title: Blood thrombogenicity is independently associated with serum TSH levels in post-non-ST elevation acute coronary syndrome.
abstract: BACKGROUND
  Higher serum TSH levels, both within the reference range and in those with subclinical hypothyroidism (SCH), have been associated with increased risk of atherosclerosis and cardiovascular (CV) events in a number of cross-sectional and longitudinal studies.
  
  
  OBJECTIVE
  Our objective was to evaluate blood thrombogenicity in patients post-non-ST elevation acute coronary syndrome (NSTE-ACS) in relation to their thyroid function. DESIGN, PATIENTS, AND OUTCOME MEASURE: At 1 week after troponin-positive NSTE-ACS, 70 patients who had been treated with optimal antiplatelet and secondary prevention therapy were studied. Patients with known thyroid disease or on medications affecting thyroid function were excluded. Blood thrombogenicity was assessed using the ex vivo Badimon perfusion chamber.
  
  
  RESULTS
  Serum TSH was associated with higher thrombus burden (β = .30; P = .01) independent of other well-established CV risk factors. Patients with SCH (n = 12; 17%) had a higher thrombus burden than euthyroid individuals as evidenced by the area of the thrombus: mean (SD) 23 608 (10 498) vs 16 661 (10 902) μm(2)/mm (P = .02). However, this association was not evident when the analysis was limited to patients with serum TSH within the reference range. In addition, neither serum free T4 nor free T3 had any significant association with thrombus area.
  
  
  CONCLUSIONS
  Serum TSH levels, particularly in the SCH range, are associated with higher thrombus burden despite optimal recommended secondary prevention therapy after NSTE-ACS. This may explain the higher CV risk seen in SCH patients. Future trials to assess the effect of individualized antithrombotic as well as thyroid hormone replacement therapy to reduce atherothrombotic risk in this population are needed.
authors.affiliation: Institutes of Cellular Medicine (G.V., K.B., S.M., A.Z.) and Institute of Genetic Medicine (S.R.), Newcastle University, Newcastle upon Tyne NE1 7RU, United Kingdom; Department of Cardiology (A.Z.), Freeman Hospital, Newcastle upon Tyne NE7 7DN, United Kingdom; and Gateshead Health National Health Service Foundation Trust (R.H., S.R.), Gateshead NE9 6SX, United Kingdom.
authors.forename: Girish
authors.initials: G
authors.lastname: Viswanathan
authors.forename: Karthik
authors.initials: K
authors.lastname: Balasubramaniam
authors.forename: Richard
authors.initials: R
authors.lastname: Hardy
authors.forename: Sally
authors.initials: S
authors.lastname: Marshall
authors.forename: Azfar
authors.initials: A
authors.lastname: Zaman
authors.forename: Salman
authors.initials: S
authors.lastname: Razvi
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology; D000368:Aged; D000818:Animals; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013552:Swine; D013927:Thrombosis / Q000097:blood* / Q000453:epidemiology / Q000209:etiology*; D013959:Thyroid Diseases / Q000097:blood / Q000150:complications / Q000453:epidemiology; D013960:Thyroid Function Tests; D013961:Thyroid Gland / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood*
chemical_list: D013972:Thyrotropin