CLINICAL STUDY Thyroid hormone and recovery of cardiac function in patients with acute myocardial infarction: a strong association? Ioannis Lymvaios 1 , Iordanis Mourouzis, Dennis V Cokkinos 2 , Meletios A Dimopoulos 1 , Savvas T Toumanidis 1 and Constantinos Pantos Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, 11527 Goudi, Athens, Greece, 1 Department of Clinical Therapeutics, ‘Alexandra’ Hospital, Universityof Athens, 11528 Athens, Greece and 2 Biomedical Research Foundation, Academy of Athens, 11527 Athens, Greece (Correspondence should be addressed to C Pantos; Email: cpantos@med.uoa.gr) Abstract Objective: This study investigated whether changes in thyroid hormone (TH) in plasma are associated with the recovery of cardiac function in patients with acute myocardial infarction (AMI). Previous experimental studies have provided evidence of potential implication of TH signaling in post-ischemic recovery of cardiac function. Methods: A total of 47 patients with AMI and early reperfusion therapy were included in this study. Myocardial injury was analyzed by peak creatinine kinase–MB (CKMB) and cardiac function was assessed by echocardiographic left ventricular ejection fraction (LVEF%). Recovery of function (DEF%) was estimated as the difference of LVEF% between 48 h and 6 months (6 mo) after AMI. Total triiodothyronine (T 3 ), thyroxine (T 4 ), and TSH were measured in plasma at different time points (24 h, 48 h, 5 d, and 6 mo). Results: A significant correlation between LVEF% and T 3 (rZ0.5, PZ0.0004) was found early after AMI (48 h), whereas no correlation was observed between CKMB and T 3 (rZK0.04, PZ0.81). A strong correlation was found between DEF% and total T 3 (rZ0.64, PZ10 K6 ) at 6 mo after AMI. Furthermore, multivariate regression analysis revealed that T 3 at 6mo (rZ0.64, r 2 Z0.41, PZ10 K6 ) was an independent determinant of DEF%. Conclusion: Changes in T 3 levels in plasma are closely correlated with the early and late recovery of cardiac function after AMI. T 3 levels at 6 mo appear to be an independent predictor of late functional recovery. European Journal of Endocrinology 165 107–114 Introduction Acute and chronic illnesses can cause changes in thyroid hormone (TH) profile, a condition known as ‘non-thyroidal illness syndrome’ (1–3). This syndrome affects nearly 70% of patients hospitalized with diseases of various etiologies (4). The physiological significance of this response is not fully understood, and there is a long-lasting dilemma whether this abnormality needs correction (1, 2). Low triiodothyronine (T 3 ) state is common in severe chronic heart failure (5), acute myocardial infarction (AMI) (6–8), and cardiac surgery (9). Furthermore, changes in TH in plasma are linked to high mortality both in patients with heart failure (5) and those with AMI (8), indicating potential implication of TH signaling in the post-ischemic cardiac recovery. Inter- estingly, this hypothesis has recently been addressed in experimental models of ischemia–reperfusion and myocardial infarction in animals and accumulating evidence reveals that TH is critical for the response of the myocardium to ischemic stress and TH may possess cytoprotective properties that are ‘silent’ in healthy tissue, manifesting only during stress (10–13). Based on this evidence, this study investigated whether changes in TH in plasma are associated with early and late recovery of cardiac function in patients with AMI. This issue has not been previously addressed and may be of clinical relevance. AMI results in loss of cardiac function due to tissue necrosis, reperfusion injury, and cardiac remodeling, causing significant morbidity and mortality with a high risk (30–75%) of developing heart failure despite modern reperfusion and pharmacological therapy (14–17). Methods Patients and measurements A total of 47 patients (61.7% male, mean age 62.3 G10.2 years) admitted to the emergency cardiac care and diagnosed with ST elevation AMI (STEMI) were included in this study. AMI diagnosis and treatment was based on the guidelines of the European Society of European Journal of Endocrinology (2011) 165 107–114 ISSN 0804-4643 q 2011 European Society of Endocrinology DOI: 10.1530/EJE-11-0062 Online version via www.eje-online.org