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There are multiple pathophysiologic processes associated with HFrEF. One such process involves impaired contractility, which is the primary myocardial defect in the pathophysiology of HFrEF.1-3
Following an index event, there is progessive decline in left ventricular (LV) contractile function.3
Cellular-level progression of HFrEF involves multiple changes to cardiomyocyte structure and function, all of which impact cardiac contractility.2
Inotropy is the contractile ability of the cardiac muscle to generate a force of contraction independent of any load or stretch applied.1,7 Contractility manifests as myocardial fiber shortening, which increases ventricular pressure.5,8