CD36 deficiency has little influence on the pathophysiology of hypertrophic cardiomyopathy

CD36 is homologous with myocardial long-chain fatty acid (LCFA) binding pro tein and has been suggested to relate to myocardial fatty acid metabolism M yocardial scintigraphy with iodine-123 15-(p-iodophenyl)-3-(R, S)-methylpen tadecanoic acid (BMIPP) revealed an impairment in LCFA metabolism chiefly i n the hypertrophic myocardium in hypertrophic cardiomyopathy (HCM). Recentl y, the incidence of CD36 deficiency has been reported to be high in HCM pat ients, and CD36 deficiency was proposed as an etiology of hereditary HCM. H owever, the pathophysiological effect of CD36 deficiency on HCM has not bee n fully investigated. We analysed the expression of CD36 antigens on both platelets and monocytes obtained from 82 patients with HCM using two-color flow cytometry, Among t he study patients, seven patients (8,5%) demonstrated type II CD36 deficien cy, whereas type I CD36 deficiency was not detected. Two of 23 patients (8. 7%) with a family history of HCM and five of 59 patients (8.5%) without a f amily history of HCM showed type II CD36 deficiency respectively Contrary t o the previous report, three of 53 patients with asymmetric septal hypertro phy (ASH) (5.7%) and four of 29 patients without ASK (13.8%) showed CD36 de ficiency. Moreover, clinical characteristics, scintigraphic Endings, echoca rdiographic data, and hemodynamic findings disclosed no significant differe nces between the HCM patients showing normal CD36 expression and those with CD36 deticiency, The incidence of CD36 deficiency in HCM patients is not higher than in the general population. Therefore, CD36 deficiency is not a characteristic fact or of KCM and has little influence on the pathyphysiology of HCM. (C) 1999 Academic Press.