Cardiac myosin inhibitor has favorable effects on cardiac structure, function and fibrosis in oHCM
New data from the CMR sub-study of FOREST-HCM showed that aficamten has favorable effects on cardiac structure, function and fibrosis in patients with obstructive hypertrophic cardiomyopathy (oHCM).
In the FOREST-HCM CMR sub-study, treatment with aficamten for 48 weeks improved cardiac remodeling and function, and stabilized myocardial fibrosis in patients with oHCM. In a total of 16 patients who completed CMR at baseline and at 48 weeks, treatment with aficamten improved LV mass index (-11.4 g/m² ±19.4; p=0.03), maximum LV septal wall thickness (-1.3 mm ±1.8; P=0.02), LA volume (-16.3 ml/m² ±26.4; P=0.05), mitral regurgitant (MR) volume (-12.9 ml ±15.1; P=0.01), and MR fraction (-9.5% ±15.1; P=0.05) from baseline to 48 weeks. Moreover, treatment with aficamten for 48 weeks stabilized interstitial and replacement myocardial fibrosis, and did not increase in the fibrosis mass (absolute mass of late gadolinium enhancement: -0.6 g ±5.0; p=0.64).
FOREST-HCM (Follow-up, Open-Label, Research Evaluation of Sustained Treatment with Aficamten in HCM) is an on-going open label extension trial of aficamten in patients with HCM. Previously, it was shown in FOREST-HCM that treatment with aficamten in patients with oHCM led to sustained reductions in LVOT gradients and cardiac biomarkers, and improved symptoms, without treatment interruptions due to low LVEF.