Mechanisms of coronary thrombosis in cigarette smoke exposure

Arterioscler Thromb Vasc Biol. 2013 Jul;33(7):1460-7. doi: 10.1161/ATVBAHA.112.300154. Epub 2013 May 16.

Abstract

Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.

Keywords: cigarette smoke exposure; coronary thrombosis; endothelial cells; plasminogen activator; von Willebrand factor.

Publication types

  • Review

MeSH terms

  • Animals
  • Coronary Thrombosis / blood
  • Coronary Thrombosis / etiology*
  • Coronary Thrombosis / mortality
  • Coronary Thrombosis / pathology
  • Coronary Vessels / metabolism*
  • Coronary Vessels / pathology
  • Disease Progression
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / pathology
  • Fibrinogen / metabolism
  • Hemostasis*
  • Humans
  • Inflammation Mediators / metabolism
  • Oxidative Stress
  • Plaque, Atherosclerotic
  • Platelet Activation
  • Prognosis
  • Risk Assessment
  • Risk Factors
  • Smoking / adverse effects*
  • Smoking / blood
  • Smoking / mortality
  • Thromboplastin / metabolism
  • Tobacco Smoke Pollution / adverse effects*
  • Tobacco Use Disorder / blood
  • Tobacco Use Disorder / complications*
  • Tobacco Use Disorder / mortality
  • Tobacco Use Disorder / pathology

Substances

  • Inflammation Mediators
  • Tobacco Smoke Pollution
  • Fibrinogen
  • Thromboplastin