Mavacamten reduced peak force by 40% at 0.33 µM and by 85% at 0.5 µM in human engineered heart tissues, while improving diastolic function by reducing diastolic stiffness.
Does mavacamten alter length-dependent contractility and diastolic function in human engineered heart tissue?
Mavacamten decreases inotropy and improves lusitropy (diastolic function) in human engineered heart tissue while preserving length-dependent contractility, providing mechanistic support for its clinical use in hypertrophic cardiomyopathy.
p-value: p=0.0009
We applied innovative methods to comprehensively characterize the length and load-dependent behaviors of engineered human cardiac muscle when treated with the cardiac β-myosin specific inhibitor mavacamten, a drug on the verge of clinical implementation for hypertrophic cardiomyopathy. We find mechanistic support for the role of mavacamten in improving diastolic function of cardiac tissue and note novel effects on work and power.
Sewanan et al. (Fri,) conducted a other in Hypertrophic cardiomyopathy (in vitro model). Mavacamten vs. Baseline (paired measurements) was evaluated on Peak force (p=0.0009). Mavacamten reduced peak force by 40% at 0.33 µM and by 85% at 0.5 µM in human engineered heart tissues, while improving diastolic function by reducing diastolic stiffness.