Myocardial blood flow and metabolism in patients with hypertrophic cardiomyopathy--a study with carbon-11 acetate and positron emission tomography.

The underlying pathophysiology of hypertrophic cardiomyopathy (HCM) is still unclear. positron emission tomography is a suitable and promising technique for the detection of possible metabolic consequences of the disease. To assess regional myocardial blood flow and metabolism, 19 asymptomatic or only mildly symptomatic patients with HCM and 10 normal control subjects were studied using carbon-11 acetate and fluorine-18-labelled deoxyglucose (FDG) as tracers of myocardial blood flow (Ao), oxygen consumption (k), and exogenous glucose utilization. In the patients, regional Ao in the hypertrophied septum and apex (H) was similar to that in the nonhypertrophied free wall (N) (91.3 +/- 3.9% vs 92.9 +/- 3.1%; p = NS). However, the k values were significantly lower in H than in N (0.044 +/- 0.012 vs 0.060 +/- 0.016/min, p < 0.0001). The k value in N and normal control subjects (0.062 +/- 0.013) was similar. Postprandial FDG uptake was lower in H than in N (70 +/- 16 vs 91 +/- 7%; p < 0.0001) in 16 patients and slightly higher in 3 patients. Fasting FDG study showed increased FDG uptake in H in 3 out of 13 patients, suggesting a disorder of the myocardial microvascular circulation. A relative decrease in hypertrophied septal and apical oxidative metabolism and glucose utilization without any corresponding perfusion defect could reflect abnormal regional aerobic metabolism in the disproportionately thickened myocardium in patients with HCM. This suggests that a primary myocardial metabolic defect might be present in patients with HCM.