lusitropic

Lusitropy refers to the rate of myocardial relaxation during diastole. A positive lusitropic effect accelerates relaxation, while a negative lusitropic effect slows it. In the heart, relaxation is closely tied to intracellular calcium handling; faster removal of calcium from the cytosol into the sarcoplasmic reticulum, aided by SERCA2a and regulated by phospholamban phosphorylation, promotes quicker diastolic relaxation. Autonomic signaling, hormonal influences, and structural heart disease can modulate lusitropy.

Clinically, lusitropy is assessed indirectly through measures of diastolic function. Common indicators include the relaxation time constants such as Tau, the rate of pressure decline during relaxation (dP/dt min), and echocardiographic indices like the E/A ratio and deceleration time. These metrics help evaluate diastolic performance and the heart’s ability to fill effectively.

Pharmacologic and physiologic agents can produce positive or negative lusitropic effects. Positive lusitropy is observed with agents that enhance calcium reuptake and calcium handling, such as certain beta-adrenergic agonists (for example, dobutamine) and phosphodiesterase-3 inhibitors (such as milrinone), as well as calcium sensitizers like levosimendan in specific contexts. Negative lusitropy can occur with aging, myocardial fibrosis, diabetes, or drugs that blunt beta-adrenergic signaling. Understanding lusitropy is particularly relevant to conditions characterized by diastolic dysfunction, including heart failure with preserved ejection fraction, where improved relaxation can aid ventricular filling.