QRS duration reflects underlying changes in conduction velocity during increased intraventricular pressure and heart failure.

Pressure overload and heart failure electrophysiological remodeling (HF-ER) in pigs are associated with decreased conduction velocity (CV) and dispersion of repolarization, which lead to higher risk of ventricular arrhythmia. This work aimed to establish the correlation between QRS complex duration and underlying changes in CV during increased intraventricular pressure (IVP) and/or HF-ER ex-vivo, and to determine whether QRS duration could be sensitive to an acute increase in left ventricular (LV) afterload in-vivo. HF-ER was induced in 7 pigs by high-rate ventricular pacing. Seven weight-matched animals were used as controls. Isolated Langendorff-perfused hearts underwent programmed ventricular stimulation to study QRS complex duration and CV under low/high IVP, using volume-conducted ECG and epicardial optical mapping, respectively. Four additional pigs underwent open-chest surgery to increase LV afterload by partially clamping the ascending aorta, while measuring QRS complex duration during sinus rhythm (SR). In 13 hearts included for analysis, both HF-ER and increased IVP showed significantly slower epicardial CV (-40% and -15%, p < 0.001 and p = 0.004, respectively), which correlated with similar widening of the QRS complex (+41% and +17%, p = 0.005 and p < 0.001, respectively). HF-ER hearts shower larger prolongation of the QRS complex than controls upon increasing the IVP (+21% vs. +12%, respectively. HF-ER*IVP interaction: p = 0.004). QRS complex widened after increasing LV afterload in-vivo (n=3), with correlation between QRS duration and aortic diastolic pressures (R = 0.58, p < 0.001). In conclusion, high IVP and/or HF-ER significantly decrease CV, which correlates with QRS widening on the ECG during ventricular pacing. Increased myocardial wall stress also widens the QRS complex during SR in-vivo.