OBJECTIVE We hypothesised that acute ischemic left ventricular failure is characterised by depressed systolic and diastolic function combined with inefficiency in oxygen to mechanical work energy transfer. METHODS Eight anaesthetised pigs (32+/-3 kg) were employed in an in vivo open chest model. Intraventricular combined pressure and conductance catheters were used to generate continuous left ventricular pressure-volume relations. Myocardial oxygen consumption (MVO(2)) was determined from coronary flow and coronary arteriovenous oxygen difference. After baseline measurements, ischemia was induced by repeated left coronary injections of 50 microm polystyrene microspheres until stroke volume was reduced by 30%. Haemodynamic and biochemical measurements were repeated 30, 90 and 150 min after microembolisation. RESULTS Coronary embolisation induced a significant reduction in stroke work (2749+/-504-1473+/-449 mmHg ml, P<0.05) at 30 min compared to baseline. Post-embolic contractility was reduced measured by the slope of the preload recruitable stroke work index (66.2+/-12.8-50.0+/-5.8 mmHg, P<0.05) and the slope of the curvilinearly fitted end-systolic pressure-volume relation in V(0) (7.1+/-2.2-4.9+/-2.2 mmHg/ml, P<0.05). The dP/dt(min) decreased (2076+/-291-1468+/-266 mmHg/s, P<0.05), but there was no significant change in diastolic stiffness or Tau. Following the 30 min measurements, there were only small changes in most indices. We found no change in myocardial oxygen consumption for basal metabolic processes or excitation-contraction coupling (unloaded MVO(2)), and there were no changes in conversion of oxygen to total mechanical work (MVO(2)-PVA slope). However, decreased mechanical efficiency (SW/MVO(2)) paralleled an increased ratio of arterial elastance to ventricular elastance. CONCLUSIONS Coronary microembolisation in pigs induce a stable ischemic left ventricular failure characterised by reduced contractility and minimally impaired diastolic function. In this acute ischemic left ventricular failure, the main contributor to all over cardiovascular inefficiency is increased ratio of arterial- to ventricular elastance, a setting that impairs mechanical efficiency. However, efficiency of oxygen to total mechanical work transfer in the myocardium is unaltered. The mechanism behind this finding is elusive and warrants further investigation.