Amiodarone and post-MI patients.
Amiodarone is a viable drug for preventing sudden cardiac death, particularly during the first year after MI. If larger trials confirm the aforementioned prospective trials of Ceremuzynski et al, Cairns et al, and the BASIS trial, the efficacy of amiodarone would outweigh the risk of its side effects during the first year after MI. Based on the long-term observation from the BASIS trial, the duration of amiodarone therapy need not be more than 1 year--which, as we have learned, is when these post-MI patients would benefit most from the drug. It is also likely that the effects of amiodarone would complement those of aspirin and angiotensin converting enzyme inhibitors. The SAVE, CONSENSUS II, and SOLVD trials demonstrated that captopril and enalapril did not reduce the mortality rate during the first year after MI, nor did they reduce the sudden cardiac death rate. Their beneficial effects became evident only during the second year and thereafter. Unlike other antiarrhythmic agents of various classes, amiodarone possesses antiarrhythmic properties but does not exert deleterious effects on ventricular function. More studies are needed to determine if the benefit of amiodarone could be enhanced by combination therapy (eg, angiotensin converting enzyme inhibitors, aspirin, or beta-blockers). Whether amiodarone will provide the same protection for patients who have poor left ventricular function or congestive heart failure is not known. The European and VA cooperative studies should help answer this question. If it turns out that amiodarone is beneficial, one must then determine whether higher doses of the drug will offer more protection, and, if so, if that greater protection would be offset by increased toxicity. How much amiodarone should be given to offer the most protection with the least risk? Another intriguing research question is this: If we treat patients with amiodarone for more than 1 year, would the drug continue to improve the mortality rate in subsequent years? Other studies are needed in patients at very high risk of sudden cardiac death (ie, those who have a low ejection fraction and high-density VPDs). A study comparing amiodarone and sotalol in high-risk patients for sudden cardiac death is also needed. These clinical studies should be carried out with basic science research investigating the actions of amiodarone at the molecular and cellular level in order to give us a better understanding of how the drug works.
Nademanee
K
K
Department of Cardiology, Denver (Colo) General Hospital 80204.
Singh
B N
BN
Stevenson
W G
WG
Weiss
J N
JN
D000638:Amiodarone / Q000378:metabolism / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D003327:Coronary Disease / Q000175:diagnosis; D016757:Death, Sudden, Cardiac / Q000517:prevention & control; D004594:Electrophysiology; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000188:drug therapy
D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D000638:Amiodarone