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Vena Cava Filters: Device for Prevention of Pulmonary Embolism and Thrombosis

Posted in Atherogenic Processes & Pathology, Atrial Fibrilation (a-Fib), Cardiac Pacing and Arrhythmias, Cardiac and Cardiovascular Surgical Procedures, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Coagulation Therapy and Internal Bleeding, congestive heart failure, Frontiers in Cardiology and Cardiovascular Disorders, Heart Failure (HF), Medical Devices R&D and Inventions, Origins of Cardiovascular Disease, Peripheral Arterial Disease & Peripheral Vascular Surgery, Pharmacotherapy of Cardiovascular Disease, Vascular Diseases, Vena Caval Filters: Device for Prevention of Pulmonary Embolism and Thrombosis, tagged , , , , , on October 4, 2016| Leave a Comment »

Inferior Vena Cava Filters: Device for Prevention of Pulmonary Embolism and Thrombosis

Reporter: Aviva Lev-Ari, PhD, RN

 

UPDATED on 7/18/2018

 

Original Investigation
Cardiology
July 13, 2018

Association of Inferior Vena Cava Filter Placement for Venous Thromboembolic Disease and a Contraindication to Anticoagulation With 30-Day Mortality

Tyson E. Turner, MD, MPH1; Mohammed J. Saeed, MBChB, MPH2; Eric Novak, MS1; et alDavid L. Brown, MD1
Author Affiliations Article Information
JAMA Network Open. 2018;1(3):e180452. doi:10.1001/jamanetworkopen.2018.0452
Key Points

Question  What is the association of inferior vena cava filter placement with 30-day mortality in patients with venous thromboembolic disease and a contraindication to anticoagulation?

Findings  In this cohort study, using 2 different statistical methods with adjustment for immortal time bias, inferior vena cava filter placement in patients with venous thromboembolic disease and a contraindication to anticoagulation was associated with an increased risk of 30-day mortality.

Meaning  Randomized clinical trials are needed to define the role of inferior vena cava filter placement in patients with venous thromboembolic disease and a contraindication to anticoagulation.

 

Abstract

Importance  Despite the absence of data from randomized clinical trials, professional societies recommend inferior vena cava (IVC) filters for patients with venous thromboembolic disease (VTE) and a contraindication to anticoagulation therapy. Prior observational studies of IVC filters have suggested a mortality benefit associated with IVC filter insertion but have often failed to adjust for immortal time bias, which is the time before IVC filter insertion, during which death can only occur in the control group.

Objective  To determine the association of IVC filter placement with 30-day mortality after adjustment for immortal time bias.

Design, Setting, and Participants  This comparative effectiveness, retrospective cohort study used a population-based sample of hospitalized patients with VTE and a contraindication to anticoagulation using the State Inpatient Database and the State Emergency Department Database, part of the Healthcare Cost and Utilization Project of the Agency for Healthcare Research and Quality, from hospitals in California (January 1, 2005, to December 31, 2011), Florida (January 1, 2005, to December 31, 2013), and New York (January 1, 2005, to December 31, 2012). Data analysis was conducted from September 15, 2015, to March 14, 2018.

Exposure  Inferior vena cava filter placement.

Main Outcomes and Measures  Multivariable Cox proportional hazard models were constructed with IVC filters as a time-dependent variable that adjusts for immortal time bias. The Cox model was further adjusted using the propensity score as an adjustment variable.

Results  Of 126 030 patients with VTE, 61 281 (48.6%) were male and the mean (SD) age was 66.9 (16.6) years. In this cohort, 45 771 (36.3%) were treated with an IVC filter, whereas 80 259 (63.7%) did not receive a filter. In the Cox model with IVC filter status analyzed as a time-dependent variable to account for immortal time bias, IVC filter placement was associated with a significantly increased hazard ratio of 30-day mortality (1.18; 95% CI, 1.13-1.22; P < .001). When the propensity score was included in the Cox model, IVC filter placement remained associated with an increased hazard ratio of 30-day mortality (1.18; 95% CI, 1.13-1.22; P < .001).

Conclusions and Relevance  After adjustment for immortal time bias, IVC filter placement was associated with increased 30-day mortality in patients with VTE and a contraindication to anticoagulation. Randomized clinical trials are needed to determine the efficacy of IVC filter placement in patients with VTE and a contraindication to anticoagulation.

 

EDITORIAL

Requiem for Liberalizing Indications for Vena Caval Filters?

Samuel Z. Goldhaber
http://dx.doi.org/10.1161/CIRCULATIONAHA.116.022730 Published: May 24, 2016

Use of inferior vena caval (IVC) filters has proliferated.

  • In 1979, ≈2000 vena caval filters were inserted.
  • In 1999, the number of IVC filters inserted annually had increased ≈25-fold to 49 000.
  • Retrievable IVC filters were first approved in 2003 and gained popularity rapidly.
  • By 2006, retrievable IVC filters accounted for about half of all IVC filters that were inserted.
  • The largest proportional increase in IVC filter use was subsequently in patients at risk for pulmonary embolism (PE) but who had had neither PE nor deep vein thrombosis (DVT).1

The Controversy by Samuel Z. Goldhaber, MD

Appropriate use of IVC filters is a hot topic. On the one hand,

  • filters hold the promise of reducing PE rates by trapping moderate and large DVT that have detached from the deep veins of the legs and pelvis and that are hurtling toward the heart. On the other hand, we do not have clear-cut definitions of which patients with PE and DVT will benefit most from this technology.
  • an array of complications can ensue, including
  1. caval perforation,2
  2. caval thrombosis,
  3. fracture,
  4. fragment embolization,
  5. intracardiac migration,3
  6. cardiac perforation, and
  7. cardiac tamponade.4

In a systematic review of retrievable IVC filters, only 34% were retrieved, and the majority remained in place permanently. Most of the complications from retrievable filters occurred with long-term use.5

Guidelines

However, it is premature to hammer nails into the coffin and to gather as a medical community for a requiem that celebrates no indication for liberalizing indications for placing an IVC filter. Instead, we need to shift the focus of the questions that we investigate and pour resources into further randomized and observational trials of IVC filter insertion in special highrisk populations.

There remain important groups of patients who may benefit from IVC filters with reduction in PE and PE-associated mortality (Table 2). In some cases, tantalizing data suggest that these populations warrant filters. In other cases, we lack data to guide us. Patients with massive PE—accompanied by cardiogenic shock requiring vasopressors to support blood pressure—are desperately ill. They are clinically unstable. An additional PE under these circumstances can be the fatal blow. Data from the National Inpatient Sample and the International Cooperative PE Registry suggest that filters in these patients may be lifesaving.

Patients with severe PE who undergo acute surgical pulmonary embolectomy are vulnerable to recurrent PE, especially during the early postoperative period where full anticoagulation cannot be immediately implemented. I have had personal experience managing this type of patient where the embolectomy is successful but the patient dies of recurrent PE.19

Table 1. Generally Accepted Consensus Recommendations for IVC Filter Insertion in Patients With VTE

  • Major bleeding on full-dose anticoagulation
  • Major contraindication to full-dose anticoagulation
  • New-onset acute PE (especially recurrent PE) despite well-documented fulldose anticoagulation for an existing VTE

IVC indicates inferior vena caval; PE, pulmonary embolism; and VTE, venous thromboembolism.

 

Table 2. Special Populations Where Benefits of IVC Filter Insertion May Outweigh Risks

  • Massive PE or high-risk submassive PE
  • Surgical pulmonary embolectomy
  • Cancer patients with VTE or at high risk of VTE with concomitant high risk of bleeding if anticoagulated
  • Surgical patients (especially during preoperative evaluation) at high risk of VTE with concomitant high risk of bleeding if anticoagulated

IVC indicates inferior vena caval; PE, pulmonary embolism; and VTE, venous thromboembolism.

http://dx.doi.org/10.1161/CIRCULATIONAHA.116.022730

References

1. Stein PD, Matta F, Hull RD. Increasing use of vena cava filters for prevention of pulmonary embolism. Am J Med. 2011;124:655–661. doi:10.1016/j.amjmed.2011.02.021.

2. Jia Z, Wu A, Tam M, Spain J, McKinney JM, Wang W. Caval penetration by inferior vena cava filters: a systematic literature review of clinical significance and management. Circulation. 2015;132:944–952. doi: 10.1161/ CIRCULATIONAHA.115.016468

3. Owens CA, Bui JT, Knuttinen MG, Gaba RC, Carrillo TC, Hoefling N, Layden-Almer JE. Intracardiac migration of inferior vena cava filters: review of published data. Chest. 2009;136:877–887. doi: 10.1378/ chest.09-0153.

4. Nicholson W, Nicholson WJ, Tolerico P, Taylor B, Solomon S, Schryver T, McCullum K, Goldberg H, Mills J, Schuler B, Shears L, Siddoway L, Agarwal N, Tuohy C. Prevalence of fracture and fragment embolization of Bard retrievable vena cava filters and clinical implications including cardiac perforation and tamponade. Arch Intern Med. 2010;170:1827–1831. doi: 10.1001/archinternmed.2010.316.

5. Angel LF, Tapson V, Galgon RE, Restrepo MI, Kaufman J. Systematic review of the use of retrievable inferior vena cava filters. J Vasc Interv Radiol. 2011;22:1522–1530.e3. doi: 10.1016/j.jvir.2011.08.024.

19. Aklog L, Williams CS, Byrne JG, Goldhaber SZ. Acute pulmonary embolectomy: a contemporary approach. Circulation. 2002;105:1416–1419.

Other related articles published in this Open Access Online Scientific Journal include the follwoing:

 

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

https://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/

Venous Thromboembolism (VTE): Blood Clots in Leg and Lungs – No. 3 Cardiovascular Killer Globally – Is Leading Cause of Premature Death and Disability in Hospitals

https://pharmaceuticalintelligence.com/2014/10/13/venous-thromboembolism-vte-blood-clots-in-leg-and-lungs-no-3-cardiovascular-killer-globally-is-leading-cause-of-premature-death-and-disability-in-hospitals/

The Relation between Coagulation and Cancer affects Supportive Treatments

https://pharmaceuticalintelligence.com/2015/10/19/the-relation-between-coagulation-and-cancer-affects-supportive-treatments/

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Etiologies of Cardiovascular Diseases: Epigenetics, Genetics and Genomics: Request for Book Review Writing on Amazon.com

Posted in BioIT: BioInformatics, BioIT: BioInformatics, NGS, Clinical & Translational, Pharmaceutical R&D Informatics, Clinical Genomics, Cancer Informatics, Cardiac and Cardiovascular Surgical Procedures, Cardiovascular Pharmacogenomics, Congenital Heart Disease, Ecosystems & Industrial Concentration in the Medical Device Sector, Epigenetics and Environmental Factors, Frontiers in Cardiology and Cardiovascular Disorders, Genetic Mutations in Congenital Heart Disease, Genome Biology, Personalized and Precision Medicine & Genomic Research, Population Health Management, Genetics & Pharmaceutical on September 11, 2016| Leave a Comment »

Etiologies of Cardiovascular Diseases: Epigenetics, Genetics and Genomics: Request for Book Review Writing on Amazon.com, Volume 2 (Volume Two: Latest in Genomics Methodologies for Therapeutics: Gene Editing, NGS and BioInformatics, Simulations and the Genome Ontology), Part 1: Next Generation Sequencing (NGS)

cvd-series-a-volume-iii


Series A: e-Books on Cardiovascular Diseases 

Series A Content Consultant: Justin D Pearlman, MD, PhD, FACC

VOLUME THREE

Etiologies of Cardiovascular Diseases:

Epigenetics, Genetics and Genomics

http://www.amazon.com/dp/B018PNHJ84

 

by  

Larry H Bernstein, MD, FCAP, Senior Editor, Author and Curator

and

Aviva Lev-Ari, PhD, RN, Editor and Curator

Introduction to Volume Three 

PART 1
Genomics and Medicine

1.1  Genomics and Medicine: The Physician’s View

1.2  Ribozymes and RNA Machines – Work of Jennifer A. Doudna

1.3  Genomics and Medicine: Contributions of Genetics and Genomics to Cardiovascular Disease Diagnoses

1.4 Genomics Orientations for Individualized Medicine, Volume One

1.4.1 CVD Epidemiology, Ethnic subtypes Classification, and Medication Response Variability: Cardiology, Genomics and Individualized Heart Care: Framingham Heart Study (65 y-o study) & Jackson Heart Study (15 y-o study)

1.4.2 What comes after finishing the Euchromatic Sequence of the Human Genome?

1.5  Genomics in Medicine – Establishing a Patient-Centric View of Genomic Data

 

PART 2
Epigenetics – Modifiable Factors Causing Cardiovascular Diseases

2.1 Diseases Etiology

2.1.1 Environmental Contributors Implicated as Causing Cardiovascular Diseases

2.1.2 Diet: Solids, Fluid Intake and Nutraceuticals

2.1.3 Physical Activity and Prevention of Cardiovascular Diseases

2.1.4 Psychological Stress and Mental Health: Risk for Cardiovascular Diseases

2.1.5 Correlation between Cancer and Cardiovascular Diseases

2.1.6 Medical Etiologies for Cardiovascular Diseases: Evidence-based Medicine – Leading DIAGNOSES of Cardiovascular Diseases, Risk Biomarkers and Therapies

2.1.7 Signaling Pathways

2.1.8 Proteomics and Metabolomics

2.1.9 Sleep and Cardiovascular Diseases

2.2 Assessing Cardiovascular Disease with Biomarkers

2.2.1 Issues in Genomics of Cardiovascular Diseases

2.2.2 Endothelium, Angiogenesis, and Disordered Coagulation

2.2.3 Hypertension BioMarkers

2.2.4 Inflammatory, Atherosclerotic and Heart Failure Markers

2.2.5 Myocardial Markers

2.3  Therapeutic Implications: Focus on Ca(2+) signaling, platelets, endothelium

2.3.1 The Centrality of Ca(2+) Signaling and Cytoskeleton Involving Calmodulin Kinases and Ryanodine Receptors in Cardiac Failure, Arterial Smooth Muscle, Post-ischemic Arrhythmia, Similarities and Differences, and Pharmaceutical Targets

2.3.2 EMRE in the Mitochondrial Calcium Uniporter Complex

2.3.3 Platelets in Translational Research ­ 2: Discovery of Potential Anti-platelet Targets

2.3.4 The Final Considerations of the Role of Platelets and Platelet Endothelial Reactions in Atherosclerosis and Novel Treatments

2.3.5 Nitric Oxide Synthase Inhibitors (NOS-I)

2.3.6 Resistance to Receptor of Tyrosine Kinase

2.3.7 Oxidized Calcium Calmodulin Kinase and Atrial Fibrillation

2.3.8 Advanced Topics in Sepsis and the Cardiovascular System at its End Stage

2.4 Comorbidity of Diabetes and Aging

2.4.1 Heart and Aging Research in Genomic Epidemiology: 1700 MIs and 2300 coronary heart disease events among about 29 000 eligible patients

2.4.2 Pathophysiological Effects of Diabetes on Ischemic-Cardiovascular Disease and on Chronic Obstructive Pulmonary Disease (COPD)

2.4.3 Risks of Hypoglycemia in Diabetics with Chronic Kidney Disease (CKD)

2.4.4  Mitochondrial Mechanisms of Disease in Diabetes Mellitus

2.4.5 Mitochondria: More than just the “powerhouse of the cell”

2.4.6  Pathophysiology of GLP-1 in Type 2 Diabetes

2.4.7 Developments in the Genomics and Proteomics of Type 2 Diabetes Mellitus and Treatment Targets

2.4.8 CaKMII Inhibition in Obese, Diabetic Mice leads to Lower Blood Glucose Levels

2.4.9 Protein Target for Controlling Diabetes, Fractalkine: Mediator cell-to-cell Adhesion though CX3CR1 Receptor, Released from cells Stimulate Insulin Secretion

2.4.10 Peroxisome proliferator-activated receptor (PPAR-gamma) Receptors Activation: PPARγ transrepression for Angiogenesis in Cardiovascular Disease and PPARγ transactivation for Treatment of Diabetes

2.4.11 CABG or PCI: Patients with Diabetes – CABG Rein Supreme

2.4.12 Reversal of Cardiac Mitochondrial Dysfunction

2.4.13  BARI 2D Trial Outcomes

2.4.14 Overview of new strategy for treatment of T2DM: SGLT2 inhibiting oral antidiabetic agents

2.5 Drug Toxicity and Cardiovascular Diseases

2.5.1 Predicting Drug Toxicity for Acute Cardiac Events

2.5.2 Cardiotoxicity and Cardiomyopathy Related to Drugs Adverse Effects

2.5.3 Decoding myocardial Ca2+ signals across multiple spatial scales: A role for sensitivity analysis

2.5.4. Leveraging Mathematical Models to Understand Population Variability in Response to Cardiac Drugs: Eric Sobie, PhD

2.5.5 Exploiting mathematical models to illuminate electrophysiological variability between individuals.

2.5.6 Clinical Effects and Cardiac Complications of Recreational Drug Use: Blood pressure changes, Myocardial ischemia and infarction, Aortic dissection, Valvular damage, and Endocarditis, Cardiomyopathy, Pulmonary edema and Pulmonary hypertension, Arrhythmias, Pneumothorax and Pneumopericardium

 

2.6 Male and Female Hormonal Replacement Therapy: The Benefits and the Deleterious Effects on Cardiovascular Diseases

2.6.1  Testosterone Therapy for Idiopathic Hypogonadotrophic Hypogonadism has Beneficial and Deleterious Effects on Cardiovascular Risk Factors

2.6.2 Heart Risks and Hormones (HRT) in Menopause: Contradiction or Clarification?

2.6.3 Calcium Dependent NOS Induction by Sex Hormones: Estrogen

2.6.4 Role of Progesterone in Breast Cancer Progression

PART 3
Determinants of Cardiovascular Diseases Genetics, Heredity and Genomics Discoveries

Introduction

3.1 Why cancer cells contain abnormal numbers of chromosomes (Aneuploidy)

3.1.1 Aneuploidy and Carcinogenesis

3.2 Functional Characterization of Cardiovascular Genomics: Disease Case Studies @ 2013 ASHG

3.3 Leading DIAGNOSES of Cardiovascular Diseases covered in Circulation: Cardiovascular Genetics, 3/2010 – 3/2013

3.3.1: Heredity of Cardiovascular Disorders

3.3.2: Myocardial Damage

3.3.3: Hypertention and Atherosclerosis

3.3.4: Ethnic Variation in Cardiac Structure and Systolic Function

3.3.5: Aging: Heart and Genetics

3.3.6: Genetics of Heart Rhythm

3.3.7: Hyperlipidemia, Hyper Cholesterolemia, Metabolic Syndrome

3.3.8: Stroke and Ischemic Stroke

3.3.9: Genetics and Vascular Pathologies and Platelet Aggregation, Cardiac Troponin T in Serum

3.3.10: Genomics and Valvular Disease

3.4  Commentary on Biomarkers for Genetics and Genomics of Cardiovascular Disease

PART 4
Individualized Medicine Guided by Genetics and Genomics Discoveries

4.1 Preventive Medicine: Cardiovascular Diseases

4.1.1 Personal Genomics for Preventive Cardiology Randomized Trial Design and Challenges

4.2 Gene-Therapy for Cardiovascular Diseases

4.2.1 Genetic Basis of Cardiomyopathy

4.3 Congenital Heart Disease/Defects

4.4 Cardiac Repair: Regenerative Medicine

4.4.1 A Powerful Tool For Repairing Damaged Hearts

4.4.2 Modified RNA Induces Vascular Regeneration After a Heart

4.5 Pharmacogenomics for Cardiovascular Diseases

4.5.1 Blood Pressure Response to Antihypertensives: Hypertension Susceptibility Loci Study

4.5.2 Statin-Induced Low-Density Lipoprotein Cholesterol Reduction: Genetic Determinants in the Response to Rosuvastatin

4.5.3 SNPs in apoE are found to influence statin response significantly. Less frequent variants in PCSK9 and smaller effect sizes in SNPs in HMGCR

4.5.4 Voltage-Gated Calcium Channel and Pharmacogenetic Association with Adverse Cardiovascular Outcomes: Hypertension Treatment with Verapamil SR (CCB) vs Atenolol (BB) or Trandolapril (ACE)

4.5.5 Response to Rosuvastatin in Patients With Acute Myocardial Infarction: Hepatic Metabolism and Transporter Gene Variants Effect

4.5.6 Helping Physicians identify Gene-Drug Interactions for Treatment Decisions: New ‘CLIPMERGE’ program – Personalized Medicine @ The Mount Sinai Medical Center

4.5.7 Is Pharmacogenetic-based Dosing of Warfarin Superior for Anticoagulation Control?

Summary & Epilogue to Volume Three

 

 

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Cardiovascular Original Research: Cases in Methodology Design for Content Co-Curation: Request for Book Review Writing on Amazon.com

Posted in Cardiac and Cardiovascular Surgical Procedures, Frontiers in Cardiology and Cardiovascular Disorders on September 11, 2016| Leave a Comment »

volume-2-cvdseriesacover

Cardiovascular Original Research:

Cases in Methodology Design for Content Co-Curation

The Art of Scientific & Medical Curation

 http://www.amazon.com/dp/B018Q5MCN8

Justin D Pearlman, MD, PhD, FACC

Larry H Bernstein, MD, FCAP

and

Aviva Lev-Ari, PhD, RN

Introduction to Volume Two

Part 1: The Methodology of Curation for Scientific Research Findings

1.1 The Methodology Explained

1.1.1 Curation by a Single Curator

1.1.2  Co-Curation by Several Experts, Authors, Writers

1.1.3 Editor’s Curation of an electronic Table of Contents (eTOCs) of an e-Book or a Hardcover Volume

1.2  The Creation Process of a Curation as an Alternative Model for Scientific Publishing

1.3  FIVE steps in the Creation Process of a Curation

1.3.1 CURATION and Co-CURATION of Scientific articles in conjunction with Experts, Authors, Writers critique and synthesis

1.3.2 Assembly of articles into e-Books using ONE of a Kind electronic Table of Contents (eTOCs) architecture

1.3.3 Assembly of e-Books into e-Series

1.3.4 Publishing of e-Series on Amazon.com

1.3.5 Distribution of e-Series to Professional Associations via their Internet website

1.4  Other Alternative Types to the Academic Publishing Model

1.5  Methodology of Curation Applied to Medical Research Findings

1.5.1 The Voice of Content Consultant on The Methodology of Curation

1.5.2  Curation is Uniquely Distinguished by the Historical Exploratory Ties that Bind

Part 2: Cardiovascular Disease – Predicted Cost of Care and the

Affordable Care Act

Introduction

2.1 Cost of Care for Cardiovascular Medical Diagnoses

2.1.1 Diagnosis of Cardiovascular Disease, Treatment and Prevention: Current & AHA Predicted Cost of Care and the Promise of Individualized Medicine Using Clinical Decision Support Systems

2.1.2 Economic Toll of Heart Failure in the US: Forecasting the Impact of Heart Failure in the United States – A Policy Statement From the American Heart Association

2.1.3 Heart Disease: Economic and Personal Effects

2.2 Impact of 2013 HealthCare Reform in the US

2.2.1 The Affordable Care Act: A Considered Evaluation. Part I.  The legislative act (ACA) and the model for implementation (Insurance Gateways).

2.2.2 The Affordable Care Act: A Considered Evaluation. Part II: The Implementation of the ACA, Impact on Physicians and Patients, and the Dis-Ease of the Accountable Care Organizations.

2.2.3 The Affordable Care Act: A Considered Evaluation.
 Part III. Final Implementation of the Affordable Care Act and a Patient and Community Outcomes Focus 

2.2.4 Post Acute Care – Driver of Variation in Healthcare Costs

2.3 Patient Protection and Affordable Care Act Featured at RAND

Part 3: Causes of Cardiovascular Diseases

3.1 Human Genome: Congenital Etiological Sources of Cardiovascular Disease

3.1.1 Genomics & Genetics of Cardiovascular Disease Diagnoses

3.1.1.1 Genomics & Genetics of Cardiovascular Disease Diagnoses: A Literature Survey of AHA’s Circulation Cardiovascular Genetics, 3/2010 – 3/2013

3.1.2 Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

3.1.2.1 Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

3.1.2.2  Transposon-mediated Gene Therapy improves Pulmonary Hemodynamics and attenuates Right Ventricular Hypertrophy: eNOS gene therapy reduces Pulmonary vascular remodeling and Arterial wall hyperplasia

3.1.3 Genetics of Conduction Disease

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

3.2 The Role of Calcium in Health and Disease

3.2.1 Identification of Biomarkers that are Related to the Actin Cytoskeleton – Part I

3.2.2 Role of Calcium, the Actin Skeleton, and Lipid Structures in Signaling and Cell Motility – Part II

3.2.3 Ca2+-Stimulated Exocytosis:  The Role of Calmodulin and Protein Kinase C in Ca2+ Regulation of Hormone and Neurotransmitter

3.2.4 Disruption of Calcium Homeostasis: Cardiomyocytes and Vascular Smooth Muscle Cells: The Cardiac and Cardiovascular Calcium Signaling Mechanism – Part VIII

3.2.5 Synaptotagmin functions as a Calcium Sensor: How Calcium Ions Regulate the fusion of vesicles with cell membranes during Neurotransmission – Part X

3.2.6 The Centrality of Ca(2+) Signaling and Cytoskeleton Involving Calmodulin Kinases and
Ryanodine Receptors in Cardiac Failure, Arterial Smooth Muscle, Post-ischemic Arrhythmia,
Similarities and Differences, and Pharmaceutical Targets

3.2.7  Atherosclerosis Independence: Genetic Polymorphisms of Ion Channels Role in the Pathogenesis of Coronary Microvascular Dysfunction and Myocardial Ischemia (Coronary Artery Disease (CAD))

3.2.8 Calcium Signaling, Cardiac Mitochondria and Metabolic Syndrome

3.3 Vasculature and Myocardium: Diagnosing the Conditions of Disease

3.3.1 State of Cardiology on Wall Stress, Ventricular Workload and Myocardial Contractile Reserve: Aspects of Translational Medicine (TM)

3.3.2 Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus

3.3.3 Cardiovascular Complications: Death from Reoperative Sternotomy after prior CABG, MVR, AVR, or Radiation; Complications of PCI; Sepsis from Cardiovascular Interventions

3.3.4 Mitral Valve Repair: Who is a Patient Candidate for a Non-Ablative Fully Non-Invasive Procedure?

Part 4: Risks and Biomarkers for Cardiovascular Diseases

4.1 The Role of Calcium in Health and Disease


4.1.1 Renal Distal Tubular Ca2+ Exchange Mechanism in Health and Disease – Part III

4.2 Vasculature and Myocardium: Diagnosing the Conditions of Disease – Biomarkers of Acute Cardiovascular Events 


4.2.1 No Early Symptoms – An Aortic Aneurysm Before It Ruptures – Is There A
Way To Know If I Have it?

4.2.2  Females and Non-Atherosclerotic Plaque: Spontaneous Coronary Artery Dissection: New Insights from Research and DNA Ongoing Study

4.2.3 Cardiovascular Diseases: Decision Support Systems for Disease
Management Decision Making

4.2.4 Dealing with the Use of the High Sensitivity Troponin (hs cTn) Assays

4.2.5 Prognostic Marker Importance of Troponin I in Acute Decompensated
Heart Failure (ADHF): Troponin I in acute decompensated heart failure:
insights from the ASCEND-HF study

4.2.6 More on the Performance of High Sensitivity Troponin T and with Amino
Terminal Pro BNP in Diabetes

4.2.7 The Cardio-Renal Syndrome (CRS) in Heart Failure (HF)

4.2.8 Vasoplegia in Orthotopic Heart Transplant Patients

4.2.9 Myocardial Infarction: The New Definition
After Revascularization

4.3 Biomarkers of Long Term Risk of Cardiovascular Disease

4.3.1 Special Considerations in Blood Lipoproteins, Viscosity, Assessment
and Treatment

4.3.2 What is the Role of Plasma Viscosity in Hemostasis and Vascular
Disease risk?

4.3.3 High-Density Lipoprotein (HDL): An Independent Predictor of
Endothelial Function & Atherosclerosis, A Modulator, An Agonist, A Biomarker
for Cardiovascular Risk

4.3.4 Artherogenesis: Predictor of CVD – the Smaller and Denser LDL
Particles

4.3.5 Hypertriglyceridemia concurrent Hyperlipidemia: Vertical Density
Gradient Ultracentrifugation a Better Test to Prevent Undertreatment of
High-Risk Cardiac Patients

4.3.6 Cholesteryl Ester Transfer Protein (CETP) Inhibitor: Potential of
Anacetrapib to treat Atherosclerosis and CAD

4.4 Conduction Dysfunction and ElectroPhysiology of the Heart


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

4.4.2 Genetic Analysis of Atrial Fibrillation

4.4.3 Oxidized Calcium Calmodulin Kinase and Atrial Fibrillation

4.4.4 Renal Function Biomarker, β-trace protein (BTP) as a Novel Biomarker for Cardiac Risk Diagnosis in Patients with Atrial Fibrilation

4.5 Cardiovascular Imaging: Diagnosing the Condition of the Disease and Determining Course of Treatment

4.5.1 Imaging Biomarker for Arterial Stiffness: Pathways in Pharmacotherapy for Hypertension and Hypercholesterolemia  Management

4.5.2 Coronary Circulation Combined Assessment: Optical Coherence Tomography(OCT), Near-Infrared Spectroscopy (NIRS) and Intravascular Ultrasound (IVUS) – Detection of Lipid-Rich Plaque and Prevention of Acute Coronary Syndrome (ACS)

4.5.3 Emerging Clinical Applications for Cardiac CT: Plaque Characterization,SPECT Functionality, Angiogram’s and Non-Invasive FFR

4.5.4 Fractional Flow Reserve (FFR) & Instantaneous wave-free ratio (iFR): An Evaluation of Catheterization Lab Tools (Software Validation) for Ischemic Assessment (Diagnostics) – Change in Paradigm: The RIGHT vessel not ALL vessel

4.5.5 Acute and Chronic Myocardial Infarction: Quantification of Myocardial Perfusion Viability – FDG-PET/MRI vs. MRI or PET alone

Part 5: Advances in Treatment of Cardiovascular Diseases




5.1 Vasculature and Myocardium: Diagnosing the Conditions of Disease

5.1.1  Erythropoietin (EPO) and Intravenous Iron (Fe) as Therapeutics for Anemia in Severe and Resistant CHF: The Elevated N-terminal proBNP Biomarker

5.1.2 Do Novel Anticoagulants Affect the PT/INR? The Cases of XARELTO(rivaroxaban) or PRADAXA (dabigatran)

5.1.3 Alternative Designs for the Human Artificial Heart: The Patients in Heart Failure – Outcomes of Transplant (donor)/Implantation (artificial) and Monitoring Technologies for the Transplant/Implant Patient in the Community

5.1.4 Vascular Surgery: International, Multispecialty Position Statement on Carotid Stenting, 2013 and Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD

5.1.5 Heart Transplant (HT) Indication for Heart Failure (HF): Procedure Outcomes and Research on HF, HT @ Two Nation’s Leading HF & HT Centers

5.1.6 Endovascular Lower-extremity Revascularization Effectiveness: Vascular Surgeons (VSs), Interventional Cardiologists (ICs) and Interventional Radiologists (IRs)

5.1.7 Clinical Indications for Use of Inhaled Nitric Oxide (iNO) in the Adult Patient Market: Clinical Outcomes after Use, Therapy Demand and Cost of Care

5.1.8  AHA, ACC Change in Requirement for Surgical Support for PCI Performance: Class IIb -> Class III, Level of Evidence A: Support Nonemergent PCI without Surgical Backup (Change of class IIb, Level of evidence B)

5.1.9 Biomaterials Technology: Models of Tissue Engineering for Reperfusion and Implantable Devices for Revascularization

5.1.10 Vascular Repair: Stents and Biologically Active Implants

5.1.11  Regeneration: Cardiac System (cardiomyogenesis) and Vasculature (angiogenesis)

5.1.12 Fight against Atherosclerotic Cardiovascular Disease: A Biologics not a Small Molecule – Recombinant Human lecithin-cholesterol acyltransferase (rhLCAT) attracted AstraZeneca to acquire AlphaCore

5.1.13 Harnessing New Players in Atherosclerosis to Treat Heart Disease

5.2 The Role of Calcium in Health and Disease

5.2.1 Calcium Cycling (ATPase Pump) in Cardiac Gene Therapy: Inhalable Gene Therapy for Pulmonary Arterial Hypertension and Percutaneous Intra-coronary Artery Infusion for Heart Failure: Contributions by Roger J. Hajjar, MD – Part VI

5.2.2 Cardiac Contractility & Myocardium Performance: Ventricular Arrhythmiasand Non-ischemic Heart Failure – Therapeutic Implications for Cardiomyocyte Ryanopathy (Calcium Release-related Contractile Dysfunction) and Catecholamine Responses – Part VII

5.2.3 Calcium-Channel Blockers, Calcium Release-related Contractile Dysfunction (Ryanopathy) and Calcium as Neurotransmitter Sensor – Part IX

5.3 Conduction Dysfunction and ElectroPhysiology of the Heart

5.3.1 Cardiac Resynchronization Therapy (CRT) to Arrhythmias: Pacemaker/Implantable Cardioverter Defibrillator (ICD) Insertion

5.4 Cardiovascular Imaging: Diagnosing the Condition of the Disease and Determining Course of Treatment

5.4.1  3D Cardiovascular Theater – Hybrid Cath Lab/OR Suite, Hybrid Surgery, Complications Post PCI and Repeat Sternotomy

Summary to Volume Two

Epilogue to Volume Two

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Chest Radiation Therapy causes Collateral Damage to the Human Heart

Posted in Aortic Valve: TAVR, TAVI vs Open Heart Surgery, Cancer Surgery of the Heart, Cardiac and Cardiovascular Surgical Procedures on August 28, 2016| Leave a Comment »

Chest Radiation Therapy causes Collateral Damage to the Human Heart

Reporter: Aviva Lev-Ari, PhD, RN

“Radiation therapy for some forms of cancer involves a large dose of radiation to the chest,” says Milind Desai, MD, Director of Cardiovascular Imaging Research at Cleveland Clinic. “The heart can suffer collateral damage as a result.”

Guideposts for identification

The key to identifying true radiation-associated heart disease, says Dr. Desai, is later injury — whether constrictive pericarditis, coronary artery disease, valvular disease or conduction abnormalities. He adds that the prevalence of radiation-associated heart disease is difficult to ascertain, due in part to its considerable latency, although it appears to be increasing.

Risk factors for radiation-associated heart disease include:

  • Total radiation dose > 20-35 Gy
  • Doses > 2 Gy/day
  • Increased volume of heart irradiated
  • Younger age
  • Time since exposure
  • Concomitant cardiotoxic chemotherapy
  • Other cardiovascular risk factors (diabetes mellitus, smoking)
  • Radiation source (cobalt)

SOURCE

https://consultqd.clevelandclinic.org/2016/02/radiation-heart-disease-learnings-diverse-daunting-entity/?utm_campaign=qd+tweets&utm_medium=social&utm_source=twitter&utm_content=160223+radiation+heart+disease+learnings&dynid=twitter-_-qd+tweets-_-social-_-social-_-160223+radiation+heart+disease+learnings

Heart Surgery to a Damaged Heart by Radiation

Patients undergoing cardiothoracic surgery at Cleveland Clinic over a three-year period had a 2.5-fold elevated mortality risk if they had a history of malignancy requiring chest irradiation compared with matched controls who underwent the same surgery but did not have a history of malignancy or chest irradiation. Most of the patients with the cancer history had had either

  • Breast cancer (53 percent) or
  • Hodgkin lymphoma (27 percent).
Long-Term Survival of Patients With Radiation Heart Disease Undergoing Cardiac Surgery

A Cohort Study

Willis Wu, Ahmad Masri, Zoran B. Popovic, Nicholas G. Smedira, Bruce W. Lytle, Thomas H. Marwick, Brian P. Griffin and Milind Y. Desai
http://dx.doi.org/10.1161/CIRCULATIONAHA.113.001435
Published: April 9, 2013

Alternative treatment approaches, including transcatheter aortic valve replacement or other percutaneous interventions, may be more appropriate after identifying risk.

 

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

Cardio-oncology and Onco-Cardiology Programs: Treatments for Cancer Patients with a History of Cardiovascular Disease

Curator: Aviva Lev-Ari, PhD, RN

https://pharmaceuticalintelligence.com/2014/01/08/cardio-oncology-and-onco-cardiology-programs-treatments-for-cancer-patients-with-a-history-of-cardiovascular-disease/

 

Series A: e-Books on Cardiovascular Diseases

Series A Content Consultant: Justin D Pearlman, MD, PhD, FACC

VOLUME THREE

Etiologies of Cardiovascular Diseases:

Epigenetics, Genetics and Genomics

http://www.amazon.com/dp/B018PNHJ84

by  

Larry H Bernstein, MD, FCAP, Senior Editor, Author and Curator

and

Aviva Lev-Ari, PhD, RN, Editor and Curator

https://pharmaceuticalintelligence.com/biomed-e-books/series-a-e-books-on-cardiovascular-diseases/volume-three-etiologies-of-cardiovascular-diseases-epigenetics-genetics-genomics/

 

  • Cardiovascular Diseases, Volume Three: Etiologies of Cardiovascular Diseases: Epigenetics, Genetics and Genomics, on Amazon since 11/29/2015

http://www.amazon.com/dp/B018PNHJ84

onepagecvdseriesaflyervol1-4

 

 

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The presence of any Valvular Heart Disease (VHD) did not influence the comparison of Dabigatran [Pradaxa, Boehringer Ingelheim] with Warfarin

Posted in Aortic Valve: TAVR, TAVI vs Open Heart Surgery, Atherogenic Processes & Pathology, Atrial Fibrilation (a-Fib), Cardiac Pacing and Arrhythmias, Cardiac and Cardiovascular Surgical Procedures, Coagulation Therapy and Internal Bleeding, Electrophysiology, Frontiers in Cardiology and Cardiovascular Disorders, Mitral Valve: Repair and Replacement, Origins of Cardiovascular Disease, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Valves & Tools, tagged , , , , , on August 16, 2016| Leave a Comment »

The presence of any Valvular Heart Disease (VHD) did not influence the comparison of Dabigatran [Pradaxa, Boehringer Ingelheim] with Warfarin

Reporter: Aviva Lev-Ari, PhD, RN

 

UPDATED on 10/22/2018

Dabigatran (Pradaxa) was no better than aspirin for prevention of recurrent stroke among patients with an embolic stroke of undetermined source in the RE-SPECT ESUS trial reported at the World Stroke Congress.

 

Pradaxa® (dabigatran etexilate)
Clinical experience of Pradaxa® equates to over 9 million patient-years in all licensed indications worldwide. Pradaxa® has been in the market for more than ten years and is approved in over 100 countries.15
Currently approved indications for Pradaxa® are:16,17
  • Prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation and a risk factor for stroke
  • Primary prevention of venous thromboembolic events in patients undergoing elective total hip replacement surgery or total knee replacement surgery
  • Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) and the prevention of recurrent DVT and recurrent PE in adults
Dabigatran, a direct thrombin inhibitor (DTI), was the first widely approved drug in a new generation of direct oral anticoagulants, available to target a high unmet medical need in the prevention and treatment of acute and chronic thromboembolic diseases.18,19,20
REFERENCES

16 Pradaxa® US Prescribing Information, 2018.
17 Pradaxa® European Summary of Product Characteristics, 2018.
18 Stangier J. Clinical pharmacokinetics and pharmacodynamics of the oral direct thrombin inhibitor dabigatran etexilate. Clin Pharmacokinet. 2008;47(5):285–95.
19 Di Nisio M. et al. Direct thrombin inhibitors. N Engl J Med.2005;353:1028–40.
20 Stangier J. et al. Pharmacokinetic Profile of the Oral Direct Thrombin Inhibitor Dabigatran Etexilate in Healthy Volunteers and Patients Undergoing Total Hip Replacement. J Clin Pharmacol. 2005;45:555–63

SOURCE

https://www.boehringer-ingelheim.com/press-release/Results-from-two-Pradaxa-trials-to-be-presented-at-WSC

 

 

Event Rate and Outcome Risk, With vs Without Valvular Heart Disease

Outcome Valvular heart disease, event rate/y, % No valvular heart disease, event rate/y, % HR (95% CI)* P
Stroke, systemic embolic event 1.61 1.41 1.09 (0.88–1.33) 0.43
Major bleeding 4.36 2.84 1.32 (1.16–1.33) <0.001
Intracranial hemorrhage 0.51 0.41 1.20 (0.83–1.74) 0.32
All-cause mortality 4.45 3.67 1.09 (0.96–1.23) 0.18
*Adjusted using propensity scores

ORIGINAL RESEARCH ARTICLE

Comparison of Dabigatran versus Warfarin in Patients with Atrial Fibrillation and Valvular Heart Disease: The RE-LY Trial

Michael D. Ezekowitz, Rangadham Nagarakanti, Herbert Noack, Martina Brueckmann, Claire Litherland, Mark Jacobs, Andreas Clemens,Paul A. Reilly, Stuart J. Connolly, Salim Yusuf and Lars Wallentin

 http://dx.doi.org/10.1161/CIRCULATIONAHA.115.020950

 

Results—There were 3950 patients with any VHD:

  • 3101 had mitral regurgitation,
  • 1179 tricuspid regurgitation,
  • 817 aortic regurgitations,
  • 471 aortic stenosis and
  • 193 mild mitral stenosis.

At baseline patients with any VHD had more

  • heart failure,
  • coronary disease,
  • renal impairment and
  • persistent atrial fibrillation.

Patients with any VHD had higher rates of

  • major bleeds (HR 1.32; 95% CI 1.16-1.5)

but similar

  • stroke or systemic embolism (SEE) rates (HR 1.09; 95% CI 0.88-1.33).

For D110 patients, major bleed rates were lower than warfarin (HR 0.73; 95% CI 0.56-0.95 with and HR 0.84; 95% CI 0.71-0.99 without VHD) and

For D150 similar to warfarin in patients with (HR 0.82; 95% CI 0.64-1.06) or without VHD (HR 0.98; 95% CI 0.83-1.15).

For D150 patients stroke/SEE rates were lower versus warfarin with (HR 0.59; 95% CI 0.37-0.93) and without VHD (HR 0.67; 95% CI 0.52-0.86) and similar to warfarin for D110 irrespective of presence of VHD (HR 0.97 CI 0.65-1.45 and 0.85 CI 0.70-1.10).

For intracranial bleeds and death rates for D150 and D110 were lower vs warfarin independent of presence of VHD.

Conclusions—The presence of any VHD did not influence the comparison of dabigatran with warfarin.

Clinical Trial Registration—URL: http://clinicaltrials.gov. Unique Identifier: NCT00262600.

SOURCES

http://circ.ahajournals.org/content/early/2016/08/05/CIRCULATIONAHA.115.020950

http://www.medscape.com/viewarticle/867482?nlid=108872_3866&src=WNL_mdplsfeat_160816_mscpedit_card&uac=93761AJ&spon=2&impID=1179558&faf=1

 

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Clinical Trials for Transcatheter Mitral Valves Annulus Repairs and TAVR: CT Structural Software for Procedural Planning and Anatomical Assessments

Posted in Aortic Valve: TAVR, TAVI vs Open Heart Surgery, Cardiac and Cardiovascular Surgical Procedures, Mitral Valve: Repair and Replacement, tagged , on August 15, 2016| Leave a Comment »

Clinical Trials for Transcatheter Mitral Valves Annulus Repairs and TAVR: CT Structural Software for Procedural Planning and Anatomical Assessments

Reporter: Aviva Lev-Ari, PhD, RN

 

 

VIEW VIDEO

http://www.dicardiology.com/videos/what-look-ct-structural-heart-planning-software/5027704022001?eid=333021707&bid=1497257

 

What to Look for in CT Structural Heart Planning Software

An interview with Jonathan Leipsic, M.D., FSCCT, chairman of the department of radiology, St. Paul’s Hospital, Vancouver, Canada, at the Society of Cardiovascular Computed Tomography (SCCT) 2016 meeting. Leipsic is heavily involved with the procedural planning and anatomical assessments for TAVR and clinical trials for new transcatheter mitral valves and annulus repairs. 

SOURCE

From: Diagnostic and Interventional Cardiology <mail@sgc-ecms.com>

Reply-To: <DoNotReply@sgc-ecms.com>

Date: Monday, August 15, 2016 at 11:20 AM

To: Aviva Lev-Ari <AvivaLev-Ari@alum.berkeley.edu>

Subject: VIDEO: What to Look for in CT Structural Heart Planning Software

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Ralph’s Story: An Entertainer at Heart

Posted in Atrial Fibrilation (a-Fib), Cardiac Pacing and Arrhythmias, CABG, Cardiac and Cardiovascular Surgical Procedures, Cardiovascular and Vascular Systems, Patient Experience, Patient Experience: Personal Memories of Invasive Medical Intervantion, Patient’s Voice: Personal Experience with Invasive Medical Procedures, Uncategorized, tagged , , , , on July 30, 2016| Leave a Comment »

Ralph’s Story: An Entertainer at Heart

Patient was diagnosed with heart disease and pulmonary hypertension in January 2016 and had a triple-bypass operation at age 69. Interview was conducted six months post-surgery.

Author: Gail S. Thornton, M.A.

Co-Editor: The VOICES of Patients, HealthCare Providers, Caregivers and Families: Personal Experience with Critical Care and Invasive Medical Procedures

 

Evergreen, Colorado, an idyllic, peaceful community with an elevation of 8,000 feet west of Denver, offers its residents and visitors a beautiful place for arts and culture, summer and winter sporting activities, and scenic beauty. In fact, Ralph Nichols has lived in the town for more than 20 years.

“This past September [2015] was, particularly, challenging for me, where winter begins quite early for us. It became increasingly painful and difficult to breathe in the freezing temperatures. It seemed that my lungs were inflamed and I couldn’t even stand the cold weather. I thought it might be the beginning of a bad cold, and I wasn’t overly concerned that there was anything terribly wrong.”

At that time, Ralph went to his family physician who performed the usual routine examination with no significant results.

“Many years ago, I developed a mild case of scleroderma, a chronic connective tissue disease. I thought that perhaps my symptoms were the result of some type of inflammation in my body that could be managed with prescription medications.”

Scleroderma is known as an autoimmune disease, which adds an inappropriate amount of collagen to various parts of the body, such as the joints, skin, and later stages, various organs, such as the lungs, in Ralph’s case. Scleroderma can cause the organs to shut down and, eventually, cause death.

“I never let this condition stop me from doing anything as it is life-long condition. It was always something I had to tolerate and work through.”

http://www.scleroderma.org/site/PageNavigator/patients_whatis.html#.V5Zrm84luKo

 

Image SOURCE: Photographs courtesy of Ralph Nichols and Gabriela Contreras.  Top left: Ralph today. Top right: Ralph recovering one month after surgery. Bottom left and center: Ralph with his medical team. Bottom right: Ralph in rehabilitation center.

Over the brutal Colorado winter, Ralph’s symptoms were getting worse. He had no idea that his life would dramatically change over the next few months. He went to see his family physician again. During this physical examination, Ralph was referred to pulmonary and cardiovascular specialists for a routine electrocardiogram, echocardiogram and stress test in order to further diagnose his symptoms. He had always been relatively healthy and fit and never been seriously ill or hospitalized.

“On the outside, Ralph was the picture of good health,” said his wife, Gabriela. “On the inside, his body was telling him that something was wrong.”

Three months later in December 2015, Ralph met with Dr. Alexandra Smart, a pulmonologist, who ordered a chest x-ray and other diagnostic tests, including a right heart catheterization. At that point, Ralph’s medical team grew. It was then determined that Ralph needed to see other cardiovascular specialists and undergo more tests. In January 2016, he met with Dr. Sameer Mehta, cardiologist at Cardiac & Thoracic Surgery Associates, in Lakewood, Colorado, who reviewed his tests to date, listened to Ralph’s symptoms, and told him he needed both a right and left heart cardiac catheterization.

 “They gave me sedation for the catheterization procedure and went through my neck with a camera to see what was going on with my lungs and heart. We were all singing together on the way to the operating room. During the procedure, my cardiologist found more than he had anticipated.”

The result was not good. Ralph had major blockages in two main arteries that supply blood to his heart muscle compounded by the fact that his lungs were affected by scleroderma.

“The catheterization was alarming. It showed that my arteries were in bad shape. They were both clogged with atherosclerotic plaque; one of them was 99 percent blocked and the other was 85 percent blocked.”

His cardiologist believed that the blockages would not respond to medications quickly or a stent.

“Even though my father had major heart disease and died two years later of cancer at the age of 56, I thought that I would be immune to this particular experience. After all, I was in good health, exercised regularly, lived a reasonable lifestyle and had a great diet.”

 Preparing for Life-Saving and Life-Changing Surgery

Unfortunately, surgery was the next step. Ralph was referred to Dr. Mehta’s colleague, Dr. Patrick D. Rudersdorf, cardiothoracic surgeon at Cardiac & Thoracic Surgery Associates.

“I didn’t leave the hospital that day as expected. Instead, I got a visit from Dr. Rudersdorf and couldn’t believe what he was telling me. My only chance to live was having triple bypass surgery which needed to be done immediately. The doctor met with me that same day to explain the procedure, answer my questions and talk through the details of the rehabilitation period after the surgery.”

Dr. Rudersdorf reassured Ralph that he was doing the right thing and calmed my fears.

“He said that I needed this life-saving surgery because I was at high risk for having a major heart attack. I was shocked, at first, at the thought of the intensity of surgery on my body. It’s a situation that no one likes to be in, but I had to make a decision about alleviating the ongoing pain and pressure in my chest along with shortness of breath due to diseased heart arteries. Coronary bypass surgery was my answer to feeling better — and it essentially gave me my life back.”

Dr. Rudersdorf moved his previously planned morning surgery to another day to accommodate me first thing in the morning. Ralph underwent triple bypass surgery at St. Anthony Hospital in Lakewood, Colorado. The procedure was complex and took eight hours. He was in the hospital for a total of 31 days.

“It was an ordeal that I thought I’d never have to experience. I had no time to call anyone, or time to even contemplate life and death…or even being scared.  My wife Gabriela spent the entire time in the hospital, supported by our dearest friends, Norma Delaney and Garret Annofsky, in addition to keeping family and friends in other parts of the United States and Mexico updated as well. Once the surgery was over, the medical team woke me up and said the procedure was successful, but I was far from being out of the woods.”

Ralph had some complications because of a condition called pulmonary hypertension, a type of high blood pressure that affects the arteries in the lungs and the right side of the heart. According to the Mayo Clinic’s web site, in one form of pulmonary hypertension, tiny arteries in the lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through the lungs, and raises pressure within the lungs’ arteries. As the pressure builds, the heart’s lower right chamber (right ventricle) must work harder to pump blood through the lungs, eventually causing the heart muscle to weaken and fail. http://www.mayoclinic.org/diseases-conditions/pulmonary-hypertension/home/ovc-20197480

“The pulmonary hypertension limited some of the medications that the doctors would have used during my recovery. It was a tough few days for me in intensive care, hooked up to about 18 monitors. The medical team had to stop and re-start my heart four different times because of atrial fibrillation — finally getting both parts of the heart to dance together in the same rhythm.”

Ralph’s heart was beating abnormally fast and irregular and not functioning the way it should. The doctors restore regular rhythm to the heart by sending an electrical shock to the heart, which is called electrical cardioversion or chemically using antiarrhythmia medications, which is called pharmacologic or chemical cardioversion.

“The doctors shocked my heart first chemically with medications when I was awake. This procedure was the scariest. I was sitting up in bed and felt my heart stop, then the medical team flushed the medication out with saline in order to restart my heart. That procedure was not successful, so that is why the doctors had to shock my heart three more times electrically.

“The reason the doctors stopped my heart was to correct the atrial fibrillation and to get my heart into regular sinus rhythm, which is a wave mode of the heart where everything is synchronized. The doctors did not want me to continue to experience atrial fibrillation because if continued, I would not be able to regain my strength.”

Ralph was finally moved from intensive care to intermediate care after five days and the medical team kept him in intermediate care another 12 days until his heart and lungs got stronger.

“From there, I didn’t go home but instead went to Evergreen Life Center for rehabilitation for two weeks to learn how to walk, climb stairs so that I could access my home on my own, and develop my strength again. The rehab team would let me leave only after making sure I had oxygen in my home.”

After that, Ralph started another phase of his rehabilitation at St. Anthony Cardiac Rehabilitation and Wellness Center. For the next three months, he took part in cardiac rehabilitation three days a week. He passed that with flying colors. Now, he is in another phase of rehabilitation, building his lung capacity two days a week.

Ralph didn’t have the means or even the will to communicate with friends during this tumultuous time, except Gabriela and several close friends who were always at the hospital and rehabilitation center who gave him the strength to continue.

“I finally returned home after many weeks with an enormous feeling of gratitude for each and every one of my friends, as well as the St. Anthony’s hospital team of doctors, nurses, and therapists, who supported me and Gabriela during this exceptional adventure that has certainly changed my life.”

Surely, this experience has been a life-changing experience for Ralph.

 Coronary Artery Bypass Facts

 Coronary artery bypass grafting (CABG, often pronounced “cabbage”) is a surgical treatment for blocked coronary arteries. Coronary arteries supply blood to the heart muscle and when blockages in these arteries form, chest pain, shortness of breath and heart attacks can occur. Catheter procedures performed by interventional cardiologists address the blockages themselves with stents. Coronary bypass surgery performed by cardiac surgeons reroutes the blood around the blockages to supply better blood supply to the heart muscle and is a better treatment option, although more invasive, for certain patients and more durable for most patients.

http://ctsurgery.com/conditions-procedures/heart-aorta/cardiac-surgery/coronary-artery-bypass-grafting-cabg/

Life for Ralph Today

Today, Ralph is regaining his strength both in mind and body. He visits the cardiovascular and pulmonary rehabilitation center three times a week for the past few months and walks on their treadmill, lifts weights and pedals the bicycle for one hour, supervised by the therapists. He also sees his medical team for regular check-ups every month, eats healthier with no fat and no salt, and takes a cocktail of medicines daily for his heart and lungs, including amiodarone, furosemide, pitavastatin, and aspirin.

“Almost six months after my surgery, although I am not in the best shape of my life, however, I am in the best spiritual place than ever before. This is a huge milestone for me. I continue to improve my strength, which will make my heart more resilient. There is nothing that I can’t do now, and I am doing everything I can to experience a normal life as far as work and regaining my strength. I find it necessary to move to a warmer climate and lower altitude in order to continue to improve.”

Ralph also is the former lead singer of The Letterman and The Sandpipers, two American easy-listening bands during the 1960-70-80s. He is an entertainer at heart with over 3,000 professional appearances to his credit. He has been performing and recording for over 50 years, traveled the world extensively and performed before members of the Vatican with Pope Pius XII and Royalty with Prince Rainier and Princess Grace Kelly, as well as notables such as Frank and Nancy Sinatra, Tony Bennett, Ronald Reagan, Merv Griffin, Danny Thomas, Shirley Bassey, Rosalind Russell and Bob Hope.

Ralph and his vocal group were dubbed by Billboard Magazine as “the greatest romantic vocal group of all time.” He is also a member of the Vocal Group Hall of Fame, a prestigious honor. He is a true legend as his group has sold more than 20 million recordings, performed live thousands of times, and whose recording of the song “Love” was left by NASA astronauts in a time capsule on the moon.

“I enjoy each and every day and appreciate all that life has to offer.”

Ralph’s next step is to get back to singing and his solo entertainment business, which he holds dear to his heart. That should be a task that he can easily accomplish.

 

Editor’s note:

We would like to thank Gabriela Contreras, a global communications consultant and patient advocate, for the tremendous help and support that she provided in scheduling time to talk with Ralph Nichols.

Ralph Nichols provided his permission to publish this interview on July 30, 2016.

 

REFERENCES/SOURCES

http://www.scleroderma.org/site/PageNavigator/patients_whatis.html#.V5Zrm84luKo

http://www.mayoclinic.org/diseases-conditions/pulmonary-hypertension/home/ovc-20197480

http://ctsurgery.com/conditions-procedures/heart-aorta/cardiac-surgery/coronary-artery-bypass-grafting-cabg/

 

Other related articles:

Retrieved from http://www.sunset.com/travel/rockies/evergreen-colorado-day-trip-travel-planner

Retrieved from http://www.secondscount.org/heart-condition-centers/info-detail-2/benefits-risks-of-coronary-bypass-surgery-2#.V5dkK_krKUk

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

2016

People with blood type O have been reported to be protected from coronary heart disease, cancer, and have lower cholesterol levels.

https://pharmaceuticalintelligence.com/2016/01/11/people-with-blood-type-o-have-been-reported-to-be-protected-from-coronary-heart-disease-cancer-and-have-lower-cholesterol-levels/

2015

A Patient’s Perspective: On Open Heart Surgery from Diagnosis and Intervention to Recovery

https://pharmaceuticalintelligence.com/2015/05/10/a-patients-perspective-on-open-heart-surgery-from-diagnosis-and-intervention-to-recovery/

No evidence to change current transfusion practices for adults undergoing complex cardiac surgery: RECESS evaluated 1,098 cardiac surgery patients received red blood cell units stored for short or long periods

https://pharmaceuticalintelligence.com/2015/04/08/no-evidence-to-change-current-transfusion-practices-for-adults-undergoing-complex-cardiac-surgery-recess-evaluated-1098-cardiac-surgery-patients-received-red-blood-cell-units-stored-for-short-or-lon/

2013

ACC/AHA Guidelines for Coronary Artery Bypass Graft Surgery

https://pharmaceuticalintelligence.com/2013/11/05/accaha-guidelines-for-coronary-artery-bypass-graft-surgery/

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

https://pharmaceuticalintelligence.com/2013/05/07/on-devices-and-on-algorithms-arrhythmia-after-cardiac-surgery-prediction-and-ecg-prediction-of-paroxysmal-atrial-fibrillation-onset/

 

Editor’s note:

I wish to encourage the e-Reader of this Interview to consider reading and comparing the experiences of other Open Heart Surgery Patients, voicing their private-life episodes in the ER that are included in this volume.

I also wish to encourage the e-Reader to consider, if interested, reviewing additional e-Books on Cardiovascular Diseases from the same Publisher, Leaders in Pharmaceutical Business Intelligence (LPBI) Group, on Amazon.com.

  •  Perspectives on Nitric Oxide in Disease Mechanisms, on Amazon since 6/2/12013

http://www.amazon.com/dp/B00DINFFYC

  • Cardiovascular, Volume Two: Cardiovascular Original Research: Cases in Methodology Design for Content Co-Curation, on Amazon since 11/30/2015

http://www.amazon.com/dp/B018Q5MCN8

  • Cardiovascular Diseases, Volume Three: Etiologies of Cardiovascular Diseases: Epigenetics, Genetics and Genomics, on Amazon since 11/29/2015

http://www.amazon.com/dp/B018PNHJ84

  • Cardiovascular Diseases, Volume Four: Regenerative and Translational Medicine: The Therapeutics Promise for Cardiovascular Diseases, on Amazon since 12/26/2015

http://www.amazon.com/dp/B019UM909A

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Thriving Three Groups on LinkedIn

Posted in 3D Printing for Medical Application, BioIT: BioInformatics, NGS, Clinical & Translational, Pharmaceutical R&D Informatics, Clinical Genomics, Cancer Informatics, BioTechnology - Venture Creation, Venture Capital, CANCER BIOLOGY & Innovations in Cancer Therapy, Cardiac and Cardiovascular Surgical Procedures, Cardiovascular Research, Computational Biology/Systems and Bioinformatics, CRISPR/Cas9 & Gene Editing, DNA repair, Drug Delivery Platform Technology, Epigenetics and Environmental Factors, FDA Regulatory Affairs, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Testing: Methodology for Diagnosis, Global Partnering & Biotech Investment, Health Law & Patient Safety, HealthCare IT, Human Immune System in Health and in Disease, Immuno-Oncology & Genomics, Immunodiagnostics, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, International Global Work in Pharmaceutical, Interventional Oncology: Radiofrequency Ablation, Transarterial Chemoembolization, Microwave Ablation and Irreversible Electroporation (IRE), Interviews with Scientific Leaders, Investment in Technological Breakthrough, Medical Devices R&D and Inventions, Origins of Cardiovascular Disease, Pharmacotherapy of Cardiovascular Disease on July 20, 2016| Leave a Comment »

Thriving Three Groups on LinkedIn

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #206: Thriving Three Groups on LinkedIn. Published on 7/20/2016

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Groups Launcher and Group Manager: Aviva Lev-Ari, PhD, RN

Cardiovascular Biotech & Pharma UK & US Networking Group

954 members

https://www.linkedin.com/groups/4357927

Leaders in Pharmaceutical Business Intelligence

350 members

https://www.linkedin.com/groups/4346921

Innovation in Israel

205 members

https://www.linkedin.com/groups/2987122

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Lysyl Oxidase (LOX) gene missense mutation causes Thoracic Aortic Aneurysm and Dissection (TAAD) in Humans because of inadequate cross-linking of collagen and elastin in the aortic wall

Posted in Abdominal Aorta, Aortic Valve: TAVR, TAVI vs Open Heart Surgery, Cardiac and Cardiovascular Surgical Procedures, Computational Biology/Systems and Bioinformatics, Congenital Heart Disease, CRISPR/Cas9 & Gene Editing, Frontiers in Cardiology and Cardiovascular Disorders, Genetic Mutations in Congenital Heart Disease, Genome Biology, Pre-Clinical Animal Model Development, Thoracic Aorta, Vascular Diseases, tagged , , on July 19, 2016| Leave a Comment »

Lysyl Oxidase (LOX) gene missense mutation causes Thoracic Aortic Aneurysm and Dissection (TAAD) in Humans because of inadequate cross-linking of collagen and elastin in the aortic wall

Mutation carriers may be predisposed to vascular diseases because of weakened vessel walls under stress conditions.

Reporter: Aviva Lev-Ari, PhD, RN

2.1.3.7

2.1.3.7   Lysyl Oxidase (LOX) gene missense mutation causes Thoracic Aortic Aneurysm and Dissection (TAAD) in Humans because of inadequate cross-linking of collagen and elastin in the aortic wall – Mutation carriers may be predisposed to vascular diseases because of weakened vessel walls under stress conditions, Volume 2 (Volume Two: Latest in Genomics Methodologies for Therapeutics: Gene Editing, NGS and BioInformatics, Simulations and the Genome Ontology), Part 2: CRISPR for Gene Editing and DNA Repair

Loss of function mutation in LOX causes thoracic aortic aneurysm and dissection in humans

  1. Vivian S. Leea,
  2. Carmen M. Halabia,b,
  3. Erin P. Hoffmanc,1,
  4. Nikkola Carmichaelc,d,
  5. Ignaty Leshchinerc,d,
  6. Christine G. Liand,e,
  7. Andrew J. Bierhalsf,
  8. Dana Vuzmanc,d,
  9. Brigham Genomic Medicine2,
  10. Robert P. Mechama,
  11. Natasha Y. Frankc,d,g,3, and
  12. Nathan O. Stitzielh,i,j,3

Author Affiliations

  1. aDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110;

  2. bDivision of Nephrology, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110;

  3. cDepartment of Medicine, Division of Genetics, Brigham and Women’s Hospital, Boston, MA 02115;

  4. dHarvard Medical School, Boston, MA 02115;

  5. eDepartment of Pathology, Brigham and Women’s Hospital, Boston, MA 02115;

  6. fMallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110;

  7. gVA Boston Healthcare System, Boston, MA 02132;

  8. hCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110;

  9. iDepartment of Genetics, Washington University School of Medicine, St. Louis, MO 63110;

  10. jMcDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63110

Edited by J. G. Seidman, Harvard Medical School, Boston, MA, and approved June 7, 2016 (received for review January 27, 2016)

  • Author contributions: V.S.L., R.P.M., N.Y.F., and N.O.S. designed research; V.S.L., C.M.H., and N.O.S. performed research; E.P.H., N.C., C.G.L., D.V., B.G.M.P., R.P.M., and N.Y.F. contributed new reagents/analytic tools; V.S.L., C.M.

Significance

The mechanical integrity of the arterial wall is dependent on a properly structured ECM. Elastin and collagen are key structural components of the ECM, contributing to the stability and elasticity of normal arteries. Lysyl oxidase (LOX) normally cross-links collagen and elastin molecules in the process of forming proper collagen fibers and elastic lamellae. Here, using whole-genome sequencing in humans and genome engineering in mice, we show that a missense mutation in LOX causes aortic aneurysm and dissection because of insufficient elastin and collagen cross-linking in the aortic wall. These findings confirm mutations in LOX as a cause of aortic disease in humans and identify LOX as a diagnostic and potentially therapeutic target.

Abstract

Thoracic aortic aneurysms and dissections (TAAD) represent a substantial cause of morbidity and mortality worldwide. Many individuals presenting with an inherited form of TAAD do not have causal mutations in the set of genes known to underlie disease. Using whole-genome sequencing in two first cousins with TAAD, we identified a missense mutation in the lysyl oxidase (LOX) gene (c.893T > G encoding p.Met298Arg) that cosegregated with disease in the family. Using clustered regularly interspaced short palindromic repeats (CRISPR)/clustered regularly interspaced short palindromic repeats-associated protein-9 nuclease (Cas9) genome engineering tools, we introduced the human mutation into the homologous position in the mouse genome, creating mice that were heterozygous and homozygous for the human allele. Mutant mice that were heterozygous for the human allele displayed disorganized ultrastructural properties of the aortic wall characterized by fragmented elastic lamellae, whereas mice homozygous for the human allele died shortly after parturition from ascending aortic aneurysm and spontaneous hemorrhage. These data suggest that a missense mutation in LOX is associated with aortic disease in humans, likely through insufficient cross-linking of elastin and collagen in the aortic wall. Mutation carriers may be predisposed to vascular diseases because of weakened vessel walls under stress conditions. LOX sequencing for clinical TAAD may identify additional mutation carriers in the future. Additional studies using our mouse model of LOX-associated TAAD have the potential to clarify the mechanism of disease and identify novel therapeutics specific to this genetic cause.

SOURCE

http://www.pnas.org/content/early/2016/07/15/1601442113.abstract

Missense LOX Mutation Linked to Aortic Rupture, Aneurysm

Jul 19, 2016

|

a GenomeWeb staff reporter

NEW YORK (GenomeWeb) – Researchers from Washington University School of Medicine have linked a LOX gene variant with aortic rupture and aneurysm.

As they reported in the online early edition of the Proceedings of the National Academy of Sciences yesterday, the researchers sequenced two first cousins from a family with a history of aortic ruptures and aneurysms to uncover a missense mutation in the lysyl oxidase (LOX) gene, which encodes a protein that cross-links elastin and collagen. When they used CRISPR/Cas9 genome engineering to introduce the mutation into a mouse model, mice heterogeneous for the mutation had disorganized aortic walls, while mice homozygous for the mutation died shortly after birth of ascending aneurysm and spontaneous hemorrhage, suggesting that the LOX variant might be causal.

Read more @ the Source

SOURCE

https://www.genomeweb.com/sequencing/missense-lox-mutation-linked-aortic-rupture-aneurysm

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SAPIEN 3 Transcatheter Aortic Valve Replacement in High-Risk and Inoperable Patients with Severe Aortic Stenosis: One-Year Clinical Outcomes

Posted in Aortic Valve: TAVR, TAVI vs Open Heart Surgery, Cardiac and Cardiovascular Surgical Procedures, Frontiers in Cardiology and Cardiovascular Disorders, Heart Failure (HF), Medical Devices R&D and Inventions, Valves & Tools on July 14, 2016| Leave a Comment »

SAPIEN 3 Transcatheter Aortic Valve Replacement in High-Risk and Inoperable Patients with Severe Aortic Stenosis: One-Year Clinical Outcomes

Reporter: Aviva Lev-Ari, PhD, RN

Circulation

July 12, 2016, Volume 134, Issue 2

 

 

The registry study — the preliminary results of which were presented at the Transcatheter Cardiovascular Therapeutics meeting in 2015 — included 583 high-risk (65%) or inoperable patients (35%) who got TAVR with the Sapien 3 device between 2013 and 2014. Procedures were performed via the transfemoral (84%) or transapical/transaortic routes (16%).

On multivariable adjustment, the predictors of 1-year mortality were

  • alternative access (hazard ratio [HR] 2.06, 95% CI 1.26-3.36),
  • moderate paravalvular leak (HR 3.75, 95% CI 1.57-8.96), and
  • disabling stroke (HR 10.33, 95% CI 4.62-233.09).

“Even with the low rate of moderate paravalvular leak rate, they found an association with 1 year mortality,” commented Kappetein. “Moderate paravalvular leak is bad for a patient!”

Within 30 days, overall stroke and disabling stroke occurred at frequencies of 1.4% and 0.9%, respectively. Between 1 month and 1 year, these rates were 4.3% and 2.4%.

Généreux appeared to be at ease with the 1-year stroke rate, adding that “this reflects it being a high-risk population.”

In order to bring mortality and stroke rates even lower, he suggested that clinicians “focus on other strategies such as anticoagulation and other medical or device therapies like left atrial appendage closure.”

Nearly all patients improved enough to move out of New York Heart Association class three and four after the procedure (90.1% at baseline versus 7.7% at 1 year, P<0.0001). Self-reported quality of life similarly improved on the Kansas City Cardiomyopathy Questionnaire, with average scores rising from 46.9 to 72.4 at 1 year (P<0.0001).

“A high-risk population is difficult because patients may have mortality related to a comorbidity such as infection and heart failure. That being said, there is still room for improvement in the care of patients beyond the device choice,” Généreux said, suggesting that appropriate anticoagulation is key.

For now, “the combination of new design features of Sapien 3, procedural improvements, operator experience and improved patient selection have all contributed to a low rate of important adverse events (including stroke) and a high rate of 1-year survival in high-risk and inoperable patients with severe aortic stenosis,” Herrmann and colleagues concluded.

SOURCE

One-Year Clinical Outcomes With SAPIEN 3 Transcatheter Aortic Valve Replacement in High-Risk and Inoperable Patients With Severe Aortic Stenosis

Howard C. Herrmann, Vinod H. Thourani, Susheel K. Kodali, Raj R. Makkar, Wilson Y. Szeto, Saif Anwaruddin, Nimesh Desai, Scott Lim, S. Chris Malaisrie, Dean J. Kereiakes, Steven Ramee, Kevin L. Greason, Samir Kapadia, Vasilis Babaliaros, Rebecca T. Hahn, Philippe Pibarot,Neil J. Weissman, Jonathon Leipsic, Brian K. Whisenant, John G. Webb, Michael J. Mack and Martin B. Leon and For the PARTNER Investigators
Download PDF
http://dx.doi.org/10.1161/CIRCULATIONAHA.116.022797
Published: July 12, 2016

Abstract

Background: In the initial PARTNER trial (Placement of Aortic Transcatheter Valves) of transcatheter aortic valve replacement for high-risk (HR) and inoperable patients, mortality at 1 year was 24% in HR and 31% in inoperable patients. A recent report of the 30-day outcomes with the low-profile SAPIEN 3 transcatheter aortic valve replacement system demonstrated very low rates of adverse events, but little is known about the longer-term outcomes with this device.

Methods: Between October 2013 and September 2014, 583 HR (65%) or inoperable (35%) patients were treated via the transfemoral (84%) or transapical/transaortic (16%) access route at 29 US sites. Major clinical events at 1 year were adjudicated by an independent clinical events committee, and echocardiographic results were analyzed by a core laboratory.

Results: Baseline characteristics included age of 83 years, 42% female, and median Society of Thoracic Surgeons score of 8.4%. At the 1-year follow-up, survival (all-cause) was 85.6% for all patients, 87.3% in the HR subgroup, and 82.3% in the inoperable subgroup. Survival free of all-cause and cardiovascular mortality in the transfemoral patients from the HR cohort was 87.7% and 93.3%, respectively. There was no severe paravalvular leak. Moderate paravalvular leak (2.7%) was associated with an increase in mortality at 1 year, whereas mild paravalvular leak had no significant association with mortality. Symptomatic improvement as assessed by the percentage of patients in New York Heart Association class III and IV (90.1% to 7.7% at 1 year; P<0.0001) and by Kansas City Cardiomyopathy Questionnaire overall summary score (improved from 46.9 to 72.4;P<0.0001) was marked. Multivariable predictors of 1-year mortality included alternative access, Society of Thoracic Surgeons score, and disabling stroke.

Conclusions: In this large, adjudicated registry of SAPIEN 3 HR and inoperable patients, the very low rates of important complications resulted in a strikingly low mortality rate at 1 year. Between 30 and 365 days, the incidence of moderate paravalvular aortic regurgitation did not increase, and no association between mild paravalvular leak and 1-year mortality was observed, although a small increase in disabling stroke occurred. These results, which likely reflect device iteration and procedural evolution, support the use of transcatheter aortic valve replacement as the preferred therapy in HR and inoperable patients with aortic stenosis.

Clinical Trial Registration : URL: http://www.clinicaltrials.gov. Unique identifier:NCT01314313.

SOURCE

http://circ.ahajournals.org/content/134/2/130.full

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