Key result
A patient with hereditary hypertrophic cardiomyopathy and type I CD36 deficiency showed no myocardial long-chain fatty acid accumulation and completely CD36-negative myocardial capillary endothelial cells.
Case Report (n=1)
Type I CD36 deficiency may be closely related to hereditary hypertrophic cardiomyopathy and the lack of myocardial long-chain fatty acid accumulation.
Links CD36 deficiency to absent myocardial fatty acid uptake in hereditary HCM; hypothesis-generating and needs validation in larger cohorts.
CD36 is a multifunctional membrane-type receptor glycoprotein that reacts with oxidized low-density lipoprotein and long-chain fatty acid (LCFA). A patient presented with hereditary hypertrophic cardiomyopathy (HCM) and type I CD36 deficiency (neither platelets nor monocytes expressed CD36) but showed no myocardial LCFA accumulation. CD36 was expressed in the capillary endothelial cells of the cardiac muscle of a control subject, while the patient's myocardial capillary endothelial cells were completely CD36-negative. These results suggest that type I CD36 deficiency is closely related to hereditary HCM and lack of myocardial LCFA accumulation.
No takes yet. Share an insight, caveat, or question.
Watanabe et al. (1998) conducted a case report in Hypertrophic Cardiomyopathy and Type I CD36 Deficiency (n=1). Type I CD36 deficiency vs. Control subject (HCM patient positive for CD36) was evaluated on Myocardial long-chain fatty acid (LCFA) accumulation and CD36 expression in myocardial capillary endothelial cells. A patient with hereditary hypertrophic cardiomyopathy and type I CD36 deficiency showed no myocardial long-chain fatty acid accumulation and completely CD36-negative myocardial capillary endothelial cells.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: