Alterations in the right ventricular function may or may not contribute to progressive cardiac dysfunction after left ventricular infarction. Ligation of the left coronary artery (LCAL) was lethal within 24 h for 25% of 100 rats, whereas none of 21 sham-operated rats died. No rats died during the following 4 weeks, after which the ischaemic area of the left ventricular wall appeared fibrotic and weighed 0.041% of the body weight. Simultaneously, the weight of the right ventricle increased from 0.037 to 0.072% of the body weight. The hypertrophied right papillary muscle had a depressed force of contraction and prolonged contraction and relaxation phases. Angiotensin converting enzyme inhibition (ACEI) started early (24 h) prevented hypertrophy and normalized the contractile pattern under basic conditions. However, isoprenaline stimulation revealed that the relaxation phase was still prolonged. Concentration-effect curves for Ca2+ indicated that the pathological relaxation observed in the hypertrophied muscles and during isoprenaline stimulation of myocardium in ACEI treated animals could be due to insufficient re-uptake of cytosolic Ca2+ by the sarcoplasmic reticulum. The results support the idea that the development of right ventricular hypertrophy may contribute to pathophysiological consequences of an infarct in the left ventricle. ACEI started after 24 h prevented hypertrophy, whereas ACEI started after 14 days did not. ACEI was unable to normalize completely the balance between energy demand and energy delivery.