Dysfunctional Ca2+ transport in heart disease jeopardizes systole and diastole, potentially triggering arrhythmogenic Ca2+ waves through mechanoelectric feedback in nonuniform cardiac muscle.
The hallmarks of the normal heartbeat are both rapid onset of contraction and rapid relaxation as well as an inotropic response to both increased end-diastolic volume and increased heart rate. At the microscopic level, Ca(2+) plays a crucial role in normal cardiac contraction. This paper reviews the cycle of Ca(2+) fluxes during the normal heartbeat, which underlie the coupling between excitation and contraction and permit a highly synchronized action of cardiac sarcomeres. Length dependence of the response of the regulatory sarcomeric proteins mediates the Frank-Starling Law of the heart. However, Ca(2+) transport may go astray in heart disease such as in congestive heart failure, and both jeopardize systole and diastole and triggering arrhythmias. The interaction between weak and strong segments in nonuniform cardiac muscle allows partial preservation of force of contraction but may further lead to mechanoelectric feedback or reverse excitation-contraction coupling mediating an early diastolic Ca(2+) transient caused by the rapid force decrease during the relaxation phase. These rapid force changes in nonuniform muscle may cause arrhythmogenic Ca(2+) waves to propagate by the activation of neighboring sarcoplasmic reticulum by diffusing Ca(2+) ions.
Hendrick E. D. J. ter Keurs (Sat,) conducted a review in Heart function and dysfunction. Ca2+ interaction with sarcomeric proteins was evaluated. Dysfunctional Ca2+ transport in heart disease jeopardizes systole and diastole, potentially triggering arrhythmogenic Ca2+ waves through mechanoelectric feedback in nonuniform cardiac muscle.