Left ventricular contractility and the energetic cost of contraction were assessed in various disease models in experimental animals utilizing frameworks of E_max (left ventricular contractility index) and pressure-volume area (PVA, a measure of total left ventricular mechanical energy expenditure) derived from the pressure-volume (P-V) diagram. Under various contractile conditions, PVA linearly correlates with myocardial oxygen consumption per beat (VO₂) in a load-independent manner. The reciprocal of the slope of the linear VO₂-PVA relation indicates "contractile efficiency" (the energy transduction efficiency from oxygen to total mechanical energy). It was similar between dog and rabbit hearts (about 40%) and was not significantly affected by enhanced contractility with calcium, epinephrine, or cardiac cooling, or by depressed contractility with propranolol, decreased coronary perfusion pressure, or stunned myocardium. However, in thyrotoxic rabbit hearts contractile efficiency was significantly depressed compared to normal hearts. On the other hand, the VO₂ intercept of the VO₂-PVA relation (PVA-independent VO₂), which reflects VO₂ for non-mechanical activities such as excitation-contraction coupling and basal metabolism, positively correlates with E_max' Therefore, the ratio of an increase in PVA-independent VO₂ to an increase in E_max indicates "oxygen cost of contractility". Oxygen cost of contractility was higher in stunned myocardium than in normal hearts, suggesting that the energy cost of calcium handling is elevated in stunned myocardium. Thus, using the frameworks of E_max and PVA, we can interconnect cardiac mechanics and energetics. Further, using the concepts of contractile efficiency and oxygen cost of contractility, we can approach the pathogenesis of variously altered contractile conditions.