Background: The dog model of chronic complete AV-block (CAVB) demonstrates a considerable incidence of (witnessed) sudden death (16/117 dogs). In this study we tried to: (1) elucidate the mechanisms of sudden death using an ECG telemetry device and (2) identify retrospectively the risk parameters indicative of this arrhythmogenic death.
Methods: Between 1994 and 1998, 78 anesthetized dogs underwent an extensive electrophysiological study including: (1) left- (LV) and right ventricular (RV) monophasic action potential (MAP) recordings to assess Delta MAPD (LV APD minus RV APD) and (2) pacing protocols (PES) to induce torsade de pointes arrhythmias (TdP) at 4--6 weeks CAVB. Eight animals experienced sudden cardiac death (SCD) during the follow-up period (mean 7+/-3 weeks CAVB). Since the response of the CAVB dog to class III drugs is not uniform we also made comparisons among the SCD group, TdP drug responders and non-responders. For this purpose we selected all animals which (1) received almokalant (n=15, 0.12 mg/kg/5 min) or ibutilide (n=9, 0.025 mg/kg/5 min) as an additional challenge to induce TdP and (2) had a follow-up period of at least 4 weeks.
Results: Six out of eight SCD dogs showed inducible TdP at baseline. Two of eight dogs had telemetric ECG surveillance and both revealed polymorphic VT as the cause of SCD. Baseline Delta MAPD of the SCD (90+/-15 ms) was significantly higher than the non-SCD group (n=70, 60+/-30 ms). Of the 24 dogs which received class III drugs, 12 belonged to the TdP responder group. Delta MAPD of the TdP responder group (80+/-15 ms) was similar to the SCD group and significantly higher compared to the non-responder group (n=12, 40+/-25 ms). QT-time and cycle length of idioventricular rhythm were not different.
Conclusion: In the CAVB dog model, SCD is (1) most probably related to TdP while (2) inducible TdP and the measure of Delta MAPD at baseline indicate susceptibility to SCD.