Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure

Background: The influence of an increased left ventricular end-diastolic pr essure (LVEDP) on the development of lethal arrhythmias in chronic heart fa ilure is unclear. We investigated the effect of chronic and acute LVEDP inc rease on the epicardial activation time of sinus (SB) and paced (PB) beats. Methods: Six dogs underwent rapid ventricular pacing at 220-280 beats/min f or 6-14 weeks for induction of heart failure. On the study day, baseline (b a) LVEDP was determined for the surviving heart failure animals (HF-ba), an d for seven control animals (C-ba). The epicardial activation time (EAT, ti me between the earliest and latest epicardial activation) for five consecut ive SB and five ventricular PB during the baseline hemodynamic state were r ecorded using a 504 electrode mapping-sock. In the control animals a 2-litr e volume (vl) was infused over 10 min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for S B and PB was redetermined. Results: Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6 +/- 1 to 17 +/- 10.8 mmHg (P = 0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P < 0.05). In contrast, in the control animals th e acute rise in LVEDP from 6.8 +/- 4.5 to 14.7 +/- 6.2 mmHg P < 0.05), shor tened the EAT for SB (C-ba vs. C-vl, P < 0.05). A similar decrease in EAT f or SB caused by acute volume load was seen in the HF animals, but did not r each significance due to the small sample size (one of the three remaining HF animals died of spontaneous ventricular fibrillation before the volume l oad). Chronic LVEDP elevation significantly prolonged the EAT for PB from 7 2 +/- 11 to 120 +/- 31 ms (C-ba vs. HF-ba) while acute LVEDP increase had n o significant effect on EAT for PB. Conclusion: Chronic HF increases LVEDP and prolongs EAT, while an acute inc rease in LVEDP shortens the EAT for sinus beats. A prolongation of EAT in h eart failure may make the heart more susceptible to ventricular arrhythmias and electromechanical dissociation.