The effect of afterload on right ventricular pacing-induced left ventricular dysfunction: a translational study

Right ventricular (RV) pacing (RVP) impairs left ventricular (LV) function. Nevertheless, the interaction between arterial afterload and RVP-associated LV dysfunction has not been investigated yet.

We sought to examine the effect of afterload on RVP-evoked LV hemodynamic changes in patients with aortic stenosis (AS) undergoing transcatheter aortic valve implantation (TAVI) as well as in a small animal model of sustained LV pressure overload (PO).

Thirty-five patients with AS and a previously implanted pacemaker underwent detailed echocardiographic examination immediately before TAVI and also on the second postoperative day. The ultrasound measurements were carried out during intrinsic, narrow QRS rhythm and during frequency-matched RVP as well. Global myocardial work index (GMWI) was calculated to assess LV contractility. In parallel, LV pressure-volume analysis was performed in Wistar rats with transverse aortic constriction (TAC) or sham operation (Sham) during intrinsic narrow QRS rhythm (termed as TAC-Vsense and Sham-Vsense) as well as during RVP (termed as TAC-Vpace and Sham-Vpace). RVP was achieved in rats by an octopolar electrophysiology catheter placed in the RV.

RVP decreased LV contractility in AS patients before and after TAVI as well. Nevertheless, the extent of RVP-evoked LV dysfunction was alleviated following pressure unloading (ΔGMWI: -37±7 vs. -25±8%, before TAVI vs. after TAVI, P<0.05). Similarly, although RVP was associated with reduced LV contractility in both the TAC (the slope of the maximum rate of LV pressure rise-end-diastolic volume relation [dPdtmax-EDV]: 92±8 vs. 53±6mmHg/s/µl, TAC-Vsense vs. TAC-Vpace; P<0.05) and Sham groups (dPdtmax-EDV: 74±5 vs. 60±9 mmHg/s/µl, Sham-Vsense vs. Sham-Vpace; P<0.05), the negative inotropic effect of RVP was found to be stronger in the TAC compared to the Sham group (ΔdPdtmax-EDV: -42±4 vs. -19±6%; TAC vs. Sham, P<0.01). Furthermore, reduction of the maximal rate of LV pressure decrease (ΔdPdtmin: -20±3 vs. -5±5%, TAC vs. Sham, P<0.01) and prolongation of the active relaxation time constant (Δτ: 22±3 vs. 6±3%, TAC vs. Sham, P<0.01) also occurred to a greater extent in case of sustained LV PO, indicating augmented diastolic dysfunction.

Our translational results indicate that RVP-induced LV dysfunction might be afterload dependent.