Silent myocardial ischemia due to coronary-artery spasm was associated with the initiation of life-threatening ventricular arrhythmias in 5 of 356 survivors of out-of-hospital cardiac arrest.
Cohort (n=356)
Can silent myocardial ischemia due to coronary-artery spasm initiate life-threatening ventricular arrhythmias in patients without flow-limiting structural coronary lesions?
Silent myocardial ischemia due to coronary artery spasm can trigger potentially fatal ventricular arrhythmias in patients without structural coronary disease, and these events can be prevented by calcium-channel blockers.
BACKGROUND: Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS: As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS: Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS: Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.
Myerburg et al. (Thu,) conducted a cohort in Out-of-hospital cardiac arrest (n=356). Silent myocardial ischemia due to coronary-artery spasm was evaluated on Initiation of life-threatening ventricular arrhythmias. Silent myocardial ischemia due to coronary-artery spasm was associated with the initiation of life-threatening ventricular arrhythmias in 5 of 356 survivors of out-of-hospital cardiac arrest.