title: Coronary endothelial dysfunction is associated with increased risk of venous thromboembolism.
abstract: BACKGROUND
  Normal endothelial function is central to physiologic anticoagulation mechanisms. Endothelial dysfunction may predispose to venous thromboembolism (VTE). We aimed to investigate if coronary endothelial dysfunction (CED) predicts development of VTE in patients presenting with coronary atherosclerosis without critical stenoses.
  
  
  METHODS
  Coronary microvascular function was evaluated in 502 patients with coronary atherosclerosis without critical stenoses by administration of intracoronary acetylcholine at the time of diagnostic study. After a median follow-up of 6.3years, patients were assessed for the development of VTE by administration of a questionnaire. Coronary microvascular endothelial dysfunction was defined as ≤50% increase in coronary blood flow from baseline in response to maximal dose of acetylcholine.
  
  
  RESULTS
  The median age was 53years (IQR: 45, 62) 68% were female and CED occurred in 279 (56%) patients. Hypertension (40.8%), diabetes (8.4%), and hyperlipidemia (58.3%) were common risk factors. There were no differences in baseline characteristics between those with and without CED. There were 9 VTE events (6 unprovoked) among patients with CED compared to no events in the control group (P=0.01).
  
  
  CONCLUSIONS
  CED was associated with the development of VTE. Endothelial injury by causing disruption of vascular hemostasis may play a role in predisposing patients to VTE.
authors.affiliation: Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Megha
authors.initials: M
authors.lastname: Prasad
authors.affiliation: Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Robert
authors.initials: R
authors.lastname: McBane
authors.affiliation: Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Martin
authors.initials: M
authors.lastname: Reriani
authors.affiliation: Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.affiliation: Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: lerman.amir@mayo.edu.
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
mesh_terms: D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000150:complications* / Q000503:physiopathology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D054556:Venous Thromboembolism / Q000453:epidemiology* / Q000503:physiopathology