title: Free triiodothyronine level indicates the degree of myocardial injury in patients with acute ST-elevation myocardial infarction.
abstract: BACKGROUND
  Previous studies have suggested that hypothyroidism correlated with coronary heart diseases (CHD) mortality in long-term cohort, but whether the thyroid function status is associated with myocardial injury in acute ST-elevation myocardial infarction (STEMI) has not been investigated sufficiently.
  
  
  METHODS
  Five hundred and eighty-two hospitalized patients from January 2010 to December 2011, with the diagnosis of STEMI, were enrolled in this study. All patients underwent testing for thyroid function status, cardiac troponin I (cTnI), cardiac enzymes, C-reactive protein (CRP). We investigated the association between thyroid hormone levels and cardiac markers (creatine kinase-MB and cTnI), and thus evaluated the potential role of thyroid function status in predicting the myocardial injury.
  
  
  RESULTS
  There were 76 patients (13.06%) who had hypothyroidism including low-T3-syndrome (34 patients, 5.84%), subclinical hypothyroidism (28 patients, 4.81%) and clinical hypothyroidism (14 patients, 2.41%). After adjusting for conventional risk factors (age, gender, smoking, diabetes mellitus, dyslipidemia, hypertension), free triiodothyronine (FT3) was significantly and negatively correlated with log-CKMB (r = -0.244, P < 0.001) and log-cTnI (r = -0.290, P < 0.001), indicating that the lower thyroid hormone level correlates with the severer cardiac injury in STEMI patients. FT3 also had a moderate negative correlation with CRP (r = -0.475, P < 0.001), which might indicate that hypothyroidism may activate the inflammation response. No significant correlation was found between other thyroid parameters (TSH, FT4) and cardiac markers.
  
  
  CONCLUSIONS
  As the lower FT3 level correlates with higher level of cardiac markers and lower left ventricular ejection fraction (LVEF), the hypothyroidism may be a predictor for myocardial injury in STEMI. And these results may warrant further study to investigate whether reversing the hypothyroidism could benefit the STEMI patients.
authors.affiliation: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
authors.forename: Wen-yao
authors.initials: WY
authors.lastname: Wang
authors.forename: Yi-da
authors.initials: YD
authors.lastname: Tang
authors.forename: Min
authors.initials: M
authors.lastname: Yang
authors.forename: Cheng
authors.initials: C
authors.lastname: Cui
authors.forename: Mu
authors.initials: M
authors.lastname: Mu
authors.forename: Jie
authors.initials: J
authors.lastname: Qian
authors.forename: Yue-jin
authors.initials: YJ
authors.lastname: Yang
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D013961:Thyroid Gland / Q000378:metabolism; D014284:Triiodothyronine / Q000097:blood*; D019210:Troponin I / Q000378:metabolism*
chemical_list: D019210:Troponin I; D014284:Triiodothyronine; D002097:C-Reactive Protein