Dyssynchronous heart failure (HF) is routinely treated with cardiac resynchronization therapy (CRT). During conventional biventricular (BV) CRT, pacing is applied to the right ventricle (RV) endocardium and the left ventricle (LV) epicardium via the coronary sinus (EPI-CRT BV ). Current best practice results in 30% to 40% of CRT patients failing to display improved clinical response.1 Recent clinical 2-5 and experimental 6,7 evidence suggests that BV CRT with an endocardial pacing strategy for the LV lead (ENDO-CRT BV ) can provide an improvement in acute hemodynamic response and stroke work over EPI-CRT BV and offers a novel approach for increasing CRT response rates. However, the relative importance of cardiac physiology or better access to optimal pacing sites in causing this improved outcome remains controversial. Identifying and understanding physiological mechanisms behind improved ENDO-CRT BV response are crucial for optimizing clinical procedures and identifying patients who will receive the maximal benefit from this therapy.In acute left bundle branch block (LBBB) canine studies, ENDO-CRT BV improved the systolic LV function over conventional EPI-CRT BV .6 Electric activation times (ATs) as measured by contact mapping were decreased with ENDO-CRT BV © 2015 American Heart Association, Inc. Original Article
Circ Arrhythm Electrophysiol
Background-Cardiac resynchronization therapy (CRT) delivered via left ventricular (LV) endocardial pacing (ENDO-CRT) is associated with improved acute hemodynamic response compared with LV epicardial pacing (EPI-CRT).The role of cardiac anatomy and physiology in this improved response remains controversial. We used computational electrophysiological models to quantify the role of cardiac geometry, tissue anisotropy, and the presence of fast endocardial conduction on myocardial activation during ENDO-CRT and EPI-CRT. Methods and Results-Cardiac activation was simulated using the monodomain tissue excitation model in 2-dimensional (2D) canine and human and 3D canine biventricular models. The latest activation times (LATs) for LV endocardial and biventricular epicardial tissue were calculated (LVLAT and TLAT), as well the percentage decrease in LATs for endocardial (en) versus epicardial (ep) LV pacing (defined as %dLV=100×(LVLAT ep −LVLAT en )/LVLAT ep and %dT=100×(TLAT ep −TLAT en )/TLAT ep , respectively). Normal canine cardiac anatomy is responsible for %dLV and %dT values of 7.4% and 5.5%, respectively. Concentric and eccentric remodeled anatomies resulted in %dT values of 15.6% and 1.3%, respectively. The 3D biventricular-paced canine model resulted in %dLV and %dT values of −7.1% and 1.5%, in contrast to the experimental observations of 16% and 11%, respectively. Adding fast endocardial conduction to this model altered %dLV and %dT to 13.1% and 10.1%, respectively. Conclusions-Our results provide a physiological explanation for improved response to ENDO-CRT. We predict that patients with viable fast-conducting endocardial tissue or distal Purkinje network or both, as we...