Objectives. This study was conducted to determine the myocardial beta-adrenoceptor density as a market of sympathetic function in patients with hypertrophic cardiomyopathy and normal control subjects. Bachground. Although some casesof hypertrophic cardiomyopthy are familial with an autosomal dominant pattern of inheritance, there remains a subtatial proportion of cases in which neither a family history nor genetic abnormalities can be demonstrated. Additional abnormalities, both genetic and acquired, may be important in the phenotypic expression of this condition. Clinical features of the ddisease and metabolic studies suggest an increased activity of the sympathetic nervous system. Methods. Eleven patients with hypertrophic cardiomyopathy, none of whom had previously received beta-blocking drugs, and eight normal control subjects underwent positron emission tomography to evaluate regional left ventricular beta-adrenoceptor density and myocardial blood flow using carbon-11-labeled CGP 12177 and oxygen-15-labeled water as tracers. Plasma catecholamines were also measured. Results. Mean (±SD) myocardial beta-adrenoceptor density was significantly less in the hypertrophic cardiomyopathy group than in the control group (7.70 ± 1.86 vs. 11.50 ± 2.18 pmol/g tissue, p <0.001). Myocardial blood flow was similar in both group (0.91 ± 0.22 vs. 0.91 ± 0.21 ml/min per g, p = NS). The distribution of beta-adrenoceptor density was uniform throughout the left ventricle in both groups. In the hypertrophic cardiomyopathy group, there was no correlation between regional wall thickness and myocardial beta-adrenoceptor density. There were no significant differences in either plasma norepinephrine or epinephrine concentrations between the two groups. Conclusions. There is a diffuse reduction in myocardial betaadrenoceptor density in patients with hypertrophic cardiomyopathy in the absence of significantly elevated circulating catechlamine concentrations. This most likely reflects downregutation of myocardial beta-adrenoceptors secondary to increased myocardial concentrations of norepinephrine and is consistent with the hypothesis that cardiac sympathetic drive is increased in this condition.
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