Key result
Ivabradine caused a mild regression of myocardial remodeling in an experimental model of ischemic heart failure, decreasing mean cardiomyocyte cross-sectional area by 1.31 times.
Why the study?
Does ivabradine improve myocardial remodeling in a rat model of ischemic heart failure?
Does ivabradine improve myocardial remodeling in a rat model of ischemic heart failure?
In a rat model of isoproterenol-induced ischemic heart failure, ivabradine attenuated myocardial remodeling and cardiomyocyte hypertrophy.
Answers are grounded in this paper and cite their sources.
May attenuate remodeling in this rat model; leaves open translation to human ischemic HF.
Aim. Experimental study of Ivabradine influence on myocardial remodeling in patients with ischemic chronic heart failure.Material and Methods. The ischemic model of heart failure (HF) was modeled in 30 mature rats by isoproterenol injection. All animals were divided into 3 groups (10 each): I – control; II – with model of HF; III – with HF model and Ivabradine usage. For calculation of metric characteristics of the cardiomyocytes UTHSCSA Image Tool® for Windows® (version 2.00) program equipment in interactive regime was used. Morphometric analysis was made by point-based calculation method with 72-network. Statistical analysis was made by standard program equipment “Statistica for Windows12.0” (StatSoft,Tulsa,OK,USA).Results. In experimental animals with model of ischemic HF the substantial hypertrophy of cardiomyocytes was observed. This process was characterized by increase in cardiomyocytes cross-sectional area, cross-sectional area of nuclei, decrease of nucleus-to-cytoplasm ratio and some discoordination of this parameter. In case of Ivabradine prescription we have noted reduction in myocardial hypertrophy processes with the following sings: decrease in mean cardiomyocytes cross-sectional area in 1.31 times (p<0,05), and mean cross-sectional area of nuclei – in 1.41 times (p<0,05).Conclusions. 1. In case of ischemic heart failure the substantial hypertrophy of cardiomyocytes with increase in mean parameters of their nuclei volume and nucleus-to-cytoplasm ratio disturbances were observed.2. Ivabradine caused a mild regression of myocardial remodeling, as evidenced by a decrease in the degree of cardiomyocytes and their nuclei hypertrophy, severity of parenchyma dystrophy and fibrosis of heart muscle.
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Fedorov et al. (2016) studied Ischemic chronic heart failure (experimental model) (n=30). Ivabradine vs. Heart failure model without treatment was evaluated on Mean cardiomyocyte cross-sectional area (µm²) (decreased by 1.31 times, p=<0.05). Ivabradine caused a mild regression of myocardial remodeling in an experimental model of ischemic heart failure, decreasing mean cardiomyocyte cross-sectional area by 1.31 times.
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