Myocardial β-adrenoceptor density has been found to be reduced in hypertrophic cardiomyopathy, even when systolic function is preserved. Our purpose in the current study was to investigate whether β-adrenoceptor down-regulation was unique to hypertrophic cardiomyopathy, or is also present in secondary myocardial hypertrophy. Myocardial β-adrenoceptor density was measured in 11 patients with hypertrophic cardiomyopathy, eight patients with left ventricular hypertrophy secondary to arterial hypertension or aortic valve disease and 18 normal control subjects, using positron emission tomography with 11C-CGP-12177 as the myocardial β-adrenoceptor ligand. Reflecting the natural incidence of the conditions, the age of the hypertrophic cardiomyopathy patients was 37 (10) [mean (SD), range 20–51] years and that of the secondary hypertrophy patients 64 (18), [range 26–80] years; P−1 compared to 10.17 (244) pmol . g−1 for a matched set of 15 controls; P−1 compared to 9.16 (2.00)pmol . g−1 for a matched set of 10 controls; P−1 in hypertrophic cardiomyopathy and 2.5 (1.0)nmol. 1−1 for the matched controls; P−1 respectively; P−1 for noradrenaline for patients and controls respectively (P=ns); and for adrenaline 0.2 (0.1) and 0.3 (0.2) nmol . 1−1 respectively, P=ns. On multiple regression analysis, no relationships could be demonstrated amongst plasma catecholamines, β-adrenoceptor, myocardial blood flow and echocardiographic E/A ratio and fractional shortening. Myocardial β-adrenoceptor density appears to be comparably decreased in both primary and secondary left ventricular hypertrophy in the presence of preserved left ventricular systolic function.