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

Abstract

To determine whether external counterpulsation influences the evolution of injury in ischaemic myocardium, we analysed 20-hour continuous electrocardiographic recordings and plasma creatine kinase (CK) time-activity curves in 39 patients with acute myocardial infarction and 10 normal subjects. CK values projected from observed changes during the first 7 hours after admission in patients with infarction were used to predict infarct size before implementation of counterpulsation for 30-minute intervals separated by 10-minute rest periods for 12 to 18 hours. CK values during the 72-hour interval after admission were compared with values projected before counterpulsation to determine whether the intervention changed the ratio of enzymatically estimated observed to predicted infarct size. Counter- pulsation augmented systemic arterial diastolic pressure and decreased pulmonary arterial occlusive pressure consistently but 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 first hour 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. Thus, external counterpulsation initiated 7 hours after an increase in plasma CK activity did not lead to apparent salvage of ischaemic myocardium despite a transitory improvement in ventricular rhythm.