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.
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?
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.
Effect estimate: WMD 16.9% reduction (95% CI 13.2-20.7%)
p-value: p=<0.001
Current myocarditis guidelines do not advocate treatment to prevent myocardial injury and scar deposition in patients with myocarditis and normal left ventricular ejection fraction. We aimed to ascertain the utility of beta blockers, calcium channel blockers and antagonists of the renin-angiotensin system in ameliorating myocardial injury, scar formation and calcification in animal in vivo models of myocarditis. The project was prospectively registered with the PROSPERO database of systematic reviews (CRD42018089336). Primary outcomes (necrosis, fibrosis and calcification) were meta-analysed with random-effects modelling. 52 studies were systematically reviewed. Meta-analysis was performed compared with untreated controls. In each study, we identified all independent comparisons of treatment versus control groups. The pooled weighted mean difference (WMD) indicated treatment reduced necrosis by 16.9% (71 controlled analyses, 95% CI 13.2-20.7%; P < 0.001), however there was less evidence of an effect after accounting for publication bias. Treatment led to a 12.8% reduction in fibrosis (73 controlled analyses, 95% CI 7.6-18.0%; P < 0.001). After accounting for publication bias this was attenuated to 7.8% but remained significant. Treatment reduced calcification by 4.1% (28 controlled analyses, 95% CI 0.2-8.0%; P < 0.0395). We observed significant heterogeneity in effect size in all primary endpoints, which was predominantly driven by differences between drug categories. Beta blockers and angiotensin-converting enzyme (ACE) inhibitors were the only agents that were effective for both necrosis and fibrosis, while only ACE inhibitors had a significant effect on calcification. This study provides evidence for a role for ACE inhibitors and beta blockers to prevent myocardial injury and scar deposition in in vivo models of myocarditis. There is a need for further well-designed studies to assess the translational application of these treatments.
Silverblatt et al. (Thu,) 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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