Sudden cardiac death in athletes.

The impact of sudden cardiac death (SCD) in athletes has been highlighted by increasing media coverage, as well as medical and lay awareness of the entities associated with SCD. Common etiologies include cardiac abnormalities such as hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD), and coronary artery anomalies, each with varying geographic incidence. New recommendations regarding noninvasive preparticipation screening have emerged in Europe, where the Italian experience of mandatory annual screening of athletes has been the forerunner in efforts to identify individuals at risk. Ongoing clinical efforts are underway to help define the role of implantable cardioverter defibrillators as a preventive measure in appropriate candidates with HCM or ARVD, as well as methods to limit the potential for SCD as a result of chest blows sustained in sports and other recreational activities by means of chest protectors and special sporting equipment for young athletes.

Device trials in heart failure: a focused summary.

Despite considerable progress in heart failure management with pharmacologic agents, measures to bring about significant improvements in morbidity and mortality are still needed. Cardiac resynchronization therapy (CRT) is a means to enhance myocardial function by stimulating the failing left ventricle at or near the time of right ventricular activation to synchronize ventricular depolarization. Current data from randomized, controlled trials suggest that CRT benefits patients with moderate to severe heart failure and have shown that this therapy significantly reduces mortality and hospital admissions in this group. In addition to CRT, implantable cardioverter-defibrillators have been evaluated in heart failure patients with significantly reduced left ventricular function and have been shown to reduce mortality from sudden cardiac death. This article summarizes recent device trials and discusses how best to apply their results to clinical practice.

Current Treatment Options for CHF Management: Focus on the Renin-Angiotensin-Aldosterone System.

Heart failure (HF) is highly prevalent in our society and its incidence is increasing in concert with the growing aged population. Experimental and clinical studies have consistently shown that HF is ameliorated by inhibition of the renin-angiotensin-aldosterone system (RAAS). Acknowledging that heightened activation of the RAAS contributes significantly to HF progression has led to the development of pharmacologic antagonists of RAAS components that have greatly improved both symptoms and prognosis of patients suffering from this syndrome. Angiotensin-converting enzyme (ACE) inhibitors represent the first developed agents that block the production of angiotensin II, and have been shown to be effective across a broad spectrum of patients with HF, including those with asymptomatic left ventricular dysfunction to overt HF. Initiation of ACE inhibitors prior to the onset of symptoms in those with left ventricular systolic dysfunction, and as early as feasible following a myocardial infarction, has been shown to reduce mortality and the development of overt HF in several clinical trials. Clinical data also support the use of angiotensin II receptor antagonists as an alternative to ACE inhibitors in patients who are allergic to, or intolerant of, ACE inhibitors. Agents that antagonize aldosterone via blockade of mineralocorticoid receptors improve clinical outcomes in patients with advanced HF or those with reduced ejection fraction and HF following an acute myocardial infarction. Maximally inhibiting the RAAS, in conjunction with other neurohormonal systems (eg, the sympathetic nervous system by b-adrenergic blockade), leads to improved clinical outcomes in HF, a highly prevalent and costly disease in our society.

Progression of coronary artery disease in non-ischemic dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is traditionally divided into ischemic and non-ischemic etiologies. We review data from clinical trials that suggest some patients in the latter subgroup develop ischemic complications including fatal myocardial infarction. However, the reasons for and magnitude of the effect are not known. Prospective screening studies and improved endpoint adjudication in clinical trials may be required to better delineate the degree to which the phenomenon occurs. Risk factor modification strategies should be applied to the non-ischemic DCM cohort, especially with continued improvements in survival rates in patients with heart failure.