Key result
Renal sympathetic denervation significantly improved left ventricular ejection fraction (43.80% vs 36.78%, p<0.05) and attenuated cardiomyocyte apoptosis compared to sham in dogs with myocardial infarction-induced heart failure.
Why the study?
Does renal sympathetic denervation improve cardiac function and attenuate myocardiocyte apoptosis in dogs with myocardial infarction-induced heart failure?
Does renal sympathetic denervation improve cardiac function and attenuate myocardiocyte apoptosis in dogs with myocardial infarction-induced heart failure?
Absolute Event Rate: 43.8% vs 36.78%
p-value: p=<0.05
Renal sympathetic denervation improves cardiac function and attenuates cardiomyocyte apoptosis and endoplasmic reticulum stress in a canine model of myocardial infarction-induced heart failure.
Supports sympathetic modulation research in ischemic HF models; leaves open clinical translation to humans.
BACKGROUND: Myocardial apoptosis is important in the pathogenesis and progression of myocardial infarction-induced heart failure (MI-HF). Renal sympathetic denervation (RDN) has become a promising therapeutic strategy for the treatment of HF. Previous studies have shown that RDN could improve heart function Yao et al. (Exp Ther Med 14:4104-4110, 2017). However, whether and how RDN regulates myocardial apoptosis in MI-HF is unclear. This study sought to evaluate the effects of RDN on cardiac function and apoptosis-related gene expression in MI-HF dogs. METHODS: Eighteen healthy mongrel dogs were randomly divided into control group(n = 6), model group(n = 6) and treatment group(n = 6). MI-HF was established in model group and treatment group by anhydrous alcohol embolization, after heart failure dogs in the treatment group and model group proceeded bilateral renal artery ablation and bilateral renal arteriography, respectively. The cardiac function parameters were evaluated by echocardiographic; the serum NT-BNP level was detected by ELISA; the degree of myocardial fibrosis was observed through masson staining; the expression of MMP-2, MMP-9 in the cardiac were got by immunohistochemistry. TUNEL method was used to observe cardiomyocyte apoptotsis and calculate the apoptosis index (AI). Relative expression of Bcl-2 and Bax, Caspase3 and GRP78 were detected using RT-PCR and Western Blot. Renal artery H&E staining and serum creatinine were conducted to access the efficacy and safety of RDN. RESULTS: Four weeks after RDN, the LVEDD, LVESD and LVEDP decreased, and the LVEF and LVSP increased in the treatment group compared with those in the control group (all P < 0.05). Moreover, NT-BNP, an indicator of cardiac function was decreased. Additionally, MMP-2 and MMP-9 levels in the myocardium decreased significantly in the treatment group. Furthermore, the levels of Bax, and caspase 3 decreased, while the level of Bcl-2 increased. Thus, myocardial apoptosis was attenuated in RDN treated dogs. We also found that the level of GRP78 which is activated in response to endoplasmic reticulum (ER) stress, was decreased. However, serum creatinine levels were not significantly different between the RND-treated dogs and the control dogs. CONCLUSION: Cardiac function was improved by RDN treatment through regulating apoptosis and ER stress in cardiomyocytes in dogs after MI.
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Wang et al. (2018) studied Myocardial infarction-induced heart failure (n=18). Renal sympathetic denervation vs. Sham procedure (model group) was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.05). Renal sympathetic denervation significantly improved left ventricular ejection fraction (43.80% vs 36.78%, p<0.05) and attenuated cardiomyocyte apoptosis compared to sham in dogs with myocardial infarction-induced heart failure.
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