title: Sudden cardiac death.
abstract: SCD continues to be an important cause of death and morbidity. Despite expanding insight into the mechanisms causing SCD, the population at high risk is not being effectively identified. Although there is still much to do in the management phase of SCD (predicting the efficacy of various therapies), recent clinical trials have helped define the relative risks and benefits of therapies in preventing SCD. Trials are underway to determine whether treating other patient populations, including asymptomatic patients after MI, will improve survival rate. The approach to reducing mortality rate will always be multifaceted; primary prevention of coronary artery disease and prompt salvage of jeopardized myocardium are 2 important aspects of this approach. In addition to interventions for MI, such as myocardial revascularization when indicated, simple and easily administered therapies that are likely to remain the most effective prophylactic interventions are aspirin, ACE inhibitors, beta-blockers, and cholesterol-lowering agents. However, the MADIT and AVID data clearly demonstrate a role for ICD therapy in a subgroup of patients who have VT/VF and are at risk of cardiac arrest. Even though the absolute magnitude of benefit associated with ICDs is still to be determined, the AVID study and other recent reports provide convincing evidence that patients who have VT/VF fare better with ICDs than with antiarrhythmic drug therapy. For the high-risk population described in this article, in addition to aggressive anti-ischemic and heart failure therapy, ICDs are now a mainstay of life-saving treatment. Still to be surmounted is the challenge of identifying patients who have nonischemic substrates and of providing them with the appropriate therapy. Guided by genetic studies and new insight into the mechanisms of such problems as congenital long QT syndrome, life-saving and life-enhancing therapies may soon be available for the management of SCD.
authors.affiliation: University of Wisconsin Medical School, St Luke's Medical Center, Milwaukee, USA.
authors.forename: J
authors.initials: J
authors.lastname: Sra
authors.forename: A
authors.initials: A
authors.lastname: Dhala
authors.forename: Z
authors.initials: Z
authors.lastname: Blanck
authors.forename: S
authors.initials: S
authors.lastname: Deshpande
authors.forename: R
authors.initials: R
authors.lastname: Cooley
authors.forename: M
authors.initials: M
authors.lastname: Akhtar
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000628:therapy; D009202:Cardiomyopathies / Q000150:complications / Q000188:drug therapy; D002648:Child; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D017147:Defibrillators, Implantable; D004562:Electrocardiography; D005260:Female; D006331:Heart Diseases / Q000150:complications* / Q000628:therapy; D006349:Heart Valve Diseases / Q000150:complications / Q000188:drug therapy; D006801:Humans; D008133:Long QT Syndrome / Q000150:complications / Q000628:therapy; D008297:Male; D012307:Risk Factors
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents