Immediate and long-term pathophysiologic mechanisms underlying the genesis of sudden cardiac death in patients with congestive heart failure.
Congestive heart failure is the most important predisposing factor to the occurrence of sudden death in patients with cardiovascular disease. As left ventricular dysfunction deteriorates and symptoms of heart failure become evident, ambulatory ventricular arrhythmias become increasingly frequent and complex, and sudden cardiac death becomes an increasingly common occurrence. When the left ventricular ejection fraction has declined to less than 30 percent and symptoms of heart failure become refractory to treatment with digitalis and diuretics, 35 to 50 percent of patients will die of a lethal cardiac arrhythmia within three years. A number of factors interact to determine the occurrence of malignant ventricular arrhythmias in patients with congestive heart failure. Myocardial fibrosis and enhanced left ventricular wall stress may alter the electrophysiologic properties of the myocardium, but these factors may not be sufficient to explain the development of lethal rhythm disturbances. Neurohormonal activation may exacerbate the frequency and complexity of ambulatory arrhythmias in these patients, but such activation can persist for long periods without fatal electrophysiologic sequelae. Recent investigations suggest that electrolyte depletion may provide an important immediate precipitating cause for the occurrence of fatal ventricular tachyarrhythmias in the patient with severe left ventricular dysfunction whose susceptibility is markedly heightened by preexisting structural, hemodynamic, or neurohormonal factors. Further work is needed to determine if prophylactic therapy directed at preventing electrolyte depletion can favorably modify the long-term outcome of these severely ill patients.
D001145:Arrhythmias, Cardiac / Q000209:etiology; D003645:Death, Sudden / Q000209:etiology*; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D018377:Neurotransmitter Agents / Q000502:physiology; D013318:Stroke Volume; D014883:Water-Electrolyte Imbalance / Q000503:physiopathology
D018377:Neurotransmitter Agents