Assessment of myocardial oxygen consumption (Vo2) and systolic pressure-volume area (PVA) in human hearts

Abstract

Several studies have recently reported that the relationship between myocardial oxygen consumption per beat (Vo2) and left ventricular (LV) systolic pressure-volume area (PVA), which represents total mechanical energy generated by contraction, is linear and independent of loading conditions in excised, supported, and intact hearts. We assessed the Vo2-PVA relationship in nine patients with heart disease. LV volume and pressure were measured simultaneously by conductance catheter and tip-micromanometer. Vo2 was calculated from the difference between arterial and coronary sinus oxygen content, and coronary sinus blood flow measured by the thermodilution method. We obtained the linear relationship between Vo2 and PVA by dextran infusions (median r = 0.917). The slope of the Vo2-PVA relationship was (1.82 +/- 0.66) x 10(-5) mlO2 mmHg-1 ml-1 and the contractile efficiency, the reciprocal of the slope of the Vo2-PVA relationship, was 40 +/- 13%. The Vo2 intercept, which reflects Vo2 for non-mechanical work, was 0.0284 +/- 0.0286 ml O2 beat-1. These results suggest that PVA is a good predictor of myocardial oxygen consumption and a powerful tool to evaluate the coupling of LV mechanical performance to energy use in human hearts.

Mechanically Unloading the Left Ventricle Before Coronary Reperfusion Reduces Left Ventricular Wall Stress and Myocardial Infarct Size

“…Furthermore, previous studies have shown that reduced LV wall stress and stroke work correlate with reduced myocardial oxygen consumption. 38,39 Our data suggest that reducing LV wall stress, stroke work, and strain may promote myocardial salvage in AMI by reducing myocardial oxygen demand and thereby attenuating the process of ongoing myocardial ischemia.By initiating mechanical support first and sustaining systemic perfusion while reducing native LV work, we have created a window in time when the process of myocardial injury is slowed and delaying coronary reperfusion is possible while incurring only minimal additional ischemic damage. By delaying reperfusion in the setting of mechanically reduced oxygen demand, time is now available for activation of signaling pathways known to promote myocardial salvage, including phosphorylation of ERK and Akt.…”

“…Furthermore, previous studies have shown that reduced LV wall stress and stroke work correlate with reduced myocardial oxygen consumption. 38,39 Our data suggest that reducing LV wall stress, stroke work, and strain may promote myocardial salvage in AMI by reducing myocardial oxygen demand and thereby attenuating the process of ongoing myocardial ischemia.…”

Assessment of Left Ventricular Viscoelastic Components Based on Ventricular Harmonic Behavior

“…Based on their diagram (Suga and Sagawa, 1974), they described the ratio of instantaneous pressure to instantaneous volume (P(t)/(V(t) − V d )) as the time varying stiffness of ventricular chamber. The standard P-V diagrams are easy to interpret and give a rough estimate of the mechanical work done by the LV (Takaoka et al, 1992). However, the pressure and the corresponding volume of the LV need to be measured invasively using sophisticated techniques, such as intravascular micromanometers and conductance catheters (Applegate et al, 1990), which restrict the clinical applications of this model.…”

A Mechanical Model of the Human Heart Relating Septal Function to Myocardial Work and Energy

“…Suga et al (1979Suga et al ( , 1983 and Takaoka (1992) have made similar estimates based on the PVA method, and ventricular free wall movement. Regardless, better models of the coronary circulation and gas transport in the myocardium are needed to make better estimates of energy consumption based the A-VO 2 difference across the coronary capillary bed.…”

“…Currently, the rate of energy consumption per heartbeat is taken to be the area enclosed by the P-V loop (Westerhoff 2000;Suga 1979a;1981;Takaoka et al 1992); however, most analyses using this method do not include the effects of the interventricular septum. The current lack of adequate amounts of measured patient data has slowed the development of functional models capable of analyzing septal and free ventricular wall mechanics.…”