inotropie

Inotropie, or inotropy, is the property of the heart muscle that determines the force of contraction during systole. A positive inotropic effect increases contractile strength, while a negative inotropic effect reduces it. Inotropie is distinct from chronotropy (heart rate) and lusitropy (relaxation).

Contractility arises from intracellular calcium handling, the sensitivity of the myofilaments to calcium, and sympathetic nervous system activity. Clinically, contractility is not measured directly in routine care; surrogates include changes in stroke volume, ejection fraction, and the maximum rate of rise of left ventricular pressure (dp/dt max). Research contexts use indices like end-systolic elastance (Ees) to assess load-independent contractility.

Pharmacologic modulation of inotropie is common in clinical practice. Positive inotropes increase contractility and are used in acute heart failure or cardiogenic shock. Examples include beta-adrenergic agonists such as dobutamine and dopamine, phosphodiesterase inhibitors such as milrinone, and calcium sensitizers such as levosimendan. Cardiac glycosides like digoxin also have inotropic effects by inhibiting the Na+/K+ ATPase, though their onset is slower and their hemodynamic impact is variable. Negative inotropes, such as certain beta-blockers, reduce contractility but have therapeutic roles in managing arrhythmias and ischemic heart disease.

Clinical considerations emphasize caution with inotropie. Positive inotropes can provoke tachyarrhythmias, increase myocardial oxygen demand, and cause hypotension. In chronic heart failure, prolonged use of positive inotropes is associated with worse outcomes, so they are typically reserved for short-term stabilization or bridge therapy with careful titration and monitoring.