This study assessed a new method of estimating the slope (Ees) of the end-systolic pressure-volume relation (ESPVR) from a single beat of the human heart. Left ventricular pressure was recorded with a high-fidelity micromanometer in patients with heart disease during left ventriculography. Peak isovolumic pressure at the end-disastolic volume was estimated by a curve-fitting technique from an isovolumic left ventricular pressure curve. The ESPVR line was drawn from the estimated peak isovolumic pressure-volume point tangential to the left upper corner of the pressure-volume loop. The slope of this estimated ESPVR line from single-beat analysis was compared with the slope of the ESPVR line obtained from three pressure-volume loops in 16 patients given angiotensin II or nitroglycerin infusion. The estimated Ees was 5.0 +/- 2.2 mm Hg/ml/m2, and the conventional Ees was 4.9 +/- 2.7 mm Hg/ml/m2. The estimated Ees showed a positive correlation with the conventional Ees (r = 0.91, p less than 0.001, SEE = 1.2 mm Hg/ml/m2). In the other 13 patients, after dobutamine infusion (5 micrograms/kg/min i.v.) the estimated Ees increased significantly from 5.6 +/- 1.4 to 7.4 +/- 2.0 mm Hg/ml/m2 (p less than 0.01). Thus, the estimated Ees approximated the conventional Ees and was sensitive to a positive inotropic intervention. We conclude that this single-beat analysis method facilitates assessment of the beat-by-beat ESPVR of the human heart.

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.

The results of the present study indicate that PVA is a reliable and valuable predictor of myocardial oxygen consumption under different contractile states in human hearts. The VO2-PVA relation could provide useful information about mechanoenergetics in diseased human hearts.

The negative chronotropic effect of a beta-blocking agent may offset the mechanoenergetical deterioration resulting from its negative inotropic effect through a reduction in oxygen expenditure for nonmechanical work. These findings suggest that the negative chronotropic effect is an important aspect of beta-blockade therapy.

Background-The results of recent studies suggest that NO synthase may increase in the failing myocardium and that NO modulates the myocardial contractile response to ␤-adrenergic stimulation. However, there are few data regarding the physiological role of NO in patients with heart failure. The aim of the present study was to address the role of NO in left ventricular (LV) contractile response to ␤-adrenergic stimulation and corresponding oxygen expenditure in human heart failure. Methods and Results-We studied 15 patients with heart failure due to idiopathic dilated cardiomyopathy (mean ejection fraction 0.33). We examined LV contractility (E max , the slope of end-systolic pressure-volume relation), LV external work (EW), myocardial oxygen consumption (MV O 2 ), and mechanical efficiency (measured as EW/MV O 2 ) with the use of conductance and coronary sinus thermodilution catheters before and during dobutamine (DOB) infusion via a peripheral vein (4.8Ϯ0.3 g ⅐ kg Ϫ1 ⅐ min Ϫ1 IV). Heart rate was kept constant with atrial pacing. We carried out a similar protocol during the intracoronary infusion of the NO synthase inhibitor N