Hormone-electrolyte interactions in the pathogenesis of lethal cardiac arrhythmias in patients with congestive heart failure. Basis of a new physiologic approach to control of arrhythmia.
Congestive heart failure is the most arrhythmogenic disorder in cardiovascular medicine. As left ventricular performance deteriorates and symptoms of dyspnea and fatigue become progressively more severe, nearly all patients with heart failure experience frequent and complex ventricular tachyarrhythmias and nearly half die suddenly during long-term follow-up. This imminent risk of sudden death appears to be present for all patients with congestive heart failure; ambulatory electrocardiographic monitoring and programmed electrical stimulation are not useful in distinguishing patient subsets that are particularly predisposed to fatal arrhythmic events. Although conventional antiarrhythmic agents are widely prescribed as a nonspecific approach to prevent sudden death in these patients, there is little evidence to indicate that these drugs possess clinically important antiarrhythmic activity in patients with congestive heart failure, and these agents frequently serve to exacerbate the heart failure state and the underlying ventricular tachyarrhythmia. A useful approach to the prevention of sudden death in patients with congestive heart failure addresses the reversible causes of lethal ventricular arrhythmias in these individuals. Both experimental and clinical evidence indicates that circulating neurohormones and electrolyte deficits (particularly of potassium and magnesium) interact to provoke malignant ventricular ectopic rhythms and that the prevention of electrolyte depletion and the use of neurohormonal antagonists may exert clinically important antiarrhythmic actions. This physiologic approach may prove to be a more effective means of ameliorating the problem of sudden death than the empiric administration of conventional antiarrhythmic drugs.
Packer
M
M
Gottlieb
S S
SS
Kessler
P D
PD
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology*; D001341:Autonomic Nervous System / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D003645:Death, Sudden / Q000517:prevention & control*; D004452:Echocardiography; D004558:Electric Stimulation; D004562:Electrocardiography; D004573:Electrolytes / Q000502:physiology*; D006333:Heart Failure / Q000150:complications* / Q000503:physiopathology; D006728:Hormones / Q000502:physiology*; D006801:Humans; D008274:Magnesium / Q000502:physiology / Q000627:therapeutic use; D011188:Potassium / Q000097:blood / Q000502:physiology / Q000627:therapeutic use; D012084:Renin-Angiotensin System; D012306:Risk
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D002395:Catecholamines; D004573:Electrolytes; D006728:Hormones; D008274:Magnesium; D011188:Potassium