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Meta-Analysis
. 2025 Feb 23;12(1):e003215.
doi: 10.1136/openhrt-2025-003215.

Efficacy of cardiac myosin inhibitors mavacamten and aficamten in hypertrophic cardiomyopathy: a systematic review and meta-analysis of randomised controlled trials

Affiliations
Meta-Analysis

Efficacy of cardiac myosin inhibitors mavacamten and aficamten in hypertrophic cardiomyopathy: a systematic review and meta-analysis of randomised controlled trials

Ayesha Aman et al. Open Heart. .

Abstract

Background: Unlike other suggested therapies, myosin inhibitors have been shown to change the course of hypertrophic cardiomyopathy by altering the contractile mechanics of cardiomyocytes. This meta-analysis sought to determine the efficacy of mavacamten and aficamten in hypertrophic cardiomyopathy.

Methods: The online databases were searched from inception to July 2024, including the Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, ClinicalTrials.gov. The meta-analytical data were pooled using risk ratios (RRs) with 95% CI, standard mean difference (SMD) and SE.

Results: A total of 6 randomised controlled trials with 826 hypertrophic cardiomyopathy patients (mean age±SD up to 59.8±14.2 years in intervention vs 60.9±10.5 years in placebo) were included in our study. Of these, 443 received a cardiac myosin inhibitor and 383 received a placebo. The resting left ventricular outflow tract (LVOT) gradient between the two groups was considerably improved by cardiac myosin inhibitors (MD -57.27; 95% CI -63.05 to -51.49). Significant differences were also observed in the post-Valsalva LVOT gradient between the two groups (MD -55.86; 95% CI -65.55 to -46.18). Significantly decreased left ventricle ejection fraction (LVEF) was also seen (MD -4.74; 95% CI -7.22 to -2.26). The New York Health Association (NYHA) class improvement between the two groups also changed significantly (RR 2.21; 95% CI 1.75 to 2.80). Cardiac myosin inhibitors also caused significant improvement in the Kansas City Cardiomyopathy Questionnaire in a Clinical Summary Score between the two groups (MD 7.71; 95% CI 5.37 to 10.05) and significant reduction in the N-terminal pro-B-type natriuretic peptide (SMD -13.27; 95% CI -17.51 to -9.03) and the cardiac troponin I (SMD -11.90; 95% CI -15.07 to -8.72).

Conclusion: According to our meta-analysis, cardiac myosin inhibitors significantly improve the resting and post-Valsalva LVOT gradient, reduce the LVEF and improve the NYHA class and cardiac biomarkers when compared with the placebo.

Prospero registration number: CRD52024586161.

Keywords: Cardiomyopathies; Cardiomyopathy, Hypertrophic; Meta-Analysis.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1. PRISMA flow diagram of included and excluded trials. PRISMA, Preferred Reporting Items for Systematic Reviews and Meta-Analyses.
Figure 2
Figure 2. Quality assessment of the included randomised controlled trials.
Figure 3
Figure 3. Forest plot of change in resting LVOT gradient. LVOT, left ventricular outflow tract.
Figure 4
Figure 4. Forest plot of sensitivity analysis of change in resting LVOT gradient. LVOT, left ventricular outflow tract.
Figure 5
Figure 5. Forest plot of change in post-Valsalva LVOT gradient. LVOT, left ventricular outflow tract.
Figure 6
Figure 6. Forest plot of sensitivity analysis of change in post-Valsalva LVOT gradient. LVOT, left ventricular outflow tract.
Figure 7
Figure 7. Forest plot of subgroup analysis of change in post-Valsalva LVOT gradient. LVOT, left ventricular outflow tract.
Figure 8
Figure 8. Forest plot of change in LVEF.
Figure 9
Figure 9. Forest plot of sensitivity analysis of change in LVEF.
Figure 10
Figure 10. Forest plot of NYHA class improvement.
Figure 11
Figure 11. Forest plot of change in KCCQ-CSS.
Figure 12
Figure 12. Forest plot of change in NT-proBNP.
Figure 13
Figure 13. Forest plot of sensitivity analysis of change in NT-proBNP.
Figure 14
Figure 14. Forest plot of change in cTnI.
Figure 15
Figure 15. Forest plot of sensitivity analysis of change in cTnI.

References

    1. Maron BJ, Maron MS. Hypertrophic cardiomyopathy. The Lancet. 2013;381:242–55. doi: 10.1016/S0140-6736(12)60397-3. - DOI - PubMed
    1. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA. 2002;287:1308–20. doi: 10.1001/jama.287.10.1308. - DOI - PubMed
    1. Iavarone M, Monda E, Vritz O, et al. Medical treatment of patients with hypertrophic cardiomyopathy: An overview of current and emerging therapy. Arch Cardiovasc Dis. 2022;115:529–37. doi: 10.1016/j.acvd.2022.06.003. - DOI - PubMed
    1. Teekakirikul P, Zhu W, Huang HC, et al. Hypertrophic Cardiomyopathy: An Overview of Genetics and Management. Biomolecules. 2019;9:878. doi: 10.3390/biom9120878. - DOI - PMC - PubMed
    1. Ho CY, Mealiffe ME, Bach RG, et al. Evaluation of Mavacamten in Symptomatic Patients With Nonobstructive Hypertrophic Cardiomyopathy. J Am Coll Cardiol. 2020;75:2649–60. doi: 10.1016/j.jacc.2020.03.064. - DOI - PubMed

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