Systolic and diastolic properties of univentricular hearts in children: insights from physiologic indices that reflect calcium cycling.

Physiologic indices that reflect intracellular Ca2+ cycling were chosen to evaluate contraction and relaxation properties of the univentricular heart. We hypothesized that these indices would be impaired in univentricular hearts. With advances in surgical palliation, an increasing number of children are surviving with univentricular hearts supporting the systemic circulation. Similar to the adult failing heart, single ventricles may also manifest impaired Ca2+ cycling, which may have important therapeutic implications. In our study, we did not actually measure Ca2+ uptake or transients in the cardiac myocyte. Rather, we used previously validated physiologic indices that are known to reflect Ca2+ cycling. Sixteen children were studied, eight with single ventricles (SV) and eight as matched control subjects. Systolic properties were studied using maximal derivative of ventricular pressure (dP/dtmax), force-frequency relationship, and mechanical restitution. Diastolic properties were assessed using time constant of relaxation (tau) and the relaxation-frequency relationship. The critical HR (HRcrit) was assessed from the force-frequency relationship and relaxation-frequency relationship. DP/dtmax and tau were calculated from micromanometric tracings at increasing HRs, generated by right atrial pacing. In SV patients, dP/dtmax was lower than in the control group at each matched HR, and the force-frequency relationship was shifted downward. Restitution of contractility was slower in patients with SV. Tau was similar in both groups at lower HRs but significantly prolonged in the SV group at faster HRs. In the SV, HRcrit was significantly shifted to the left. These findings indicate impaired systolic and diastolic properties of univentricular heart, especially at increased HRs. Because these physiologic indices reflect Ca2+ cycling, it is speculated that the phenomenon of Ca2+ cycling may be impaired in the myocytes of univentricular hearts.