Mechanisms of thrombosis in obesity

Curr Opin Hematol. 2013 Sep;20(5):437-44. doi: 10.1097/MOH.0b013e3283634443.


Purpose of review: Obesity has become a worldwide epidemic that is driving increased morbidity and mortality from thrombotic disorders such as myocardial infarction, stroke, and venous thromboembolism. Effective prevention and treatment of thrombosis in obese patients is limited by an incomplete understanding of the underlying prothrombotic mechanisms and by uncertainties about risks, benefits, and dosing of anticoagulant drugs in this patient population.

Recent findings: This review summarizes our current understanding of established and emerging mechanisms contributing to the obesity-induced prothrombotic state. The mechanistic impact of chronic inflammation and impaired fibrinolysis in mediating obesity-associated thrombosis is highlighted. Recent data demonstrating the aberrant expression of adipokines and microRNAs, which appear to function as key modulators of proinflammatory and prothrombotic pathways in obesity, are also reviewed. Finally, some challenges and new approaches to the prevention and management of thrombotic disorders in obese and overweight patients are discussed.

Summary: Obesity-driven chronic inflammation and impaired fibrinolysis appear to be major effector mechanisms of thrombosis in obesity. The proinflammatory and hypofibrinolytic effects of obesity may be exacerbated by dysregulated expression and secretion of adipokines and microRNAs, which further increase the risk of thrombosis and suggest new potential targets for therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipokines / blood
  • Adipose Tissue / metabolism
  • Anticoagulants / therapeutic use
  • Fibrinolysis / physiology
  • Humans
  • Obesity / blood
  • Obesity / complications*
  • Platelet Aggregation Inhibitors / therapeutic use
  • Thrombosis / blood
  • Thrombosis / drug therapy
  • Thrombosis / etiology*


  • Adipokines
  • Anticoagulants
  • Platelet Aggregation Inhibitors