Key result
Poge heart-saving decoction reduces LVEDd and LVEDs and reverses ventricular remodeling in heart failure rats.
Why the study?
Poge heart-saving decoction has been used to treat heart failure in China, but its effect on cardiac function and underlying mechanism required exploration.
Does Poge heart-saving decoction improve cardiac function and reverse ventricular remodeling in an adriamycin-induced heart failure rat model?
RCT (n=60)
randomly divided
No
Does Poge heart-saving decoction improve cardiac function and reverse ventricular remodeling in an adriamycin-induced heart failure rat model?
p-value: p=<0.05
In a rat model of adriamycin-induced heart failure, Poge heart-saving decoction improved cardiac function and reversed ventricular remodeling, potentially through RAAS inhibition.
Hypothesis-generating in rodent heart failure; leaves open any clinical translation or therapeutic role in humans.
BACKGROUND: Poge heart-saving decoction (PHSD) has been used as a medicine treating heart failure in China for many years. The study aimed to explore the effect of PHSD on cardiac function in heart failure conditions and its underlying mechanism. METHODS: Adriamycin was used to induce the model of heart failure (HF) in rats. Sixty rats were randomly divided into six groups: blank control group, sham group, 9.33 g/kg group (low-PHSD, test group), 13.995 g/kg group (moderate-PHSD, test group), 18.66 g/kg group (high-PHSD, test group), and fosinopril group (4.67 mg/kg, comparison test group). Cardiac ultrasound was used to evaluate the cardiac function of the rats, and radioimmunoassay was used to measure aldosterone (ALD) and angiotensin II (AngII) levels in the serum. RESULTS: < 0.05). The histopathological changes of the myocardium in the sham group showed the disorganized fiber, shaded staining, fracture, and zonation. The fracture of the myocardium was relieved in all groups except the sham group and the blank control group. CONCLUSION: Therefore, PHSD could shorten LVEDd and LVEDs of rats and reverse ventricular remodeling. The mechanism might be related to the inhibition of the activation level of renin-angiotensin-aldosterone system (especially ALD and AngII) and decreasing the postload of the heart.
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Liu et al. (2020) conducted an RCT in Heart failure (n=60). Poge heart-saving decoction (PHSD) vs. Blank control, sham group, and fosinopril (4.67 mg/kg) was evaluated on Cardiac function (LVEDd, LVEDs) and ventricular remodeling (p=<0.05). Poge heart-saving decoction shortened LVEDd and LVEDs and reversed ventricular remodeling in a rat model of heart failure (P<0.05).
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