title: Dose-related effect of statins in venous thrombosis risk reduction.
abstract: BACKGROUND
  Atherosclerosis and venous thromboembolism share similar pathophysiology based on common inflammatory mediators. The dose-related effect of statin therapy in venous thromboembolism remains controversial. This study investigated whether the use of antiplatelet therapy and statins decrease the occurrence of venous thromboembolism in patients with atherosclerosis.
  
  
  METHODS
  We conducted a retrospective cohort study reviewing 1795 consecutive patients with atherosclerosis admitted to a teaching hospital between 2005 and 2010. Patients who had been treated with anticoagulation therapy were excluded. Patients who either used statins for <2 months or never used them were allocated to the nonuser group.
  
  
  RESULTS
  The final analysis included 1100 patients. The overall incidence of venous thromboembolism was 9.7%. Among statin users, 6.3% (54/861) developed venous thromboembolism, compared with 22.2% (53/239) in the nonuser group (hazard ratio [HR] 0.24; P <.001). After controlling for confounding factors, statin use was still associated with a lower risk of developing venous thromboembolism (HR 0.29; P <.001). High-dose statin use (average 50.9 mg/day) (HR 0.25; P <.001) lowered the risk of venous thromboembolism compared with standard-dose statins (average 22.2 mg/day) (HR 0.38; P <.001). Dual antiplatelet therapy with aspirin and clopidogrel decreased occurrence of venous thromboembolism (HR 0.19; P <.001). Interestingly, combined statins and antiplatelet therapy further reduced the occurrence of venous thromboembolism (HR 0.16; P <.001).
  
  
  CONCLUSIONS
  The use of statins and antiplatelet therapy is associated with a significant reduction in the occurrence of venous thromboembolism with a dose-related response of statins.
authors.affiliation: Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA. danai_md@hotmail.com
authors.forename: Danai
authors.initials: D
authors.lastname: Khemasuwan
authors.forename: Young Kwang
authors.initials: YK
authors.lastname: Chae
authors.forename: Shikha
authors.initials: S
authors.lastname: Gupta
authors.forename: Alejandra
authors.initials: A
authors.lastname: Carpio
authors.forename: Jeong Hyun
authors.initials: JH
authors.lastname: Yun
authors.forename: Stefan
authors.initials: S
authors.lastname: Neagu
authors.forename: Anabella B
authors.initials: AB
authors.lastname: Lucca
authors.forename: Matias E
authors.initials: ME
authors.lastname: Valsecchi
authors.forename: Jorge I
authors.initials: JI
authors.lastname: Mora
mesh_terms: D000368:Aged; D001241:Aspirin / Q000008:administration & dosage; D050197:Atherosclerosis / Q000188:drug therapy / Q000453:epidemiology; D002544:Cerebral Infarction / Q000188:drug therapy / Q000453:epidemiology; D000077144:Clopidogrel; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D015994:Incidence; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000453:epidemiology; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D016016:Proportional Hazards Models; D011655:Pulmonary Embolism / Q000453:epidemiology / Q000517:prevention & control; D012189:Retrospective Studies; D040242:Risk Reduction Behavior; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D054556:Venous Thromboembolism / Q000453:epidemiology / Q000517:prevention & control*
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin