Key result
Beta blockers, CCBs, and RAS antagonists reduce myocardial necrosis ~17% in myocarditis animal models.
Why the study?
Current myocarditis guidelines do not advocate treatment to prevent myocardial injury and scar deposition in patients with myocarditis and normal left ventricular ejection fraction.
Do beta blockers, calcium channel blockers, and renin-angiotensin system antagonists reduce necrosis, fibrosis, and calcification in animal models of myocarditis?
Population
52 animal in vivo studies of myocarditis
Comparison
Beta blockers, calcium channel blockers, or renin-angiotensin system antagonists vs untreated controls
Design
Systematic review and meta-analysis
Authors
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May inform human myocarditis trials; extends animal evidence to fibrosis and calcification.
Meta-Analysis (n=2,220)
Do beta blockers, calcium channel blockers, and renin-angiotensin system antagonists reduce necrosis, fibrosis, and calcification in animal models of myocarditis?
Effect estimate: WMD 16.9% reduction (95% CI 13.2-20.7%)
p-value: p=<0.001
ACE inhibitors and beta blockers significantly reduce myocardial necrosis, fibrosis, and calcification in animal models of myocarditis, suggesting a potential role for these therapies in preventing myocardial injury.
Silverblatt et al. (2019) conducted a meta-analysis in Myocarditis (animal models) (n=2,220). Beta blockers, calcium channel blockers, and renin-angiotensin system antagonists vs. Untreated controls (sham treatment) was evaluated on Necrosis (WMD 16.9% reduction, 95% CI 13.2-20.7%, p=<0.001). Treatment with beta blockers, calcium channel blockers, and renin-angiotensin system antagonists reduced myocardial necrosis by 16.9% compared to untreated controls in animal models of myocarditis.
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