Abstract
Heart failure can reflect impaired myofilament-level contraction. In healthy hearts, myofilaments become more sensitive to Ca2+ as cells are stretched. This fundamental property of myocardium is termed length-dependent activation and contributes to the Frank-Starling response. Mavacamten is a drug that binds to myosin. Mavacamten is under investigation as a potential therapy for heart disease. To investigate how mavacamten affects molecular-level contraction in failing human myocardium, we analyzed the contractile properties of permeabilized myocardial strips from the left-ventricular free wall of hearts that were explanted during a transplant at the University of Kentucky.
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