Right or Left Ventricular Pacing in Young Minipigs with Chronic Atrioventricular Block: Long-Term in-vivo Cardiac Performance, Morphology, Electrophysiology and Cellular Biology
Background—Left ventricular (LV) dyssynchrony may occur as a result of right ventricular (RV) pacing and is a known risk factor for the development of heart failure. In children with complete atrioventricular (AV) block pacing-induced dyssynchrony lasting for decades might be especially deleterious for LV function. To determine the hemodynamic and ultra-structural remodelling following either RV-free wall or LV-apical pacing we used a chronic minipig model.
Methods and Results—14 Piglets aged 8 weeks underwent AV node ablation and were paced AV sequentially from either the RV-free wall or the LV-apex at 120 beats per minute (bpm) for 1 year (7 age-matched minipigs served as controls with spontaneous heart rates of 104±5 bpm). Echocardiographic examinations, pressure-volume-loops, patch clamp investigations, examinations of connexin43, calcium-handling proteins and histomorphology were carried out. RV-free wall paced minipigs exhibited significantly more LV dyssynchrony than LV-apex paced animals, which was accompanied by worsening of LV function (maximum LV mechanical delay/LV ejection fraction: RV-free wall pacing 154±36ms /28±3%, LV-apical pacing 52±19ms/45±2%, control 47±14ms/62±1%; P=0.0001). On cellular level, both pacemaker groups exhibited significant reduction of L-type calcium and peak-sodium current, shortening of action potential duration and amplitude, an increase in cell capacity and alterations in the calcium-handling proteins which was similar for RV-free wall and LV-apex paced animals.
Conclusions—The observed molecular remodelling seemed to be more dependent on heart rate than on dyssynchrony. LV apical pacing is associated with less dyssynchrony, a more physiological LV contraction pattern and preserved LV function as opposed to RV-free wall pacing.
- Received November 9, 2011.
- Accepted April 6, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited