Ventricular Fibrillation Complicating Acute Myocardial Infarction: Outcome
Our groups included patients developing VF during AMI. We separated them according to preestablished electrocardiographic criteria into two groups which were comparable in age, coronary risk factors, and previous cardiac diseases. Those two types of tachyarrhythmias could be correlated with specific phases of infarction based upon electrocardiographic natural evolution of AMI. Increased ventricular vulnerability to fibrillation can occur secondary to a complete coronary occlusive event Investigations designed to assess the correlation between ST-segment alterations and coronary dynamics demonstrated that ST-segment elevation with a peaked positive T wave is an initial electrocardiographic expression of transmural myocardial ischemia, resulting from sudden reduction of coronary blood flow. The fact that less than 20 percent of the patients were found to have type 1 arrhythmia may suggest that in a substantial number of patients, it takes place during the so-called prehospital phase, whereas type 2, the multiform variety, was found to be the dominant pattern during the phase of hospitalization.
The ischemic mechanism considered is well supported by clinical observations in patients with variant angina. In these patients, coronary spasm and transmural myocardial ischemia may account for the development of ventricular arrhythmias noted during the period of ST-segment elevation which represents the most prominent electrocardiographic finding of the vasospastic attack.
Restoration of coronary blood flow is frequently associated with ventricular arrhythmias. Reentry or enhanced automaticity (or both) may play a role in the genesis of reperfiision arrhythmias during ischemia or infarction. Reestablishment of coronary blood flow after relief of spasm may also be responsible for the development of VF and sudden death in patients with vasospastic angina, even with no evidence of significant coronary artery disease.
Of the 27 patients with type 2 VF, 25 were found to develop VF during stage 2 of AMI, once pathologic Q waves were already recognized in the ECG. Rapid release of creatine kinase is a useful marker of early spontaneous recanalization. The appearance of Q waves, which used to be regarded as a marker of myocardial necrosis, was closely parallel to the “washout” of cardiac enzymes observed after reopening of an occluded coronary vessel. Therefore, these data suggest that the likely substratum involves reperfusion changes of the ischemic myocardium. The destruction of cells which were damaged by ischemia and the release of myocardial metabolites accumulated during occlusion may account for the electrical instability during reestablishment of coronary artery patency.
Category: Myocardial Infarction
Tags: electrocardiographic, myocardial infarction, ventricular fibrillation