Cardiac work and myocardial substrate extraction in congestive cardiomyopathy

Thompson, D.S.; Naqvi, N.; Juul, S.M.; Swanton, R.H.; Wilmshurst, P.; Coltart, D.J.; Jenkins, B.S.; Webb-Peploe, M.M.

British Heart Journal 47(2): 130-136


ISSN/ISBN: 0007-0769
PMID: 7059392
Accession: 004881852

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Left ventricular pressure, cardiac output, coronary sinus blood flow and myocardial substrate extraction were measured in 10 patients with congestive (dilated) cardiomyopathy and in a control group of 9 patients investigated for chest pain who proved to have no angiographic or metabolic evidence of ischemic heart disease. Hemodynamic and angiographic measurements confirmed that the patients with cardiomyopathy had severe left ventricular disease. Coronary sinus blood flow and myocardial O2 consumption were greater in the patients with cardiomyopathy, but were similar in the 2 groups when normalized for ventricular mass. Efficiency, estimated from the O2 cost of external work, was grossly reduced in the cardiomyopathy group. No major differences in substrate extraction were demonstrated between the groups. Myocardial lactate production was not observed in any patient with cardiomyopathy. Free fatty acid and glycerol release were observed in several control subjects but in none of the patients with cardiomyopathy. Measurements were repeated during pacing in 5 of the cardiomyopathy group and in each of the control subjects. The latter showed a normal response to pacing, while of the former, 4 sustained increases in end-diastolic pressure, 2 showed large reductions in both cardiac output and coronary flow, and only 1 increased coronary flow during pacing. Despite the failure of coronary flow to increase, lactate extraction remained high. These results show that anerobic carbohydrate metabolism is not an important energy source for the myopathic heart and suggest that ischemia does not contribute to poor left ventricular function. No gross abnormality of oxidative metabolism was identified, implying that low efficiency lay in the poor contractile performance of the myopathic heart.