The management of obstructive hypertrophic cardiomyopathy (HCM) has been transformed by the advent of cardiac myosin inhibitors (CMIs), such as mavacamten and aficamten. Unlike traditional pharmacotherapy, which primarily addresses symptoms, CMIs target the underlying mechanism of sarcomeric hypercontractility, offering significant reductions in left ventricular outflow tract (LVOT) gradients and improved functional capacity. This review evaluates the evolving role of CMIs in refining surgical candidate selection and postoperative care. Clinically, CMIs function as an in vivo “biological test” to distinguish between dynamic, functional obstruction—often manageable with medication—and fixed anatomical obstruction driven by complex septal or mitral substrates. While clinical trials demonstrate that CMIs can delay or prevent the need for SRT in a significant proportion of patients, surgery remains the definitive solution for those with dominant structural anomalies or drug intolerance. Consequently, the therapeutic paradigm is shifting from a binary “drugs or surgery” approach to a synergistic model. In this framework, CMIs optimize the identification of patients truly requiring structural myectomy while serving as a valuable adjunct for managing residual hypercontractility, ultimately facilitating a personalized, multidisciplinary approach to HCM treatment.
Ferraresi et al. (Wed,) studied this question.
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