The myocardial oxygen consumption (MVO(2)) to left ventricular pressure-volume area (PVA) relationship is assumed unaltered by substrates, despite varying phosphate-to-oxygen ratios and possible excess MVO(2) associated with fatty acid consumption. The validity of this assumption was tested in vivo. Left ventricular volumes and pressures were assessed with a combined conductance-pressure catheter in eight anesthetized pigs. MVO(2) was calculated from coronary flow and arterial-coronary sinus O(2) differences. Metabolism was altered by glucose-insulin-potassium (GIK) or Intralipid-heparin (IH) infusions in random order and monitored with [(14)C]glucose and [(3)H]oleate tracers. Profound shifts in glucose and fatty acid oxidation were observed. Contractility, coronary flow, and slope of the MVO(2)-PVA relationship were unchanged during GIK and IH infusions. MVO(2) at zero PVA (unloaded MVO(2)) was 0.16 +/- 0.13 J x beat(-1) x 100 g(-1) higher during IH compared with GIK infusion (P = 0.001), a 48% increase. The study demonstrates a marked energetic advantage of glucose oxidation in the myocardium, profoundly affecting the MVO(2)-PVA relationship. This may in part explain the "oxygen-wasting" effect of lipid-enhancing interventions such as adrenergic drugs and ischemia.

Mechanoenergetic inefficiency in postischemic nonnecrotic myocardium may partly be explained by an increased fatty acid (FA) oxidation rate. In the present study, left ventricular (LV) postischemic energy transfer was characterized in 10 intact anesthetized pigs. The LV was stunned by 11 brief left main coronary artery occlusions/reperfusions (20-min accumulated ischemia). Seven pigs served as time controls. The relationship between myocardial oxygen consumption (MVO(2)) and LV pressure-volume area (PVA) was assessed. [(14)C]glucose and [(3)H]oleate markers were used to discriminate between glucose and FA consumption. In stunned hearts, severe postischemic dysfunction was observed, and contractile efficiency was reduced (increased MVO(2)-PVA slope, P = 0.001). Unloaded (nonmechanical) MVO(2) was not affected by ischemia. We observed only a small transient increase in FA preference and conclude that the contribution from increased FA utilization to postischemic mechanoenergetic inefficiency is insignificant. Disrupted postischemic chemical-to-mechanical energy transfer in vivo is, therefore, related to inefficient energy utilization in the contractile apparatus.

The end-systolic pressure-volume relationship is regarded as a useful index for assessing the contractile state of the heart. However, the need for preload alterations has been a serious limitation to its clinical applications, and there have been numerous attempts to develop a method for calculating contractility based on one single pressure-volume loop. We have evaluated four of these methods. Pressure-volume data were obtained by combined pressure and conductance catheters in 37 pigs. All four methods were applied to 88 steady-state pressure-volume files, including eight files sampled during dopamine infusions. Estimates of single-beat contractility (elastance) were compared with preload-varied multiple-beat elastance [E(es(MB))]. All methods had a low average bias (-0.3 to 0.5 mmHg/ml) but limits of agreement (+/-2 SD) were unacceptably high (+/-2.6 to +/-3.8 mmHg/ml). In the dopamine group, E(es(MB)) showed an increase of 1.7 +/- 0.8 mmHg/ml (mean +/- SD) compared with baseline (P < 0.001). None of the single-beat methods predicted this increase in contractility. It is therefore doubtful whether any of the methods allow for single-beat assessment of contractility.

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