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This review examines the intricate relationship between obesity and venous thromboembolism (VTE), highlighting the underlying pathophysiological mechanisms and clinical implications. Obesity is an established independent risk factor for VTE, which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). The risk of VTE escalates with increasing body mass index (BMI) and is particularly associated with abdominal adiposity. Dysfunctional adipose tissue (AT) in obesity promotes a pro-thrombotic state through chronic low-grade inflammation and impaired fibrinolysis. This inflammation is driven by stress within hypertrophied adipocytes, which leads to localized hypoxia, cellular dysfunction, and ultimately, cell death. This inflammation is driven by adipocyte stress and the infiltration of immune cells. The adipokine leptin exemplifies the complex link between obesity and VTE. While leptin has pro-thrombotic effects, low leptin levels are paradoxically associated with an increased morbidity and mortality in patients with acute PE, a phenomenon termed the "obesity paradox". Furthermore, metabolic syndrome significantly increases the risk of recurrent VTE, with the risk growing with each additional metabolic component. Ultimately, a deeper understanding of the molecular and cellular links between obesity and VTE is essential for developing targeted strategies to reduce risk and improve outcomes in this vulnerable population.
Zawadzka et al. (Wed,) studied this question.