title: Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome.
abstract: BACKGROUND
  It is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event.
  
  
  METHODS
  Fifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5-10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T3), free T3, thyroxine (T4), free T4, troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group.
  
  
  RESULTS
  The T3 and free T3 levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T4, free T4 and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T3 and free T3 levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T3, free T3, T4 and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively).
  
  
  CONCLUSIONS
  TFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state.
authors.affiliation: Dicle University Medical Faculty Department of Cardiology, Diyarbakir, Turkey. kencan@dicle.edu.tr
authors.forename: Kenan
authors.initials: K
authors.lastname: Iltumur
authors.forename: Gonul
authors.initials: G
authors.lastname: Olmez
authors.forename: Zuhal
authors.initials: Z
authors.lastname: Ariturk
authors.forename: Tuncay
authors.initials: T
authors.lastname: Taskesen
authors.forename: Nizamettin
authors.initials: N
authors.lastname: Toprak
mesh_terms: D016887:Cardiopulmonary Resuscitation; D003327:Coronary Disease / Q000097:blood* / Q000150:complications*; D052279:Creatine Kinase, MB Form / Q000097:blood; D004554:Electric Countershock; D005067:Euthyroid Sick Syndromes / Q000097:blood / Q000150:complications / Q000175:diagnosis; D005260:Female; D005500:Follow-Up Studies; D006323:Heart Arrest / Q000097:blood* / Q000209:etiology* / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D016019:Survival Analysis; D013960:Thyroid Function Tests; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D019210:Troponin I / Q000097:blood
chemical_list: D019210:Troponin I; D014284:Triiodothyronine; D013972:Thyrotropin; D052279:Creatine Kinase, MB Form; D013974:Thyroxine