Energy conversion efficiency in human left ventricle.
BACKGROUND
Left ventricular mechanical efficiency is one of the most important measures of left ventricular pump performance. Several clinical studies, however, have shown that mechanical efficiency does not fall substantially as the heart fails. To clarify the insensitivity of mechanical efficiency to the change in pump performance, we analyzed human left ventricular mechanical efficiency, applying the concept of left ventricular systolic pressure-volume area (PVA).


RESULTS
PVA correlates linearly with myocardial oxygen consumption per beat (MVO2): MVO2 = a.PVA+b, and represents the total mechanical energy of contraction. We determined MVO2-PVA relation and external work in 11 patients with different contractile states. We also calculated the energy transfer from MVO2 to PVA (PVA/MVO2 efficiency), that from PVA to external work (work efficiency), and mechanical efficiency (external work/MVO2). Left ventricular pressure-volume loops were constructed by plotting the instantaneous left ventricular pressure against the left ventricular volume at baseline and during pressure loading. The contractile properties of the ventricle were defined by the slope of the end-systolic pressure-volume relation (Ees). Pressure elevation raised external work by 41.4%, PVA by 71.2%, and MVO2 by 54.5%. These changes were associated with a decrease in work efficiency and an increase in PVA/MVO2 efficiency. The opposite directional changes in these two efficiencies rendered the mechanical efficiency constant. The slope, a, of the relation between MVO2 and PVA was relatively constant (2.46 +/- 0.33) over the range of 0.8-8.8 mm Hg/ml of Ees, but the oxygen axis intercept, b, tended to decrease with the reduction in Ees. PVA/MVO2 efficiency correlated inversely (r = -0.66, p less than 0.05) with Ees, whereas work efficiency correlated linearly with Ees (r = 0.91, p less than 0.01).


CONCLUSIONS
Mechanical efficiency is not appreciably affected by changes in loading and inotropic conditions as long as the left ventricular contractility is not severely depressed.
Kameyama
T
T
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Asanoi
H
H
Ishizaka
S
S
Yamanishi
K
K
Fujita
M
M
Sasayama
S
S
D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D004735:Energy Transfer / Q000502:physiology; D006801:Humans; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009203:Myocardial Infarction / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*