Efficacy of cardiac resynchronization in acutely infarcted canine hearts with electromechanical dyssynchrony

Abstract

Background Patients with acute MI, left bundle branch block (LBBB), and marked LV decompensation suffer nearly 50% early mortality. Whether CRT improves hemodynamic status in this condition is unknown. We tested CRT in this setting, using a canine model of delayed lateral wall activation combined with 2-hours of coronary artery occlusion-reperfusion. Objective To evaluate the acute hemodynamic effects of CRT during and immediately after myocardial infarction. Methods Adult dogs (n=8) underwent open-chest 2-hour mid-left anterior descending artery occlusion (LAD) followed by 1-hour reperfusion. Four pacing modes were compared: right atrial pacing, pseudo-left bundle block (RV-pacing), and CRT with the left-ventricular (LV) lead positioned at either the lateral wall (LW-CRT) or peri-infarct zone (PIZ-CRT). Continuous LV pressure-volume data, regional segment length, and proximal LAD flow rates were recorded. Results At baseline, both RVP and PIZ-CRT reduced anterior wall regional work by ~50% (versus RA pacing). During coronary occlusion, this territory became dyskinetic, and dyskinesis rose further with both CRT modes as compared to pseudo-LBBB. Global cardiac output, stroke work, and ejection fraction all still improved by 11–23%. After reperfusion, both CRT modes elevated infarct-zone regional work and blood flow by ~10% over pseudo-LBBB, and improved global function. Conclusion CRT improves global chamber systolic function in chambers with delayed lateral wall activation during and following sustained coronary occlusion. It does so while modestly augmenting infarct-zone dyskinesis during occlusion and improving regional function and blood-flow upon reperfusion. These findings support CRT in the setting of early post-MI dyssynchronous heart failure.

Treatment strategies for the right heart in pulmonary hypertension

“…As a cautionary remark we stress that, as opposed to LV failure, 59–61 the supporting evidence for pacing in RV failure is still limited. Stress in the ventricular wall is a complex interplay of afterload, the moment in time of maximal load, ventricular volume, and muscle shortening.…”