Key result
Cardiac shock wave therapy cuts fibrosis by ~56% and improves LVEF in heart failure rats.
Why the study?
Although cardiac shock wave therapy is effective for post-AMI heart failure, its beneficial effects on anti-fibrosis and the underlying molecular mechanism remain poorly understood.
Does cardiac shock wave therapy improve ventricular function and reduce fibrosis in a rat model of post-infarction heart failure?
Does cardiac shock wave therapy improve ventricular function and reduce fibrosis in a rat model of post-infarction heart failure?
Absolute Event Rate: 52.13% vs 30.42%
p-value: p=<0.05
Cardiac shock wave therapy mitigates post-infarction heart failure and cardiac fibrosis in rats by activating the PI3K/Akt signaling pathway.
CSWT anti-fibrotic effects in rat AMI models; leaves open translation to human HF therapy.
Objection: Cumulative studies have identified the effectiveness of cardiac shock wave therapy (CSWT) in treating heart failure after acute myocardial infarction (AMI), but little have been discussed with regard to the beneficial effects of CSWT on anti-fibrosis along with the underlying mechanism. In this study, we investigated whether CSWT could reduce post-AMI fibrosis and further explored the molecular mechanism. Methods: Rat heart failure (HF) models induced by ligating the left anterior descending coronary artery were established and validated by echocardiography. Eligible animals were randomly categorized into five groups: the sham group, the HF group, the HF + CSWT group, the HF + LY294002 group, and the HF + CSWT + LY294002 group. The cardiac weight, serum level of BNP, NT-pro BNP and echocardiography parameters were measured to assess cardiac function in different groups. Masson's trichrome staining was used to assess the proportions of the fibrotic area. The expression level of CD34, αSMA was measured by RT-PCR, Immunohistochemistry and Immunofluorescent analyses and the level of PI3K/Akt was quantified by Immunohistochemistry and Western blotting. Results: The application of CSWT significantly improved cardiac function and reduced myocardial fibrosis and level of CD34 and αSMA, compared to the HF group. CSWT led to significant elevations of p-PI3K and p-Akt expression levels compared to that of the HF group and the inhibition of the PI3K/Akt pathway abolished the observed beneficial effects of CSWT. Conclusion: CSWT can facilitate the alleviation of cardiac fibrosis induced by AMI through the activation of PI3K/Akt signaling pathway.
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Wang et al. (2021) studied Post-infarction heart failure (n=50). Cardiac shock wave therapy (CSWT) vs. No CSWT (Heart failure control) was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.05). Cardiac shock wave therapy significantly improved left ventricular ejection fraction (52.13% vs 30.42%) and reduced myocardial fibrosis area (23.63% vs 53.89%) compared to untreated heart failure rats.
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