Abstract
BackgroundLeft ventricular (LV) remodeling following large transmural myocardial infarction (MI) remains a pivotal clinical issue despite the advance of medical treatment over the past few decades. Identification of new medications to improve the remodeling process and prevent progression to heart failure after MI is critical. Thyroid hormones (THs) have been shown to improve LV function and remodeling in animals post-MI and in the human setting. However, changes in underlying cellular remodeling resulting from TH treatment are not clear.MethodsMI was produced in adult female Sprague–Dawley rats by ligation of the left descending coronary artery. L-thyroxine (T4) pellet (3.3 mg, 60 days sustained release) was used to treat MI rats for 8 weeks. Isolated myocyte shape, arterioles, and collagen deposition in the non-infarcted area were measured at terminal study.ResultsT4 treatment improved LV ±dp/dt, normalized TAU, and increased myocyte cross-sectional area without further increasing myocyte length in MI rats. T4 treatment increased the total LV tissue area by 34%, increased the non-infarcted tissue area by 41%, and increased the thickness of non-infarcted area by 36% in MI rats. However, myocyte volume accounted for only ~1/3 of the increase in myocyte mass in the non-infarct area, indicating the presence of more myocytes with treatment. T4 treatment tended to increase the total length of smaller arterioles (5 to 15 μm) proportional to LV weight increase and also decreased collagen deposition in the LV non-infarcted area. A tendency for increased metalloproteinase-2 (MMP-2) expression and tissue inhibitor of metalloproteinases (TIMPs) -1 to −4 expression was also observed in T4 treated MI rats.ConclusionsThese results suggest that long-term T4 treatment after MI has beneficial effects on myocyte, arteriolar, and collagen matrix remodeling in the non-infarcted area. Most importantly, results suggest improved survival of myocytes in the peri-infarct area.
Highlights
Left ventricular (LV) remodeling after myocardial infarction (MI) includes infarct expansion and hypertrophy of non-infarcted myocardium, fibrosis, LV chamber dilatation, LV functional deterioration and progression to heart failure [1,2,3]
T4 treatment significantly increased heart weight, heart weight-to-body weight ratio, and LV weight in MI animals compared to untreated MI animals
MI rats with small infarcts less than 7 mm were excluded from this study
Summary
Left ventricular (LV) remodeling after myocardial infarction (MI) includes infarct expansion and hypertrophy of non-infarcted myocardium, fibrosis, LV chamber dilatation, LV functional deterioration and progression to heart failure [1,2,3]. Slow progression to chronic heart failure continues with large transmural MI as the loss of infarcted tissue and volume overload (chamber dilation) is often out of proportion to the hypertrophic response. Searching for new medications that can further improve the remodeling process is critical for preventing heart failure following MI. Left ventricular (LV) remodeling following large transmural myocardial infarction (MI) remains a pivotal clinical issue despite the advance of medical treatment over the past few decades. Identification of new medications to improve the remodeling process and prevent progression to heart failure after MI is critical. Changes in underlying cellular remodeling resulting from TH treatment are not clear
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