The study also showed that 15 mg to 20 mg of rivaroxaban each day was linked with an increased risk of fatal bleeding (two trials, OR 2.37, 95% CI 1.30-4.29). On the other hand, 10 mg of rivaroxaban each day or 5 mg taken twice a day (three trials, OR 1.47, 95% CI 0.72-2.97) and 5 mg of apixaban taken twice per day (one trial, OR 0.66, 95 % CI 0.19-2.35) were not linked with an increased risk.

Increased risk of major bleeding compared with aspirin was seen with 15 mg to 20 mg dose of rivaroxaban each day (two trials, OR 2.64, 95% CI 1.68-4.16) and a 10 mg dose of rivaroxaban once a day or 5 mg twice per day (three trials, OR 1.56, 95% CI 1.31-1.85).

Primary Source

JAMA Neurology

Source Reference: Huang W, et al “Association of intracranial hemorrhage risk with non–vitamin k antagonist oral anticoagulant use vs aspirin use a systematic review and meta-analysis” JAMA Neurology 2018; DOI: 10.1001.

SOURCE

https://www.medpagetoday.com/cardiology/strokes/74552?xid=nl_mpt_cardiodaily_2018-08-17&eun=g99985d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=AHAWeekly_081718&utm_term=AHA%20Cardiovascular%20Daily%20-%20Active%20Users%20180%20days

 

UPDATED on 10/9/2017

Xarelto Flop in Stroke Prevention Trial; Syncope Device; Workout by Watching Hockey, Theater?

Recent developments of interest in cardiovascular medicine

  • by Crystal Phend,Senior Associate Editor, MedPage TodayOctober 09, 2017

https://www.medpagetoday.com/Cardiology/Prevention/68421

Rivaroxaban (Xarelto) flopped for preventing recurrent strokes and increased bleeding compared with aspirin in top-line results from the phase III NAVIGATE ESUS trial, Bayer and Janssen announced. (Genetic Engineering and Biotechnology News)

Xarelto (Rivaroxaban): Anticoagulant Therapy gains FDA New Indications and Risk Reduction for: (DVT) and (PE), while in use for Atrial fibrillation, increase in Gastrointestinal (GI) Bleeding Reported compared with Coumadin

Rivaroxaban Gains FDA Indications For The Treatment And Prevention Of DVT And PE

The FDA today expanded the indication for rivaroxaban (Xarelto, Johnson & Johnson) to include the treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) and to reduce the risk of recurrent DVT and PE.

The oral anticoagulant is already approved to reduce the post-surgical risk of DVT and PE  after hip and knee replacement surgery and to reduce the risk of stroke in people with atrial fibrillation. The new indication was granted under the FDA’s priority review program.

“Xarelto is the first oral anti-clotting drug approved to treat and reduce the recurrence of blood clots since the approval of warfarin nearly 60 years ago,” said Richard Pazdur,  director of the FDA’s Office of Hematology and Oncology Products, in an FDA press release.

Here is the FDA press release:

FDA expands use of Xarelto to treat, reduce recurrence of blood clots
The U.S. Food and Drug Administrationtoday expanded the approved use of Xarelto (rivaroxaban) to include treating deep vein thrombosis (DVT) or pulmonary embolism (PE), and to reduce the risk of recurrent DVT and PE following initial treatment.Blood clots occur when blood thickens and clumps together. DVT is a blood clot that forms in a vein deep in the body. Most deep vein blood clots occur in the lower leg or thigh. When a blood clot in a deep vein breaks off and travels to an artery in the lungs and blocks blood flow, it results in a potentially deadly condition called PE.Xarelto is already FDA-approved to reduce the risk of DVTs and PEs from occurring after knee or hip replacement surgery (July 2011), and to reduce the risk of stroke in people who have a type of abnormal heart rhythm called non-valvular atrial fibrillation (November 2011).

The FDA reviewed Xarelto’s new indication under the agency’s priority review program, which provides an expedited six-month review for drugs that offer major advances in treatment or that provide treatment when no adequate therapy exists.

“Xarelto is the first oral anti-clotting drug approved to treat and reduce the recurrence of blood clots since the approval of warfarin nearly 60 years ago,” said Richard Pazdur, M.D., director of the Office of Hematology and Oncology Products in the FDA’s Center for Drug Evaluation and Research.

Other drugs approved by FDA to treat or reduce the risk of blood clots include Lovenox (enoxaparin), generic versions of enoxaparin, Arixtra (fondaparinux), Fragmin (dalteparin), Coumadin (warfarin), and heparin.

The safety and effectiveness of Xarelto for the new indications were evaluated in three clinical studies. A total of 9,478 patients with DVT or PE were randomly assigned to receive Xarelto, a combination of enoxaparin and a vitamin K antagonist (VKA), or a placebo. The studies were designed to measure the number of patients who experienced recurrent symptoms of DVT, PE or death after receiving treatment.

Results showed Xarelto was as effective as the enoxaparin and VKA combination for treating DVT and PE. About 2.1 percent of patients treated with Xarelto compared with 1.8 percent to 3 percent of patients treated with the enoxaparin and VKA combination experienced a recurrent DVT or PE. Additionally, results from a third study showed extended Xarelto treatment reduced the risk of recurrent DVT and PE in patients. About 1.3 percent of patients treated with Xarelto compared with 7.1 percent of patients receiving placebo experienced a recurrent DVT or PE.

The major side effect observed with Xarelto is bleeding, similar to other anti-clotting drugs.

Xarelto is marketed by Raritan, N.J.-based Janssen Pharmaceuticals Inc.

For more information:

FDA: Office of Hematology and Oncology Products

FDA: Approved Drugs: Questions and Answers

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

 

SOURCE:

http://www.forbes.com/sites/larryhusten/2012/11/02/rivaroxaban-gains-fda-indications-for-the-treatment-and-prevention-of-dvt-and-pe/?goback=%2Egde_2069447_member_181862591

Cardiac Atrial Fibrillation

ATLANTA, Georgia — Patients with atrial fibrillation receiving anticoagulant therapy are more likely to experience gastrointestinal (GI) bleeding when treated with rivaroxaban than when treated with warfarin, according to a new analysis of data from ROCKET AF.

Christopher Nessel, MD, from research and development at Johnson & Johnson in Raritan, New Jersey, reported the findings here at CHEST 2012: American College of Chest Physicians Annual Meeting.

“Compared with warfarin, the risk of GI bleeding is increased with rivaroxaban, but the incidence of life-threatening or fatal GI bleeding is lower,” Dr. Nessel told Medscape Medical News. “A careful benefit/risk assessment is needed prior to prescribing rivaroxaban for high-risk patients,” he added.

The analysis examined the incidence and outcomes of GI hemorrhage in 14,264 patients with nonvalvular atrial fibrillation enrolled in ROCKET AF.

The patients were randomized to either rivaroxaban or dose-adjusted warfarin. All GI bleeding events were recorded during treatment and for 2 days after the last dose was administered. Severity of bleeding was defined by a corresponding drop in hemoglobin or transfusion of more than 2 units of red cells.

The composite principal safety end point for GI bleeding events (upper GI, lower GI, and rectal bleeding) occurred more frequently in the 394 patients receiving rivaroxaban than in the 290 receiving warfarin (3.61% vs 2.60% per year; hazard ratio [HR], 1.39; 95% confidence interval [CI], 1.19 to 1.61). Major bleeding was more frequent with rivaroxaban than with warfarin (2.00% vs 1.24% per year; HR, 1.61; 95% CI, 1.30 to 1.99), as was clinically relevant nonmajor bleeding (1.75% vs 1.39% per year; HR, 1.26; 95% CI, 1.20 to 1.55).

Patients who experienced major GI bleeding were more likely to have experienced GI bleeding in the past, to have mild anemia, to have a lower creatinine clearance, to be previous or current smokers, and to be older than patients who did not experience a GI bleeding during the trial (n = 13,552). They were also less likely to be female and to have previously experienced a stroke or transient ischemic attack.

The incidence of severe bleeding (transfusion of at least 4 units) was similar in the rivaroxaban and warfarin groups (49 vs 47). Six patients developed fatal bleeding: 1 in the rivaroxaban group and 5 in the warfarin group.

Data May Give Clinicians Pause When Considering Rivaroxaban

“The data presented extend the observations from the ROCKET AF clinical study,” Dr. Nessel said. “Specifically, the analyses identified characteristics of nonvalvular atrial fibrillation patients that may predispose them to the occurrence of GI hemorrhage. The data also indicated that the overall fatality rates for bleeds of this nature are very low.”

Independent commentator James Wisler, MD, from the division of cardiovascular disease at Duke University Medical Center in Durham, North Carolina, pointed out that this study underscores the importance of critically evaluating these newer anticoagulants when considering their use in a given patient.

“The decision regarding which anticoagulant to use for a given patient is complex, and risks and benefits need to be considered thoughtfully,” he told Medscape Medical News. He added that the results of this study might give some physicians pause about initiating a newer anticoagulant, such as rivaroxaban, in a given patient with atrial fibrillation and an unfavorable risk profile, such as those with a previous GI bleed.

“While the previously published results from ROCKET AF suggested that the risk profiles were similar between rivaroxaban and warfarin, these results demonstrate that there is indeed a subpopulation of patients who may be better served with warfarin than rivaroxaban,” he explained.

According to Dr. Wisler, both this analysis and the initial ROCKET AF study demonstrate that rivaroxaban is associated with fewer episodes of severe or fatal bleeding events, despite the increase in major and clinically relevant nonmajor bleeding observed in the specific subgroup of this study. “Currently, it is unclear why this discrepancy exists,” he added.

He recommends that clinicians take a careful patient history to assess bleeding risk factors when considering the initiation of a newer anticoagulant such as rivaroxaban.

“While perhaps more convenient and efficacious, certain patient populations, such as that evaluated in this study, may receive net harm from these newer agents,” he said.

SOURCE:

CHEST 2012: American College of Chest Physicians Annual Meeting. Presented October 22, 2012.

http://journal.publications.chestnet.org/issue.aspx?journalid=99&issueid=25283

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Atrial Fibrillation: The Latest Management Strategies

Reporter: Aviva Lev-Ari, PhD, RN

UPDATED on 8/5/2013

Ischemic strokes are the most common type of AFib-related stroke5 and can be extremely debilitating.6,7 It’s important to help your patients understand the risk of ischemic stroke and how you can help lower that risk.

Nearly 9 out of 10 AFib-related strokes are ischemic, and most are cardioembolic5,8,9

  • Cardioembolic strokes are most commonly caused by AFib9,10
  • Hemorrhagic strokes account for approximately 10% of AFib-related strokes5
  • AFib-related ischemic strokes are primarily caused by an embolus formed in the left atrial appendage of the heart11

Ischemic strokes can be devastating, often resulting in irreversible brain damage2

  • Debilitating effects of a stroke include paralysis, slurred speech, and memory loss12
    • Every second, ≈32,000 brain cells can die due to hypoxia from lack of blood flow4
    • In 1 minute, nearly 2 million brain cells can die—increasing the risk of disability or death2-4
  • Severely disabling stroke is frequently rated by patients as equivalent to or worse than death13

Strokes are a leading cause of disability in the US14

The good news is you can significantly reduce your AFib patients’ risk of ischemic stroke with anticoagulation therapy.11,15,16 By keeping them appropriately anticoagulated, you can help your patients avoid the devastation of ischemic stroke.11

AFib=atrial fibrillation.

References

  1. Types of stroke. Johns Hopkins Medicine Web site. http://www.hopkinsmedicine.org/healthlibrary/printv.aspx?d=85,P00813. Accessed August 9, 2012.
  2. Maas MB, Safdieh JE. Ischemic stroke: pathophysiology and principles of localization. Hospital Physician Neurology Board Review Manual. 2009;13:1-16.http://www.turner-white.com/pdf/brm_Neur_V13P1.pdf. Accessed February 1, 2013.
  3. Rosamond WD, Folsom AR, Chambless LE, et al. Stroke incidence and survival among middle-aged adults: 9-year follow-up of the Atherosclerosis Risk in Communities (ARIC) cohort. Stroke. 1999;30:736-743.
  4. Saver JL. Time is brain—quantified. Stroke. 2006;37:263-266.
  5. Mercaldi CJ, Ciarametaro M, Hahn B, et al. Cost efficiency of anticoagulation with warfarin to prevent stroke in Medicare beneficiaries with nonvalvular atrial fibrillation. Stroke. 2011;42:112-118.
  6. Vemmos KN, Tsivgoulis G, Spengos K, et al. Anticoagulation influences long-term outcome in patients with nonvalvular atrial fibrillation and severe ischemic stroke. Am J Geriatr Pharmacother. 2004;2:265-273.
  7. Lin HJ, Wolf PA, Kelly-Hayes M, et al. Stroke severity in atrial fibrillation. The Framingham Study. Stroke. 1996;27:1760-1764.
  8. Grau AJ, Weimar C, Buggle F, et al. Risk factors, outcome, and treatment in subtypes of ischemic stroke: the German Stroke Data Bank. Stroke. 2001;32:2559-2566.
  9. Bogousslavsky J, Van Melle G, Regli F, Kappenberger L. Pathogenesis of anterior circulation stroke in patients with nonvalvular atrial fibrillation: the Lausanne Stroke Registry. Neurology. 1990;40:1046-1050.
  10. Freeman WD, Aguilar MI. Prevention of cardioembolic stroke. Neurotherapeutics. 2011;8:488-502.
  11. Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm SocietyCirculation. 2006;114:700-752.
  12. Effects of stroke. American Stroke Association Web site. http://www.strokeassociation.org/STROKEORG/AboutStroke/EffectsofStroke/Effects-of-Stroke_UCM_308534_SubHomePage.jsp. Accessed December 8, 2012.
  13. Gage BF, Cardinalli AB, Owens DK. The effect of stroke and stroke prophylaxis with aspirin or warfarin on quality of life. Arch Intern Med. 1996;156:1829-1836.
  14. Centers for Disease Control and Prevention (CDC). Prevalence of Stroke—United States, 2006-2010. MMWR Morb Mortal Wkly Rep. 2012;61:379-382.
  15. Singer DE, Chang Y, Fang MC, et al. The net clinical benefit of warfarin anticoagulation in atrial fibrillation. Ann Intern Med. 2009;151:297-305.
  16. Lip GYH, Andreotti F, Fauchier L, et al. Bleeding risk assessment and management in atrial fibrillation patients: a position document from the European Heart Rhythm Association, endorsed by the European Society of Cardiology Working Group on Thrombosis. Europace. 2011;13:723-746.

SOURCE

http://www.medscape.com/infosite/afib/public/

Straightforward, informed answers to your most important questions about living

with atrial fibrillation – the most common sustained cardiac arrhythmia.

Written by

Hugh G. Calkins, M.D., Director of the Arrhythmia Service

and Electrophysiology Lab at The Johns Hopkins Hospital,

and Ronald Berger, M.D.,

If you’ve ever run up a flight of stairs, chased a tennis ball across the court, or reacted in fright at a scary movie, you know what a pounding heart feels like…

But for the 2.3 million Americans who suffer from atrial fibrillation (AF or AFib), a racing heart is a way of life. Simple tasks like getting out of bed in the morning or rising from a chair can cause dizziness, weakness, shortness of breath, or heart palpitations. For these people, AF severely impairs quality of life – and even when symptoms stemming from AF are mild, the disorder can seriously impact health, increasing the risk of stroke and heart failure.

AF can be a debilitating even deadly condition. Fortunately, it can be successfully managed – but there are various approaches for treating AF or preventing a recurrence. How do you and your doctor choose which approach is right for you?

If you or a loved one has AF, there are so many questions: Do I need an anticoagulant… should I be taking medication to control my heart rate… will my symptoms respond to cardioversion… if I need an antiarrhythmic drug to control AF episodes, which one should I take… when is an ablation procedure appropriate… and more.

It’s critically important to learn everything you can now — so you can partner with your doctor effectively, ask the right questions, and understand the answers.

To help you, we asked two eminent experts at Johns Hopkins to share their expertise and hands-on experience with arrhythmia patients in an important new report, Atrial Fibrillation: The Latest Management Strategies.

Dr. Hugh Calkins and Dr. Ronald Berger are ideally positioned to help you understand and manage your AF. Together with their colleagues at Johns Hopkins, they perform approximately 2,000 electrophysiology procedures and 200 pulmonary vein isolation procedures for atrial fibrillation each year.

Hugh Calkins, M.D. is the Nicholas J. Fortuin, M.D. Professor of Cardiology, Professor of Pediatrics, and Director of the Arrhythmia Service, the Electrophysiology Lab, and the Tilt Table Diagnostic Lab at The Johns Hopkins Hospital. He has clinical and research interests in the treatment of cardiac arrhythmias with catheter ablation, the role of device therapy for treating ventricular arrhythmias, the evaluation and management of syncope, and the study of arrhythmogenic right ventricular dysplasia.

Ronald Berger, M.D., Ph.D., a Professor of Medicine and Biomedical Engineering at Johns Hopkins, is Director of the Electrophysiology Fellowship Program at The Johns Hopkins Hospital. He serves on the editorial board for two major journals in the cardiovascular field and has written and coauthored more than 100 articles and book chapters.

Atrial Fibrillation: The Latest Management Strategies is now available to you in a digital PDF download and print version.

“I feel like my heart is going to jump out of my chest…” 

An arrhythmia is an abnormality in the timing or pattern of the heartbeat, causing the heart to beat too rapidly, too slowly, or irregularly. Sounds pretty straightforward, but there’s a lot we don’t know about why the heart rhythm goes awry… or the best way to treat it.

In Atrial Fibrillation: The Latest Management Strategies, we focus on what we DO know. In page after page of this comprehensive report, we address your most serious concerns about living with AF, such as:

  • I don’t have any symptoms. Is my problem definitely AF?
  • Can drinking alcohol trigger or worsen AF?
  • Is every person who has AF at risk for a stroke?
  • If my doctor suspects AF, will I have to wear an implantable or event monitor to be sure?
  • Why does AF often show up later in life?
  • What would you recommend to the older patient – 75 and older – who has AF but no bothersome symptoms?
  • What do you recommend for the person with longstanding persistent AF?
  • Is the AF experienced by an otherwise healthy person different from that of a person with underlying heart disease or other health issues?
  • What are the differences among: paroxysmal AF, persistent AF, and longstanding persistent AF?
  • What is the “pill-in-the-pocket” approach to AF?

Anticoagulation Therapy: What You Should Know

While AF is generally not life threatening, for some patients it can increase the likelihood of blood clots forming in the heart. And if a clot travels to the brain, a stroke will result. Anticoagulation therapy is used to prevent blood clot formation in people with AF…

  • Why is anticoagulation therapy with warfarin (Coumadin) needed for some people with AF?
  • How is the use of warfarin monitored?
  • How does a doctor determine if a patient with AF needs to take warfarin?
  • What’s the CHADS2 score and how is it used?
  • If a patient’s CHADS2 score is 1, how do you decide between aspirin and warfarin, or nothing at all?
  • Why is it so difficult to keep within therapeutic range with warfarin?
  • Can I test my INR (a test measuring how long it takes blood to clot) at home?
  • What happens if my INR is too high?
  • What options are available if a patient cannot take warfarin?
  • What are the benefits of dabigatran, a new blood-thinning alternative to warfarin therapy?

Symptom Control: The Art of Rate and Rhythm Control

For many patients and their doctors, it’s difficult to achieve and maintain heart rhythm. Two key management strategies are used: heart rate and heart rhythm control. In Atrial Fibrillation: The Latest Management Strategies, you’ll read an in-depth discussion of the benefits of rate versus rhythm control for AF:

  • What have we learned from the AFFIRM study, and how has this knowledge affected the management of AF?
  • What is catheter ablation of the AV (atrioventricular) node?
  • Why is cardioversion needed?
  • Are there different types of cardioversion?
  • What is chemical cardioversion? What is electrical cardioversion?
  • Can medication be used to convert the heart back to normal sinus rhythm?
  • Which antiarrhythimic drugs are used to treat AF?
  • How is catheter ablation for AF performed?
  • What is pulmonary vein antrum isolation (PVAI) and how is it performed?
  • Who are the best candidates for PVAI?

There’s more to Atrial Fibrillation: The Latest Management Strategies, much more.

We explain surgical ablation of AF, a procedure performed through small incisions in the chest wall… discuss when it’s appropriate to seek a second opinion… take a close look at strokes and explain the warning signs and differences among ischemic, thrombotic, embolic, and hemorrhagic strokes… and provide an arrhythmia glossary of key AF terms used by electrophysiologists and cardiologists.

Direct to You From Johns Hopkins

Atrial Fibrillation: The Latest Management Strategies is designed to give you unprecedented access to the expertise of the hospital ranked #1 of America’s Best Hospitals for 21 consecutive years 1991-2011 by U.S. News & World Report. You simply won’t find a more knowledgeable and trustworthy source of the medical information you require. A tradition of discovery and medical innovation is the hallmark of Johns Hopkins research. Since its founding in 1889, The Johns Hopkins Hospital has led the way transferring the discoveries made in the laboratory to the administration of effective patient care. No one institution has done more to earn the trust of the men and women diagnosed with AF and other cardiovascular conditions.

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Curator: Aviva Lev-Ari, PhD, RN

Intravascular Stimulation/Ablation of Autonomics are procedures, aka Renal Arterial Denervation, that since 1999 has greater promise for treatment of a diseases assumed to be related to an imbalance of autonomic tone.  Dr. Scherlag prefers the name “cardiac sympathetic denervation”.  As he has outlined, the ablation of autonomics in the renal artery has more of an effect on the heart than it does on the kidneys. I do agree that the procedure has  a cardiac effect obtained by autonomic modulation in essence.

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

Pioneering work in this field, the first to stimulate/ablate autonomic nerves effecting the heart from the intravascular space was accomplished by Dr. Scherlag and others. The greatest accomplishment was “Method and apparatus for  transvascular treatment of tachycardia and fibrillation. US Patent 6,292,695. Filed June 17, 1999.

Dr. Scherlag writes, [T]he possibility that parasympathetic or sympathetic nerves running on blood vessels  could be stimulated or ablated from inside the vasculature was initially demonstrated using basket electrode catheters in a series of experimental studies (1-6) and formally patented in 1999 (7).

Treatment of Hypertension by renal arterial denervation from inside the vasculature using a basket electrode catheters by ultra sound or by RF energy is fully documented in my post Treatment of Refractory Hypertension via Percutaneous Renal Denervation

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

Clinical Trials and the Ecosystem of all leading manufacturers of Medical Devices for Renal Arterial Denervation, including videos for demonstration of the procedure are presented in my post, link above.

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.

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

http://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

REFERENCES

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.

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Reporter: Aviva Lev-Ari, PhD, RN

 

Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease

Original Article

Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease

J.B. Olesen and Others

The prevalence of both atrial fibrillation and chronic kidney disease increases with age. The prevalence of atrial fibrillation is 2.3% among persons 40 years of age or older and 5.9% among those 65 years of age or older, and the prevalence of end-stage renal disease increases from approximately 3.5% among persons 45 to 64 years of age to nearly 6% among those 75 years of age or older. Many patients have both disorders, and the number of such patients is increasing, owing in part to the aging population and the improved survival in both diseases.

Clinical Pearls

  What is the effect of chronic kidney disease on the risk of stroke?

The U.S.-based Renal Data System has reported that chronic kidney disease increases the risk of stroke by a factor of 3.7, and end-stage renal disease (i.e., disease requiring renal-replacement therapy) increases the risk by a factor of 5.8. Atrial fibrillation increases the risk of stroke by a factor of 5, and chronic kidney disease increases the risk of stroke among patients without atrial fibrillation.

  What is a CHA2DS2-VASc score?

This study evaluated the risk of stroke or systemic thromboembolism, with adjustment for CHA2DS2-VASc risk factors. The CHA2DS2-VASc score extends the CHADS2 algorithm to include additional nonmajor risk factors for stroke, including vascular disease (V), age between 65 to 74 years (A), and female gender (sex category or Sc).

Morning Report Questions

Q. What were the results of this study of patients with atrial fibrillation and chronic kidney disease with respect to risk of stroke or systemic embolism? 

A. This study demonstrated that warfarin treatment was associated with a significantly decreased risk of stroke or systemic thromboembolism overall and among patients requiring renal-replacement therapy, and with a nonsignificantly decreased risk among patients with non–end-stage chronic kidney disease. In an analysis that compared all patients who had any renal disease with those who had no renal disease, warfarin decreased the risk of stroke or systemic thromboembolism (hazard ratio, 0.76; 95% CI, 0.64 to 0.91; P=0.003), as did warfarin plus aspirin (hazard ratio, 0.74; 95% CI, 0.56 to 0.98; P=0.04). Aspirin alone was associated with an increased risk of stroke or systemic thromboembolism overall and among patients who had any renal disease, as compared with those who had no renal disease (hazard ratio, 1.17; 95% CI, 1.01 to 1.35; P=0.04).

Table 3. Hazard Ratios for Stroke or Systemic Thromboembolism.

Q. How did the risk of bleeding differ among patients with and without kidney disease? 

A. The risk of bleeding was higher among patients with non–end-stage chronic kidney disease and among patients requiring renal-replacement therapy as compared to patients without renal disease, and treatment with warfarin, aspirin, or both incrementally increased this risk. Among all patients who had any renal disease, as compared with those who had no renal disease, there was an increased risk of bleeding with warfarin (hazard ratio, 1.33; 95% CI, 1.16 to 1.53; P<0.001), aspirin (hazard ratio, 1.17; 95% CI, 1.02 to 1.34; P=0.03), and warfarin plus aspirin (hazard ratio, 1.61; 95% CI, 1.32 to 1.96; P<0.001). Among patients with non–end-stage chronic kidney disease, the risk of bleeding increased with a higher dose of loop diuretics. The risk of bleeding was highest among patients with chronic glomerulonephritis and lowest among those with chronic tubulointerstitial nephropathy.

Table 4. Hazard Ratios for Bleeding.

 Original article

Stroke and Bleeding in Atrial Fibrillation with Chronic Kidney Disease

Jonas Bjerring Olesen, M.D., Gregory Y.H. Lip, M.D., Anne-Lise Kamper, M.D., D.M.Sc., Kristine Hommel, M.D., Lars Køber, M.D., D.M.Sc., Deirdre A. Lane, Ph.D., Jesper Lindhardsen, M.D., Gunnar Hilmar Gislason, M.D., Ph.D., and Christian Torp-Pedersen, M.D., D.M.Sc.

N Engl J Med 2012; 367:625-635  August 16, 2012

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Reporter: Aviva Lev-Ari, PhD, RN

Extreme Performance Athletes May Be at Risk for Cardiac Arrhythmias

http://bidmc.org/CentersandDepartments/Departments/CardiovascularInstitute/CVINewsletter/TooMuchGoodThing.aspx

World-class rowing champion Frederick SchochWorld-class rowing champion Frederick Schoch

You probably know that regular, moderate exercise can result in many health benefits. But you may be surprised to learn that prolonged, intensive endurance exercise on an Olympian scale can actually damage your heart.

Scientists and doctors have demonstrated that long-term training and competition in extreme endurance sports such as marathons, iron-man triathlons, competitive rowing and long-distance bicycle races may cause structural changes to the heart and large arteries.

Athlete’s heart syndrome” was first described more than 100 years ago as an apparently benign condition in which the elite athlete’s heart enlarges and thickens. For many years, doctors noted that abnormal electrocardiograms were common for extreme athletes, but no evidence pointed to an association with serious arrhythmias or sudden cardiac death. However, there is accumulating evidence that chronic extreme athletic activity may lead to potentially harmful changes in the heart in some individuals.

For example, a review published recently in the Mayo Clinic Proceedingsdemonstrated that approximately 12 percent of apparently healthy marathon runners showed microscopic areas of fibrosis, or scarring, in the heart chambers. The significance of these changes is not clear, but they could predispose the heart to abnormal rhythms in some cases.

A two-year follow-up revealed that the rate of coronary heart disease was significantly higher in extreme marathon runners than in moderate runners.

A 2011 Swedish study showed that elite cross-country skiers with long years of endurance training had a 29 percent higher risk of developing a variety of abnormal heart rhythms, some benign as well as some more serious.

Extreme Athletics and Atrial Fibrillation

High-profile professional athletes who are believed to have died of fatal arrhythmias include NFL star Reggie White, who died at 43 in 2004, and legendary ultra-marathoner Micah True, who died at 58 earlier this year.

Researchers believe high-endurance sports may promote the occurrence of atrial fibrillation in susceptible persons. This arrhythmia, which involves uncomfortable episodes of irregular, rapid heartbeat caused by faulty electrical signals in the heart, is usually not life-threatening. However, in about 5 percent of those with the condition, it can lead to heart failure and stroke.

“Physicians are becoming increasingly aware that extreme training regimens and endurance-style competitions can, in rare instances, lead to potentially dangerous abnormal cardiac rhythms,” says Alfred E. Buxton, MD, Director of the Clinical Electrophysiology Laboratory at Beth Israel Deaconess Medical Center’sCardioVascular Institute.

Physicians need to take into account the current research, follow new developments and be prepared to advise certain patients to make lifestyle changes based on the new data, he says.

One Athlete’s Story

Mark E. Josephson, MDMark E. Josephson, MD

Mark E. Josephson, MD, Chief of Cardiovascular Medicine at the CardioVascular Institute — and an internationally recognized expert in electrophysiology and catheter ablation — has treated numerous rowers and other high-performance athletes who have suffered from atrial fibrillation. One example is Frederick Schoch, a world-class rowing champion and executive director of Boston’s celebrated annual Head of the Charles Regatta.

Schoch was diagnosed with paroxysmal atrial fibrillation in 2009 after he experienced heavy breathing and lightheadness following his crew’s fifth consecutive first-place finish in the Regatta’s 50 and older category. Schoch learned that atrial fibrillation can cause blood clots in the left atrium (upper chamber) and can lead to heart failure and stroke. Treatments may include medications (such as beta-blockers or anti-arrhythmic drugs), interventions (such as catheter ablation) and/or surgery.

To regulate his heart rate, Schoch’s primary care physician prescribed the drug diltiazem, but his episodes persisted and he feared he would never be able to compete again.

“Rowing is in my DNA,” says Schoch, whose father was an Olympic rower. “But with afib, I couldn’t even walk up the stairs.”

In 2010, a fellow rower referred Schoch to Dr. Josephson, who has treated more than 1,000 cardiac arrhythmia patients.

Back in the Boat

After hearing Schoch’s story, Dr. Josephson performed a catheter ablation, an interventional procedure that reduces the frequency of paroxysmal atrial fibrillation symptoms about 70 percent of the time. The procedure typically lasts two hours and involves inserting a catheter through the groin and puncturing the membrane between the heart’s right and left atria. Catheters are placed at the pulmonary veins (which are the source of atrial fibrillation triggers in 90 percent of paroxysmal afib cases), while the cardiologist delivers a high-frequency, low-voltage current to the site. This burns the tissue to isolate the pulmonary vein from the atrius so that triggers can’t initiate atrial fibrillation.

Schoch spent one night at BIDMC and returned to work two days later. He resumed his training, and in 2011, just one year after his procedure, he led his team to their sixth first-place finish in the Regatta’s senior division. Currently, he is serving as a television analyst, commenting on rowing at the 2012 Summer Olympics. He is also training for the next Head of the Charles Regatta in October.

“I am eternally grateful to Dr. Josephson,” says Schoch. “I hope that my experience can be helpful to others.”

Do Not Stop Exercising!

While the findings cited here are unsettling, they shouldn’t discourage anyone from being physically active. For most adults, the American Heart Associationrecommends 150 minutes of moderate exercise a week (30 minutes a day on five days), or 75 minutes per week of vigorous exercise. Exercise is almost as effective when divided into several shorter periods during the day for convenience.

The result will be increased physical capacity and mental well-being, and a significant reduction in cardiovascular disease risk factors such as high blood pressure, excess weight and unhealthy cholesterol levels. Regular exercise helps fend off not only heart disease and stroke, but also many cancers, osteoporosis, diabetes, arthritis and depression.

“Moderate exercise is certainly good for your heart and your overall health,” says Dr. Buxton. “However, as is usually the case in life, moderation should be the guideline. Beyond 30 to 60 minutes per day, you may reach a point of diminishing returns. So don’t overdo it, but take comfort in knowing that with the right diagnosis and treatment, atrial fibrillation can be managed successfully.”

Above content provided by the CardioVascular Institute at Beth Israel Deaconess Medical Center. For advice about your medical care, consult your doctor.

Posted August 2012

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Reporter: Aviva Lev-Ari, PhD, RN

Written by
Hugh G. Calkins, M.D., Director of the Arrhythmia Service
 and Electrophysiology Lab at The Johns Hopkins Hospital,
 and Ronald Berger, M.D.

  • Hugh Calkins, M.D. is the Nicholas J. Fortuin, M.D. Professor of Cardiology, Professor of Pediatrics, and Director of the Arrhythmia Service, the Electrophysiology Lab, and the Tilt Table Diagnostic Lab at The Johns Hopkins Hospital. He has clinical and research interests in the treatment of cardiac arrhythmias with catheter ablation, the role of device therapy for treating ventricular arrhythmias, the evaluation and management of syncope, and the study of arrhythmogenic right ventricular dysplasia.
  • Ronald Berger, M.D., Ph.D., a Professor of Medicine and Biomedical Engineering at Johns Hopkins, is Director of the Electrophysiology Fellowship Program at The Johns Hopkins Hospital. He serves on the editorial board for two major journals in the cardiovascular field and has written and coauthored more than 100 articles and book chapters. 

If you’ve ever run up a flight of stairs, chased a tennis ball across the court, or reacted in fright at a scary movie, you know what a pounding heart feels like… But for the 2.3 million Americans who suffer from atrial fibrillation (AF or AFib), a racing heart is a way of life. Simple tasks like getting out of bed in the morning or rising from a chair can cause dizziness, weakness, shortness of breath, or heart palpitations. For these people, AF severely impairs quality of life – and even when symptoms stemming from AF are mild, the disorder can seriously impact health, increasing the risk of stroke and heart failure. AF can be a debilitating even deadly condition. Fortunately, it can be successfully managed – but there are various approaches for treating AF or preventing a recurrence. How do you and your doctor choose which approach is right for you? If you or a loved one has AF, there are so many questions: Do I need an anticoagulant… should I be taking medication to control my heart rate… will my symptoms respond to cardioversion… if I need an antiarrhythmic drug to control AF episodes, which one should I take… when is an ablation procedure appropriate… and more. It’s critically important to learn everything you can now — so you can partner with your doctor effectively, ask the right questions, and understand the answers. To help you, we asked two eminent experts at Johns Hopkins to share their expertise and hands-on experience with arrhythmia patients in an important new report, Atrial Fibrillation: The Latest Management Strategies. Dr. Hugh Calkins and Dr. Ronald Berger are ideally positioned to help you understand and manage your AF. Together with their colleagues at Johns Hopkins, they perform approximately 2,000 electrophysiology procedures and 200 pulmonary vein isolation procedures for atrial fibrillation each year. 

Anticoagulation Therapy: What You Should Know

While AF is generally not life threatening, for some patients it can increase the likelihood of blood clots forming in the heart. And if a clot travels to the brain, a stroke will result. Anticoagulation therapy is used to prevent blood clot formation in people with AF…

  • Why is anticoagulation therapy with warfarin (Coumadin) needed for some people with AF?
  • How is the use of warfarin monitored?
  • How does a doctor determine if a patient with AF needs to take warfarin?
  • What’s the CHADS2 score and how is it used?
  • If a patient’s CHADS2 score is 1, how do you decide between aspirin and warfarin, or nothing at all?
  • Why is it so difficult to keep within therapeutic range with warfarin?
  • Can I test my INR (a test measuring how long it takes blood to clot) at home?
  • What happens if my INR is too high?
  • What options are available if a patient cannot take warfarin?
  • What are the benefits of dabigatran, a new blood-thinning alternative to warfarin therapy?
Symptom Control: The Art of Rate and Rhythm Control

For many patients and their doctors, it’s difficult to achieve and maintain heart rhythm. Two key management strategies are used: heart rate and heart rhythm control. In Atrial Fibrillation: The Latest Management Strategies, you’ll read an in-depth discussion of the benefits of rate versus rhythm control for AF:

  • What have we learned from the AFFIRM study, and how has this knowledge affected the management of AF?
  • What is catheter ablation of the AV (atrioventricular) node?
  • Why is cardioversion needed?
  • Are there different types of cardioversion?
  • What is chemical cardioversion? What is electrical cardioversion?
  • Can medication be used to convert the heart back to normal sinus rhythm?
  • Which antiarrhythimic drugs are used to treat AF?
  • How is catheter ablation for AF performed?
  • What is pulmonary vein antrum isolation (PVAI) and how is it performed?
  • Who are the best candidates for PVAI? 

http://www.johnshopkinshealthalerts.com/catalog/special_report/6044-1.html

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