Why the study?
To evaluate the efficacy, safety, and possible mechanisms of Astragalus membranaceus for viral myocarditis.
Does Astragalus membranaceus improve clinical outcomes and reduce myocardial injury markers in patients and animal models with viral myocarditis?
Does Astragalus membranaceus improve clinical outcomes and reduce myocardial injury markers in patients and animal models with viral myocarditis?
Astragalus membranaceus may offer cardioprotective effects in viral myocarditis by reducing myocardial injury markers and improving clinical efficacy, though the quality of existing evidence is generally low.
AM improves VM treatment efficiency and lowers myocardial injury markers without added adverse events; extends animal data but low-quality RCTs leave practice change premature.
Astragalus membranaceus (AM) is a traditional Chinese medicine, which possesses a variety of biological activities in the cardiovascular systems. We conducted a clinical and preclinical systematic review of 28 randomized clinical control studies with 2522 participants and 16 animal studies with 634 animals to evaluate the efficacy, safety, and possible mechanisms of AM for viral myocarditis (VM). The search strategies were performed in 7 databases from inception to January 2020. Application of the Cochrane Collaboration’s tool 7-item checklist, SYRCLE’s tool 10-item checklist, and Rev-Man 5.3 software to analyze the risk of bias of studies and data. The results show the score of clinical study quality ranged from 3 to 7 points with an average of 3.32, and the score of animal study quality ranged from 2 to 5 points with an average of 3. In clinical study, AM significantly reduced serum myocardial enzymes and cardiac troponin I levels and improved the clinical treatment efficiency in VM patients compared with the control group ( <a:math xmlns:a="http://www.w3.org/1998/Math/MathML" id="M1"> <a:mi>P</a:mi> <a:mo><</a:mo> <a:mn>0.05</a:mn> </a:math> ). There was no significant difference in the incidence of adverse reactions ( <c:math xmlns:c="http://www.w3.org/1998/Math/MathML" id="M2"> <c:mi>P</c:mi> <c:mo>></c:mo> <c:mn>0.05</c:mn> </c:math> ). Significant increase of the survival rate and decrease of the cardiac cardiology score, cardiac enzymes, and cardiac troponin I were compared with the placebo group in animal studies ( <e:math xmlns:e="http://www.w3.org/1998/Math/MathML" id="M3"> <e:mi>P</e:mi> <e:mo><</e:mo> <e:mn>0.05</e:mn> </e:math> ). The possible mechanisms of AM are largely through antivirus and antivirus receptors, anti-inflammatory, antioxidation, antiapoptotic, antifibrosis, and reducing cardiac calcium load. In conclusion, the findings suggested that AM is a cardioprotection candidate drug for VM.
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Zheng et al. (2020) studied this question.
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