Key result
Emerging mitotropes and myotropes offer potential alternatives to traditional calcitropes for HF and cardiogenic shock.
This review highlights the mechanisms and risks of current calcitrope inotropes in heart failure and cardiogenic shock, while introducing emerging mitotrope and myotrope alternatives.
Reduced systolic function is central to the pathophysiology and clinical sequelae of acute decompensated heart failure (ADHF) with reduced ejection fraction and cardiogenic shock. These clinical entities are the final common pathway for marked deterioration of right or left ventricular function and can occur in multiple clinical presentations including severe ADHF, myocardial infarction, post-cardiac surgery, severe pulmonary hypertension, and advanced or end-stage chronic heart failure. Inotropic therapies improve ventricular systolic function and may be divided into three classes on the basis of their mechanism of action (calcitropes, mitotropes, and myotropes). Most currently available therapies for cardiogenic shock are calcitropes which can provide critical haemodynamic support, but also may increase myocardial oxygen demand, ischaemia, arrhythmia, and mortality. Emerging therapies to improve cardiac function such as mitotropes (e.g. perhexiline, SGLT2i) or myotropes (e.g. omecamtiv mecarbil) may provide useful alternatives in the future.
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DesJardin et al. (2021) conducted a review in Heart failure and cardiogenic shock. Inotropic therapies (calcitropes, mitotropes, and myotropes) was evaluated. Inotropic therapies for heart failure and cardiogenic shock can be divided into calcitropes, mitotropes, and myotropes, with emerging therapies potentially offering alternatives to current calcitropes.
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