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Published on: May 23, 2025
Platelet CD36 links overweight and a prothrombotic phenotype in patients with non-valvular atrial fibrillation
Hua Wang1, Wei-Hong Yan1, Lei Gong2
1Department of Cardiology, Yantai Yuhuangding Hospital, Qingdao Medical College, Qingdao University, Yantai, China.
Insights
Platelet CD36 may link overweight and increased clotting risk in non-valvular atrial fibrillation (NVAF). Targeting platelet CD36 could help prevent prothrombotic states in overweight NVAF patients.
Area of Science:
- Cardiology
- Hematology
- Metabolic Disorders
Background:
- Overweight is linked to a prothrombotic state in non-valvular atrial fibrillation (NVAF), but mechanisms are unclear.
- Understanding these links is crucial for stroke risk management in NVAF patients.
Purpose of the Study:
- To investigate the role of platelet CD36 in the association between overweight and stroke risk in NVAF patients.
- To evaluate platelet CD36 expression and its correlation with body mass index (BMI) and platelet activation.
Main Methods:
- A cross-sectional study included 182 NVAF patients, categorized into normal weight and overweight groups.
- Clinical, echocardiographic, and biochemical data were collected.
- Platelet CD36 and integrin αIIbβ3 expression were measured using flow cytometry.
Main Results:
- Overweight patients (62.64%) showed significantly higher BMI, cholesterol, triglycerides, and left atrium dimensions.
- Platelet CD36 expression was significantly elevated in overweight patients, correlating positively with BMI and platelet activation markers.
- Platelet CD36 and BMI were identified as independent risk factors for platelet activation in NVAF.
Conclusions:
- Platelet CD36 appears to mediate the relationship between overweight and platelet hyperactivity in NVAF.
- Targeting platelet CD36 may offer a novel strategy to mitigate the prothrombotic state in overweight NVAF patients.
Introduction:
The pathophysiological mechanisms linking the overweight and prothrombotic state of non-valvular atrial fibrillation (NVAF) are incompletely understood. Our objective was to evaluate the effect of platelet CD36 on the risk of stroke associated with overweight in NVAF patients.
Methods:
A cross-sectional study enrolled 182 subjects with NVAF in two groups: normal weight (18.5 < body mass index(BMI) < 25.0 kg/m2) and overweight (BMI ≥ 25.0 kg/m2). Clinical data, medical history, vital signs, transthoracic echocardiography parameters, and medication were recorded. Biochemical characteristics including blood glucose and serum lipid were analyzed in the Laboratory.
Results:
The expression of platelet CD36 and integrin αIIbβ3 was detected by flow cytometry. Among the 182 patients with NVAF, 68 (37.36%) were classified as normal weight, 114 (62.64%) as overweight. With an increase in BMI, waist-hip ratio, cholesterol, triglycerides, left atrium diameters, and the ratio of mitral inflow E velocity to myocardial e' velocity in the mitral annulus (E/e') increased significantly (P < 0.05). The mean fluorescent intensity of platelet CD36 increased significantly in overweight patients (P < 0.01), in line with platelet activation biomarkers (platelet integrin αIIbβ3). Platelet CD36 was positively correlated with BMI and platelet integrin αIIbβ3, respectively (P < 0.05). Additionally, platelet CD36 and BMI were independent risk factors for platelet activation in patients with NVAF.
Conclusions:
Platelet CD36 is speculated to mediate the complex crosstalk between overweight and platelet hyperactivity, leading to the prothrombotic state in overweight patients with NVAF. Platelet CD36 could be a potential target for preventing the prothrombotic state in overweight patients with NVAF.
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