Polymorphous ventricular tachycardia early after acute myocardial infarction.

V entricular tachyarrhythmias are a major cause of cardiac death within the early hours of an evolving acute myocardial infarction. Diverse cytochemical and metabolic alterations develop in the ischemic and periischemic zones after coronary artery occlusion and subsequent reperfusion. 1,2 These alterations change rapidly over time and may cause various morphologically distinct ventricular arrhythmias in the different stages of an acute myocardial infarction.1~3 One type of malignant ventricular tachyarrhythmia that appears during an acute myocardial infarction is polymorphous ventricular tachycardia (VT). 3,4 The electrophysiologic mechanism and the therapy differ from those of other forms of vT.5~~ The occurrence of polymorphous VT in the early stages of an acute myocardial infarction has been infrequently reported,4 although an incidence of 1.2 to 2% during overall hospitalization for acute myocardial infarction had been reported.4 This report describes the clinical and electrocardiographic features of patients with polymorphous VT in the early stages of an evolving acute myocardial infarction. Data for this study were collected retrospectively from patients admitted to the coronary care unit from January 1989 to August 1991 with an evolving acute myocardial infarction. The criteria for the diagnosis of an acute myocardial infarction were: severe chest pain of >30 minutes duration, characteristic evolutionary electrocardiographic changes and a typical elevation of serum creatine kinase. All patients had a continuous 3lead electrocardiographic recording for 2 to 4 hours after admission, using 3 leads simultaneously that demonstrated maximal ST elevations. Of 954 patients, admitted during that period, 7 patients had polymorphous VT documented within the first 4 hours after admission. Of the 954 patients, 402 received intravenous thrombolytic therapy (42%). The following data were recorded: age, sex, previous history of coronary artery disease, Killip functional class on admission, and the time that elapsed from the onset of cardiac symptoms and from the initiation of thrombolytic therapy to the onset of ventricular arrhythmia. Serum potassium and calcium levels on admission were noted. Normal values for our laboratory are: potassium, 3.5 to 5.0 mmollliter, calcium, 2.12 to 2.62 mmollliter. Medication taken before polymorphous VT and therapy for arrhythmia were recorded. The heart rate, rhythm and the QT interval were determined using the last complexes before the onset of the ar-