PhD Scientific Days 2026

Poster Session 2.Q - Cardiovascular Medicine and Research

Increased sensitivity to right ventricular pacing in left ventricular pressure overload – a translational study of left ventricular mechanics in aortic stenosis

Name of the presenter

Turschl, Timea Katalin

Institute/workplace of the presenter

Heart and Vascular Center, Semmelweis University

Authors

Dr. Timea Katalin Turschl¹, Dr. Zsuzsanna Ladanyi¹, Dr. Timea Balint¹, Dr. David Nagy¹, Dr. Andrea Ferencz¹, Dr. Alexandra Fabian¹, Dr. Marton Tokodi¹, Adam Szijarto¹, Dr. Andrea Nagy¹, Dr. Andrea Molnar¹, Prof. Dr. Endre Zima¹, Dr. Levente Molnar¹, Dr. Attila Kovacs¹, Dr. Mihaly Ruppert¹, Dr. Balint Karoly Lakatos¹, Prof. Dr. Bela Merkely¹
1: Heart and Vascular Center, Semmelweis University

Text of the abstract

Right ventricular pacing (RVP) induces a dyssynchronous left ventricular (LV) activation pattern, which reduces myocardial contractility. Hemodynamic loading conditions also influence LV performance as chronic pressure overload promotes adverse remodeling and heart failure.

Thus, we hypothesized that pressure overload amplifies pacing-associated LV dysfunction.

We conducted a translational study combining a rodent model and a clinical cohort. In 16 Wistar rats, pressure overload was induced by transverse aortic constriction (TAC, n=8), with sham-operated controls (n=8). RVP was induced by an octapolar electrophysiology catheter. LV pressure–volume analysis and echocardiography were performed during intrinsic rhythm and RVP. In the clinical study 29 patients with severe aortic stenosis (AS) and previously implanted pacemakers undergoing transcatheter aortic valve replacement (TAVR) were enrolled. Echocardiography was performed before and after the intervention during intrinsic rhythm and frequency-matched RVP. Ejection fraction (EF), global longitudinal strain (GLS), and myocardial work indices (GWI, GCW) were assessed.

In rodents, TAC induced hypertrophic remodeling with enhanced baseline contractility. Pressure–volume analysis confirmed impaired contractility (PRSW, SW) and relaxation (EDPVR, Tau) during pacing. With echocardiography, RVP reduced EF, GWI and GCW in both groups, with greater impairment in TAC animals. GWI and PRSW both demonstrated a significant interaction between pressure overload and pacing.

In the clinical study, the resolution of afterload after TAVR increased EF but reduced myocardial work indices. RVP worsened EF and GLS and impaired myocardial work, with decreases in GWI and GCW, increased GWW, resulting in reduced GWE. Interaction between pacing and loading conditions was observed for EF, GWI and GCW.

These findings indicate that an increase in afterload worsens the impairment of LV function in RVP. In AS patients with RVP, increased afterload may further complicate pacing-related LV dysfunction, allowing us to hypothesize that an earlier TAVR implantation might be beneficial to this patient population.

This research was supported by the Semmelweis 250+ grant of Semmelweis University.