Abstract 5334: Vulnerability to Ventricular Fibrillation in Failing Heart is the Result of Rate-dependent Enhancement of Dispersion of Action Potential Duration and Spatially Discordant Alternans
Congestive heart failure (CHF) predisposes to ventricular fibrillation (VF). We have reported the rate-dependent shortening of action potential duration (APD) and reduction of ICa-L in the ventricle of pacing-induced CHF rabbit (Heart Rhythm 2008). However, much remains to be clarified as to the electrophysiological properties in CHF leading to an increase in the ventricular vulnerability. In pacing-induced CHF rabbit hearts (350bpm, 3weeks, n=26), action potential signals were analyzed by a high-resolution optical mapping. Normal rabbit was employed as control (CTL, n=21). APD in CHF was significantly longer at slow stimulation rates (245±8 ms and 224±10 ms at BCL 2000 ms), but it was significantly shorter at high rates compared with CTL (129±11 ms and 141±6 ms at BCL 200 ms). Conduction velocity (CV) was significantly reduced in CHF (by 16% at BCL 200 ms). At all BCLs tested, spatial APD dispersion (APD-D) was significantly greater in CHF than in CTL by 25–50%. In CHF, the shorter the BCL was, the greater the normalized APD-D (APD-D/averaged APD, Figure⇓) became. At higher rates (BCL<150 ms), spatially concordant APD alternans (SCA) was induced in CTL, whereas spatially discordant APD alternans (SDA) was elicited in CHF (Figure⇓). The SCA was followed by 2:1conduction block, whereas SDA was almost always followed by the wave breakup (WB), culminating in the initiation of VF. The incidence of VF during dynamic pacing was significantly higher in CHF (82%) than in Control (14%). In CHF, prominent rate-dependent enhancement of APD-D and SDA leads to the initiation of VF. The persistent tachycardia may increase the vulnerability to VF in CHF.