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

Objective: The aim was to examine the effect of coronary artery diseas e on human left ventricular energetics by a comparison of left ventric ular oxygen consumption and heat production. The usefulness of measure ment of left ventricular heat production for the detection of the expe cted change in left ventricular energetics produced by atrial pacing t o a faster heart rate was also assessed. Methods: Forty six patients ( mean age 57 years; 31 men) undergoing cardiac catheterisation and coro nary arteriography for the investigation of chest pain were studied. N ormal left ventricular function and normal coronary arteries were pres ent in eight and 38 had atheromatous coronary artery disease. Left ven tricular 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 co ronary sinus after injection of cold saline into the pulmonary artery. Mean external left ventricular power was calculated from mean arteria l blood pressure- and cardiac output. Left ventricular mechanical effi ciency was derived from heat production and the energy value of myocar dial oxygen use, assuming aerobic metabolism. In 27 patients studies w ere 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 wi th 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=0.00 3). During atrial pacing to a faster heart rate left ventricular energ y 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 mea n external power was not altered. As the extra energy used during paci ng was ''wasted'' as heat, there was a significant fall in left ventri cular 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 a rtery disease on the energetics of left ventricular function. They als o show that the method and equipment can detect the expected alteratio n in left ventricular energetics produced by atrial pacing. The measur ement of left ventricular heat production and oxygen consumption allow s assessment of the total left ventricular energy flux, and may be use ful for the evaluation of drug treatment with such as inotropes and va sodilators. and for the investigation of the functional consequences o f left ventricular disease.