Abstract 3071: Reversible Transmural Electrical Dyssynchrony in Pacing-Induced Congestive Heart Failure
Introduction: Inter and Intra-ventricular dyssynchrony can develop during congestive heart failure (CHF). We investigated transmural electrical conduction properties within the LV wall during CHF and subsequent recovery.
Methods: Biventricular pacemakers were implanted in 8 normal mongrel dogs (mean weight: 38 kg), and continuous RV pacing (230 –250 bpm) was initiated to induce CHF. Echocardiography, catheterization, and LV myocardial biopsy were performed biweekly while pacing was temporarily stopped. At each catheterization, an intracardiac electrode-catheter was placed at the LV endocardium against the pacemaker coronary sinus lead tip located at the LV epicardium. Intrinsic transmural electrical conduction delay was measured by recording endocardial electrograms via the electrode-catheter and epicardial electrograms via the pacemaker coronary sinus lead, both in posterolateral LV. The conduction delay was also assessed during LV pacing via the endocardial catheter and measuring the time to the coronary sinus lead tip. Pacing was stopped in 4 dogs with CHF to allow for recovery of function. All times were corrected for heart rate.
Results: All dogs developed CHF within 2– 4 wks of pacing from baseline (EF: 27±8 vs. 49±4%; LVEDP: 20±9 vs. 6±3 mmHg; QRS: 98±8 vs. 70±14 msec with no LBBB). There was no change in LV wall thickness during CHF compared to baseline (0.9 cm), while LV myocyte size increased (21.7±6.6 vs. 16.2±1.5 μm). Transmural endocardial-to-epicardial intrinsic electrical conduction time lengthened during CHF compared to baseline (35±13 vs. 10±5msec, P<0.001). In dogs recovering from CHF 2– 4 wks after cessation of pacing, intrinsic transmural endocardial-to-epicardial conduction time shortened compared to CHF (10±9 vs. 39±1ms, n=4), which was consistent with LV endocardial pacing (recovery: 47.5±6 ms; CHF: 70.7±9 ms, n=3).
Conclusions: Electrical transmural dyssynchrony develops as a consequence of pacing-induced CHF, and is reversible upon recovery of cardiac function. These changes are not associated with LV wall thickness. This novel finding suggests another aspect of ventricular dyssynchrony that may not be reflected by routine noninvasive modalities and warrants further investigation.