LEFT-VENTRICULAR ENERGETICS - HEAT-PRODUCTION BY THE HUMAN HEART

Objective: The aim was to examine the effect of coronary artery disease on human left ventricular energetics by a comparison of left ventricular oxygen consumption and heat production. The usefulness of measurement of left ventricular heat production for the detection of the expected change in left ventricular energetics produced by atrial pacing to a faster heart rate was also assessed. Methods: Forty six patients (mean age 57 years; 31 men) undergoing cardiac catheterisation and coronary arteriography for the investigation of chest pain were studied. Normal left ventricular function and normal coronary arteries were present in eight and 38 had atheromatous coronary artery disease. Left ventricular heat production was calculated from coronary blood flow, the coronary arteriovenous (aorta-coronary sinus) temperature difference. and the areas under thermodilution curves recorded in the aorta and coronary sinus after injection of cold saline into the pulmonary artery. Mean external left ventricular power was calculated from mean arterial blood pressure- and cardiac output. Left ventricular mechanical efficiency was derived from heat production and the energy value of myocardial oxygen use, assuming aerobic metabolism. In 27 patients studies were repeated during atrial pacing from the coronary sinus. Results: At rest under basal conditions left ventricular heat production was 2.4(SD 1.0) W in patients with normal hearts and 3.1(1.4) W in patients with coronary disease (NS). Mechanical efficiency was 44.2(9.7)% in the normal patients and 30.7(10.9)% in those with coronary disease (p=0.003). During atrial pacing to a faster heart rate left ventricular energy supply increased from 4.6(2.7) W to 5.9(3.3) W (p<0.0005), and heat production increased from 3.0(1.6) W to 4.6(2.4) W (p<0.0005), but mean external power was not altered. As the extra energy used during pacing was ''wasted'' as heat, there was a significant fall in left ventricular mechanical efficiency with pacing from 33.9(13.5)% to 18.9(15.2)% (p<0.0005). Conclusions: These results show the effect of coronary artery disease on the energetics of left ventricular function. They also show that the method and equipment can detect the expected alteration in left ventricular energetics produced by atrial pacing. The measurement of left ventricular heat production and oxygen consumption allows assessment of the total left ventricular energy flux, and may be useful for the evaluation of drug treatment with such as inotropes and vasodilators. and for the investigation of the functional consequences of left ventricular disease.