ObjectiveTo explore whether platelet activation is associated with systemic inflammatory responses. MethodsWe conducted a cross-sectional study to enroll all aortic dissection (AD) patients (AD group) from January 1, 2015 to June 30, 2015 in the Emergency Department. According to the characteristics of AD patients, we matched hypertension (hypertension group) and health participants (health group) with AD patients at a proportion of 1:1:1. Blood samples were collected on admission for blood routine test [mean platelet volume (MPV)/platelet (PLT)] and inflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-6] analysis. We compared all parameters among the three groups and performed bivariate correlation analyses. ResultsExpressions of TNF-α and IL-6 in the AD group [(20.9±4.5), (168.8±75.1) pg/mL] were significantly higher than those in the hypertension group [(4.3±1.9), (8.4±2.9) pg/mL] and healthy group [(5.4±1.6), (8.7±3.8) pg/mL] (P＜0.05). MPV/PLT in the AD group was significantly higher than that in the hypertension group and healthy group (0.106±0.035 vs 0.049±0.010, P＜0.05; 0.106±0.035 vs 0.054±0.019, P＜0.05). There were positive correlations between MPV/PLT and TNF-α (r=0.516, P=0.002), and between MPV/PLT and IL-6 (r=0.633, P＜0.001) in the AD group. ConclusionIn summary, our study shows that platelets of AD patients can be activated, and the degree of activation is associated with systemic inflammatory responses.
Venous thromboembolism is the third most common cardiovascular disease worldwide, including deep vein thrombosis in the lower extremities and pulmonary embolism, affecting approximately 5% of the global population. It has a high recurrence rate and mortality rate, and poses a significant burden. The traditional Virchow triangle theory laid the foundation for its pathological research. Platelets, as a key component, undergo a complex and multi-dimensional activation process, not only initiating and amplifying the coagulation cascade reaction, but also constructing a thrombogenic network through interactions with immune cells, endothelial cells, etc. This article elaborates on the core mechanism, driving pathways, specific pathological effects, and clinical value of platelet activation in venous thromboembolism, combined with insights from clinical practice and cutting-edge research, with the aim of providing new ideas for the prevention and treatment of venous thromboembolism.