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.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0008-6363(01)00226-7 | DOI Listing |
Heart Rhythm
July 2019
Department of Cardiology, Peking University First Hospital, Beijing, China; Key Laboratory of Medical Electrophysiology of Ministry of Education, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, China. Electronic address:
Background: Increased CO levels in the general circulation and/or in the myocardium are common under pathologic conditions.
Objective: The purpose of this study was to test the hypothesis that an increase in CO levels, and not just the subsequent extra- or intracellular acidosis, would augment late sodium current (I) and contribute to arrhythmogenesis in hearts with reduced repolarization reserve.
Methods: Monophasic action potential durations at 90% completion of repolarization (MAPD) from isolated rabbit hearts, I, and extra- (pH) and intracellular pH (pH) values from cardiomyocytes using the whole-cell patch-clamp techniques and 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester (BCECF-AM), respectively, were measured.
Sci Rep
April 2017
Department of Cardiology, Peking University First Hospital, Beijing, 100034, China.
Cardiac arrhythmias associated with intracellular calcium inhomeostasis are refractory to antiarrhythmic therapy. We hypothesized that late sodium current (I ) contributed to the calcium-related arrhythmias. Monophasic action potential duration at 90% completion of repolarization (MAPD) was significantly increased and ventricular arrhythmias were observed in hearts with increased intracellular calcium concentration ([Ca]) by using Bay K 8644, and the increase became greater in hearts treated with a combination of ATX-II and Bay K 8644 compared to Bay K 8644 alone.
View Article and Find Full Text PDFJ Interv Card Electrophysiol
June 2002
Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.
Unlabelled: Heterogeneity in cardiac repolarization (Delta APD) is known to be arrhythmic. In the dog model of chronic complete AV-block and acquired long QT syndrome, an increase in Delta MAPD (defined as left ventricular monophasic action potential duration (MAPD) minus right ventricular MAPD) is often associated with changes in T-wave morphology. The purpose of this study was to correlate known changes in Delta MAPD with the planimetric total area of the T-wave on the surface ECG (integral of J-T, mVx ms).
View Article and Find Full Text PDFCardiovasc Res
May 2001
Department of Cardiology, Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.
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.
Cardiovasc Res
August 1991
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Study Objective: The aim was to determine whether the rate, the magnitude, or both, of increased left ventricular wall stress in vivo has consistent and prominent effects on repolarisation, afterdepolarisations, or arrhythmogenicity.
Design: Ten anaesthetised dogs underwent transient proximal aortic occlusion. Wall stress was estimated from pressure-volume data obtained by volume catheter, normalised to preocclusion values, and correlated with simultaneously determined changes in monophasic action potential duration (MAPd).
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!