Why the study?
Mavacamten can cause left ventricular systolic dysfunction in obstructive hypertrophic cardiomyopathy, but clinical cohort rates differ from trials, prompting investigation into predictive baseline features.
May inform closer echocardiographic monitoring in mavacamten-treated obstructive HCM; leaves open whether risk-stratified interventions improve outcomes.
The cardiac myosin inhibitor mavacamten is used to alleviate symptoms in obstructive hypertrophic cardiomyopathy (oHCM).1, 2 However, it can cause left ventricular systolic dysfunction (LVSD), which occurred in 8.7% of patients in EXPLORER-HCM and 13.8% in VALOR-HCM,3, 4 and less frequently in clinical cohorts.5 Given differences in baseline demographics, we hypothesized that certain features would be associated with LVSD. Accordingly, we examined predictors of LVSD in a single-center cohort of symptomatic adults with oHCM, left ventricular outflow tract (LVOT) gradients of ≥30 mmHg at rest or ≥50 mmHg with provocation refractory to first-line therapy, NYHA class ≥2 symptoms treated with mavacamten for ≥8 weeks who enrolled in the HCM program registry All patients signed informed consent as approved by the NYU Grossman School of Medicine institutional review board.
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Massera et al. (2026) studied this question.
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