Effects of external counterpulsation on enzymatically estimated infarct size and ventricular arrhythmia.

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Abstract
Twenty-hour continuous ECG recordings and plasma creatine kinase (CK) time-activity curves in 39 patients with acute myocardial infarction and 10 normal subjects were analyzed. CK values projected from observed changes during the first 7 h after admission in patients with infarction were used to predict infarct size before implementation of counterpulsation for 30 min intervals separated by 10 min rest periods for 12-18 h. CK values during the 72 h interval after admission were compared with values projected before counterpulsation to determine whether the intervention changes the ratio of enzymatically estimated observed to predicted infarct size. Counterpulsation augmented systemic arterial diastolic pressure and decreased pulmonary arterial occlusive pressure consistently affected CK activity in normal subjects only minimally (mean peak 0.060 IU/ml). Among patients with infarction treated with counterpulsation, the incidence and rate of premature ventricular complexes, couplets, and runs did not differ significantly from values in control patients matched for early ventricular arrhythmia despite a slight transitory decrease of ventricular arrhythmia within the 1st h of counterpulsation (P < 0.01). The ratio of observed to predicted infarct size was virtually identical in treated compared with control patients matched for predicted infarct size. External counterpulsation initiated 7 h after an increase in plasma CK activity did not lead to apparent salvage of ischemic myocardium despite a transitory improvement in ventricular rhythm.