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

心脏再同步治疗对急性梗死犬心脏电机械不同步的疗效

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Abstract

BACKGROUND: Patients with acute myocardial infarction (MI), left bundle branch block (LBBB), and marked left ventricular (LV) decompensation suffer from nearly 50% early mortality. Whether cardiac resynchronization therapy (CRT) improves hemodynamic status in this condition is unknown. We tested CRT in this setting by using a canine model of delayed lateral wall (LW) activation combined with 2 hours of coronary artery occlusion-reperfusion. OBJECTIVE: This study aimed to evaluate the acute hemodynamic effects of CRT during and immediately after MI. METHODS: Adult dogs (n = 8) underwent open-chest 2-hour mid-left anterior descending artery occlusion followed by 1-hour reperfusion. Four pacing modes were compared: right atrial pacing, pseudo-left bundle block (right ventricular pacing), and CRT with the LV lead positioned at either the LW (LW-CRT) or the peri-infarct zone (peri-infarct zone-CRT). Continuous LV pressure-volume data, regional segment length, and proximal left anterior descending flow rates were recorded. RESULTS: At baseline, both right ventricular pacing and peri-infarct zone CRT reduced anterior wall regional work by ~50% (vs right atrial 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% as compared to pseudo-LBBB, as well as improved global function. CONCLUSION: CRT improves global chamber systolic function in left ventricles with delayed LW activation during and after sustained coronary occlusion. It does so while modestly augmenting infarct zone dyskinesis during occlusion and improving regional function and blood flow after reperfusion. These findings support CRT in the setting of early post-MI dyssynchronous heart failure.

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