Related Experiment Videos
CD36 deficiency has little influence on the pathophysiology of hypertrophic cardiomyopathy
T Nakamura1, H Sugihara, T Inaba
1Second Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Insights
CD36 deficiency is not more common in hypertrophic cardiomyopathy (HCM) patients than the general population. This study found CD36 deficiency does not significantly impact HCM pathophysiology or characteristics.
Area of Science:
- Cardiology
- Genetics
- Metabolism
Background:
- CD36, homologous to myocardial long-chain fatty acid (LCFA) binding protein, is implicated in myocardial fatty acid metabolism.
- Impaired LCFA metabolism is observed in hypertrophic cardiomyopathy (HCM) myocardium.
- Previous studies suggested a high incidence of CD36 deficiency in HCM patients, proposing it as an etiology of hereditary HCM.
Purpose of the Study:
- To investigate the pathophysiological effect of CD36 deficiency on HCM.
- To determine if CD36 deficiency is a characteristic factor in HCM patients.
Main Methods:
- Analyzed CD36 antigen expression on platelets and monocytes from 82 HCM patients using two-color flow cytometry.
- Compared clinical characteristics, scintigraphic, echocardiographic, and hemodynamic findings between HCM patients with and without CD36 deficiency.
Main Results:
- Type II CD36 deficiency was detected in 8.5% of HCM patients, with no significant difference based on family history or asymmetric septal hypertrophy (ASH).
- No significant differences were found in clinical, scintigraphic, echocardiographic, or hemodynamic data between HCM patients with normal CD36 expression and those with CD36 deficiency.
- The incidence of CD36 deficiency in HCM patients was not higher than in the general population.
Conclusions:
- CD36 deficiency is not a characteristic factor of HCM.
- CD36 deficiency has minimal influence on the pathophysiology of HCM.
Abstract:
CD36 is homologous with myocardial long-chain fatty acid (LCFA) binding protein and has been suggested to relate to myocardial fatty acid metabolism. Myocardial scintigraphy with iodine-123 15-(p-iodophenyl)-3-(R, S)-methylpentadecanoic acid (BMIPP) revealed an impairment in LCFA metabolism chiefly in the hypertrophic myocardium in hypertrophic cardiomyopathy (HCM). Recently, the incidence of CD36 deficiency has been reported to be high in HCM patients, and CD36 deficiency was proposed as an etiology of hereditary HCM. However, the pathophysiological effect of CD36 deficiency on HCM has not been 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 the study patients, seven patients (8.5%) demonstrated type II CD36 deficiency, 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 family history of HCM showed type II CD36 deficiency respectively. Contrary to the previous report, three of 53 patients with asymmetric septal hypertrophy (ASH) (5.7%) and four of 29 patients without ASH (13.8%) showed CD36 deficiency. Moreover, clinical characteristics, scintigraphic findings, echocardiographic data, and hemodynamic findings disclosed no significant differences between the HCM patients showing normal CD36 expression and those with CD36 deficiency. The incidence of CD36 deficiency in HCM patients is not higher than in the general population. Therefore, CD36 deficiency is not a characteristic factor of HCM and has little influence on the pathyphysiology of HCM.