Jonathan Weinstock

Cardiovascular Toxicities of Performance-Enhancing Substances in Sports

Athletes commonly use drugs and dietary supplements to improve athletic performance or to assist with weight loss. Some of these substances are obtainable by prescription or by illegal means; others are marketed as supplements, vitamins, or minerals. Nutritional supplements are protected from Food and Drug Administration regulation by the 1994 US Dietary Supplement Health and Education Act, and manufacturers are not required to demonstrate proof of efficacy or safety. Furthermore, the Food and Drug Administration lacks a regulatory body to evaluate such products for purity. Existing scientific data, which consist of case reports and clinical observations, describe serious cardiovascular adverse effects from use of performance-enhancing substances, including sudden death. Although mounting evidence led to the recent ban of ephedra (ma huang), other performance-enhancing substances continue to be used frequently at all levels, from elementary school children to professional athletes. Thus, although the potential for cardiovascular injury is great, few appropriately designed studies have been conducted to assess the benefits and risks of using performance-enhancing substances. We performed an exhaustive OVID MEDLINE search to Identify all existing scientific data, review articles, case reports, and clinical observations that address this subject. In this review, we examine the current evidence regarding cardiovascular risk for persons using anabolic-androgenic steroids including 2 synthetic substances, tetrahydrogestrinone and androstenedione (andro), stimulants such as ephedra, and nonsteroidal agents such as recombinant human erythropoietin, human growth hormone, creatine, and beta-hydroxy-beta-methylbutyrate.

Failure of Commercially Available Chest Wall Protectors to Prevent Sudden Cardiac Death Induced by Chest Wall Blows in an Experimental Model of Commotio Cordis

OBJECTIVE. Sudden cardiac death that results from chest wall blows (commotio cordis) the second leading cause of death in young athletes. Most events are caused by blows from projectiles, such as baseballs or lacrosse balls, with a substantial proportion occurring despite the use of a chest protector. In the present experiment, we tested the effectiveness of commercially available chest protectors in preventing ventricular fibrillation (VF) that results from chest wall strikes with baseballs and lacrosse balls. METHODS. Twelve different baseball or lacrosse chest protectors were evaluated in juvenile swines that were subjected to 40-mph baseball or lacrosse ball blows to the precordium during the vulnerable period of repolarization for VF and were compared with control impacts without chest protectors. Seven baseball chest protectors were hit by regulation baseballs, and 5 lacrosse chest protectors were tested by blows with standard lacrosse balls. Each animal received 2 chest blows for each protector and 2 control impacts without a chest protector, with the sequence of impacts assigned randomly. RESULTS. VF was elicited by 12 (32%) of 37 strikes in control animals without baseball chest protectors. None of the baseball chest wall protectors tested were shown to decrease significantly the occurrence of VF when compared with controls. VF was elicited by 11 (46%) of 24 strikes in control animals without lacrosse chest protectors. None of the lacrosse chest wall protectors tested decreased significantly the occurrence of VF when compared with controls. CONCLUSION. In our experimental animal model of commotio cordis, commercially available baseball and lacrosse chest wall protectors were ineffective in protecting against VF that was triggered by chest blows and, by inference, sudden cardiac death. Improvements in materials and design of chest wall barriers are necessary to reduce the occurrence of these tragic events and make the athletic field safer for youths.

Use of antiarrhythmics and implantable cardioverter-defibrillators in congestive heart failure.

As much as half of the mortality in patients with congestive heart failure (CHF) resulting from left ventricular systolic dysfunction is attributable to sudden cardiac death. Thus, the identification of risk and prevention of sudden death are important components of treating this population of patients. Antiarrhythmic drugs have been shown to be either neutral or harmful when studied in patients with prior myocardial infarction and impaired left ventricular function. Amiodarone, when studied in patients with CHF, may be of benefit. This benefit may be more pronounced in patients with nonischemic cardiomyopathy. Implantable cardioverter defibrillators (ICDs) are of clear benefit when used in the primary and secondary prevention of sudden death in selected populations. Studies soon to be completed should clarify the role of the cardioverter-defibrillator in patients with CHF. Antiarrhythmic medications are often used in conjunction with ICDs for a variety of reasons. However, these drugs have the potential to adversely affect defibrillator function, and knowledge of these effects is important when using this strategy.

Clinical results with catheter ablation: AV junction, atrial fibrillation and ventricular tachycardia.

With the limitations of pharmacologic and device therapies for atrial fibrillation and ventricular tachycardia, catheter ablation is assuming a larger role in the management of patients with these common arrhythmias. Multiple case series and clinical trials have helped to define the evolving role of these techniques for ablation of the atrioventricular node, atrial fibrillation, and ischemic ventricular tachycardia. Based on very low complication rates, excellent efficacy and proven outcomes with radiofrequency ablation of the atrioventricular node, this approach with permanent pacing should play a larger role in the treatment of symptomatic patients with permanent atrial fibrillation. While linear ablation of atrial fibrillation has limited clinical utility for the treatment of this common arrhythmia, the results of multiple case series of focal atrial fibrillation ablation indicate the potential for an expanding role of this curative technique. Catheter ablation techniques for ventricular tachycardia in the setting of coronary artery disease have a role as supplemental therapy to the implantable cardioverter defibrillator in patients with recurrent pharmacologically refractory ventricular arrhythmias requiring frequent device interventions.

Subcutaneous Implantable Cardioverter Defibrillator in Patients With Hypertrophic Cardiomyopathy: An Initial Experience

Background The subcutaneous implantable cardioverter defibrillator (S‐ICD) has been developed to avert risks associated with transvenous defibrillator leads. The technology is attractive for younger patients, such as those with hypertrophic cardiomyopathy (HCM). However, there are limited data on S‐ICD use in HCM. Methods and Results HCM patients identified at risk for sudden death were considered for S‐ICD implantation. Patients were screened for potential oversensing by surface electrocardiography (ECG). At implant, defibrillation threshold (DFT) testing was performed at 65, 50, and 35 joules (J). Twenty‐seven patients were considered for S‐ICD implantation, and after screening, 23 (85%) remained eligible. The presence of a bundle branch block was associated with screening failure, whereas elevated body mass index (BMI) showed a trend toward association. One patient passed screening at rest, but failed with an ECG obtained after exercise. At implant, the S‐ICD terminated ventricular fibrillation (VF) with a 65J shock in all 15 implanted patients and a 50J shock was successful in 12 of 15. A 35J shock terminated VF in 10 of 12 patients. DFT failure at 50 J was associated with a higher BMI. There were no appropriate shocks after a median follow‐up of 17.5 (3–35) months, and 1 patient received an inappropriate shock attributable to a temporary reduction in QRS amplitude while bending forward, resulting in oversensing, despite successful screening. Conclusions In a high‐risk HCM cohort without a pacing indication referred for consideration of an ICD, the majority were eligible for S‐ICD. The S‐ICD is effective at recognizing and terminating VF at implant with a wide safety margin.

Short QT syndrome review

The short QT syndrome (SQTS) was recently recognized as a familial clinical-electrocardiographic entity characterized by ion channel mutations, leading to sudden cardiac death, short refractory periods, and inducible ventricular fibrillation. The genetic inheritance pattern is autosomal dominant with positive family history of sudden cardiac death. To date, three principal genetic mutations in potassium channels have been linked to short QT syndrome. The electrocardiogram (ECG) is characterized by a short QT interval of typically less than 320 ms with tall peaked, narrow symmetrical T waves. Short refractory periods lead to a propensity to develop atrial or ventricular fibrillation at electrophysiology study. The following review addresses the genetics, pathophysiology, clinical presentation, and treatment of short QT syndrome.

Advances in Sudden Death Prevention: The Emerging Role of a Fully Subcutaneous Defibrillator

Randomized clinical trials support the use of implantable defibrillators for mortality reduction in specific populations at high risk for sudden cardiac death. Conventional transvenous defibrillator systems are limited by implantation-associated complications, infection, and lead failure, which may lead to delivery of inappropriate shocks and diminish survival. The development of a fully subcutaneous defibrillator may represent a valuable addition to therapies targeted at sudden death prevention. The PubMed database was searched to identify all clinical reports of the subcutaneous defibrillator from 2000 to the present. We reviewed all case series, cohort analyses, and randomized trials evaluating the safety and efficacy of subcutaneous defibrillators. The subcutaneous defibrillator is a feasible development in sudden cardiac death therapy and may be useful particularly to extend defibrillator therapy to patients with complicated anatomy, limited vascular access, and congenital disease. The subcutaneous defibrillator should not be considered in patients with an indication for cardiac pacing or who have ventricular tachycardia responsive to antitachycardia pacing. Further investigation is needed to compare long-term, head-to-head performance of subcutaneous defibrillators and conventional transvenous defibrillator systems.

Advances in mechanisms of atrial fibrillation: structural remodeling, high-frequency fractionated electrograms, and reentrant AF drivers.

The mechanisms to explain atrial fibrillation (AF) have been widely debated. Although contemporary experimental techniques have provided more insight, hypotheses regarding AF propagation conceived in the early half of the century remain minimally altered and relevant today. Modern mapping technologies have implicated multiwavelet reentry as the electrophysiologic basis to explain AF propagation within the atrial myocardium; however, reentry has also been observed within pulmonary veins and may behave as a focal trigger. The ability to terminate AF by catheter ablation has provided additional clues to explain AF induction and sustenance. The presence of complex fractionated electrograms (CFAE) and subsequent successful CFAE-directed ablation suggest that diseased atrial myocardium is a necessary substrate for AF maintenance. Atrial remodeling creates differential areas of refractory periods and conduction velocity, which, in turn, creates a suitable environment for AF. This review addresses the complex relationship between remodeled atrial myocardium and reentry and explores the role of CFAEs in AF maintenance.

The Heart of an Athlete: Black, White, and Shades of Grey with No Gold Standard

The heart of the athlete has intrigued cardiologists since the original description of increased cardiac dimensions in elite Nordic skiers more than a century ago.1 Athletes exhibit structural and electric cardiac abnormalities that mimic findings associated with cardiovascular disease.2 Some early observers regarded the heart of a conditioned athlete as weakened by strenuous training and thereby subject to progressive deterioration in function.3 Structural findings include chamber enlargement and ventricular hypertrophy.2,3 Electric abnormalities include increased QRS voltage, abnormal Q waves, and T-wave inversions.2,3 Currently, the athlete’s heart is regarded as a benign increase in cardiac mass with circulatory and morphological alterations in response to athletic training.2,3 Contemporary evidence supports the notion that this represents adaptive physiology, not preclinical disease.2,3 Despite considerable advances in diagnostic tests, significant challenges remain in differentiating the athlete’s heart from some types of cardiac disease.2–4 ECG and morphological changes found in athletes can mimic findings of hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC), and other cardiovascular diseases.2–4 The absence of a definitive diagnostic test or gold standard for many cardiovascular commonly results in diagnostic uncertainty.2–4 Article see p 1783 This overlap of normal and abnormal findings has represented a clinical challenge because diagnostic criteria lacked sufficient sensitivity and specificity to reliably distinguish physiological enlargement of the athlete’s RV from ARVC.5 The importance of this distinction is underscored by the fact that in the United States, ARVC is responsible for 4% of cases of athletic sudden deaths.2 Sudden deaths are attributed to ARVC in 22% of athletes in the Veneto region of Italy.2 Because of the recognized shortcomings of the 1994 International Task Force Criteria for the diagnosis …

Ventricular Tachyarrhythmias in Patients With Hypertrophic Cardiomyopathy and Defibrillators: Triggers, Treatment, and Implications

Triggers and ICD interventions of ventricular arrhythmias in patients with hypertrophic cardiomyopathy (HCM) offer insight into mechanisms and treatment.