Long-term thyroid hormone administration improves myocardial performance after myocardial infarction in rats

Abstract

Thyroid hormone (TH) is critical for tissue differentiation at early stages of development, induces physiological hypertrophy and regulates the expression of important contractile proteins. Furthermore, TH controls the response to stress by regulating important cardioprotective molecules such as heat shock proteins (HSPs). Thus, the present study investigated whether TH administration immediately after acute myocardial infarction can favorably remodel the postinfarcted myocardium. Acute myocardial infarction was induced in rats by coronary artery ligation (AMI, n=10) while SHAM operated animals served as controls (SHAM, n=8). TH was administered for 13 weeks (AMI-THYR, n=9). Cardiac contractile function and left ventricular (LV) chamber remodeling was assessed by serial echocardiography and in Langendorff heart preparations. AMI significantly reduced LV ejection fraction (EF%); 30.0 (s.e.m, 2.3) vs. 73.8 (1.8) in SHAM, p<0.05. +dp/dt and −dp/dt (in mm Hg/s) were 4051 (343) and 2333 (118) respectively for SHAM, 2102 (290) and 1368 (181) for AMI, p<0.05. With TH treatment, EF% was increased to 49.5 (2.7) in AMI-THYR, p<0.05 while +dp/dt and −dp/dt (in mm Hg/s) were 3708 (231) and 2035 (95) for AMI-THYR, p<0.05 vs. AMI. A marked elevation of the expression of β-MHC was found in the viable myocardium of AMI hearts which was prevented by TH. HSP70 myocardial content was decreased in AMI hearts and significantly increased after TH treatment. An ellipsoidal reshaping of LV chamber was observed with TH; cardiac sphericity index, (ratio of long/short axis, SI), was 1.98 (0.03) for SHAM, 1.52 (0.05) for AMI and 1.72 (0.02) for AMI-THYR, p<0.05. In conclusion, long-term TH administration immediately after AMI results in sustained improvement of cardiac haemodynamics.