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  • Author: Iordanis Mourouzis x
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Ioannis Lymvaios, Iordanis Mourouzis, Dennis V Cokkinos, Meletios A Dimopoulos, Savvas T Toumanidis and Constantinos Pantos


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.


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 (ΔEF%) was estimated as the difference of LVEF% between 48 h and 6 months (6 mo) after AMI. Total triiodothyronine (T3), thyroxine (T4), and TSH were measured in plasma at different time points (24 h, 48 h, 5 d, and 6 mo).


A significant correlation between LVEF% and T3 (r=0.5, P=0.0004) was found early after AMI (48 h), whereas no correlation was observed between CKMB and T3 (r=−0.04, P=0.81). A strong correlation was found between ΔEF% and total T3 (r=0.64, P=10−6) at 6 mo after AMI. Furthermore, multivariate regression analysis revealed that T3 at 6 mo (r=0.64, r 2=0.41, P=10−6) was an independent determinant of ΔEF%.


Changes in T3 levels in plasma are closely correlated with the early and late recovery of cardiac function after AMI. T3 levels at 6 mo appear to be an independent predictor of late functional recovery.

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Constantinos Pantos, Athanasios Dritsas, Iordanis Mourouzis, Antonios Dimopoulos, Georgios Karatasakis, Georgios Athanassopoulos, Sofia Mavrogeni, Athanasios Manginas and Dennis V Cokkinos

Objective: Previous experimental studies have provided evidence showing that changes in thyroid hormone signaling correspond to alterations in myocardial function in animal models of heart failure. The present study further explores whether thyroid hormone alterations are correlated with the functional status of the myocardium in patients with heart failure.

Methods: In this study, 37 patients with mean ejection fraction (EF%) of 26.2 (8.2) were included. Myocardial performance was assessed by echocardiography and cardiopulmonary exercise testing. Total tri-iodothyronine (T3), thyroxine, and TSH levels were measured in plasma.

Results: Total T3 was strongly correlated with VO2max (r = 0.78, P = 2 × 10−8). Furthermore, multivariate analysis revealed that total T3 was an independent predictor of VO2max (P = 0.000 005). A weaker but significant correlation was also found between total T3 and EF% (r = 0.56, P = 0.0004), systolic (r = 0.43, P = 0.009) and diastolic (r = 0.46, P = 0.004) blood pressure.

Conclusions: changes in thyroid hormone were closely correlated to myocardial functional status in patients with heart failure. These data probably indicate a possible role of thyroid hormone in the pathophysiology of heart failure and confirm previous experimental reports.

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Constantinos Pantos, Iordanis Mourouzis, Christodoulos Xinaris, Alexandros D Kokkinos, Konstantinos Markakis, Antonios Dimopoulos, Matthew Panagiotou, Theodosios Saranteas, Georgia Kostopanagiotou and Dennis V Cokkinos

The present study investigated whether changes in thyroid hormone (TH) signalling can occur after acute myocardial infarction (AMI) with possible physiological consequences on myocardial performance. TH may regulate several genes encoding important structural and regulatory proteins particularly through the TRα1 receptor which is predominant in the myocardium. AMI was induced in rats by ligating the left coronary artery while sham-operated animals served as controls. This resulted in impaired cardiac function in AMI animals after 2 and 13 weeks accompanied by a shift in myosin isoforms expression towards a fetal phenotype in the non-infarcted area. Cardiac hypertrophy was evident in AMI hearts after 13 weeks but not at 2 weeks. This response was associated with a differential pattern of TH changes at 2 and 13 weeks; T3 and T4 levels in plasma were not changed at 2 weeks but T3 was significantly lower and T4 remained unchanged at 13 weeks. A twofold increase in TRα1 expression was observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, while TRα1 expression remained unchanged at 2 weeks. A 2.2-fold decrease in TRβ1 expression was found in the non-infarcted area at 13 weeks, P<0.05, while no change in TRβ1 expression was seen at 2 weeks. Parallel studies with neonatal cardiomyocytes showed that phenylephrine (PE) administration resulted in 4.5-fold increase in the expression of TRα1 and 1.6-fold decrease in TRβ1 expression versus untreated, P<0.05. In conclusion, cardiac dysfunction which occurs at late stages after AMI is associated with increased expression of TRα1 receptor and lower circulating tri-iodothyronine levels. Thus, apo-TRα1 receptor state may prevail contributing to cardiac fetal phenotype. Furthermore, down-regulation of TRβ1 also contributes to fetal phenotypic changes. α1-adrenergic signalling is, at least in part, involved in this response.