Thomsen Morten B, Truin Michiel, van Opstal Jurren M, Beekman Jet D M, Volders Paul G A, Stengl Milan, Vos Marc A
Department of Medical Physiology, Heart Lung Centre Utrecht, Yalelaan 50, NL-3584 CM Utrecht, The Netherlands.
Basic Res Cardiol. 2005 May;100(3):279-87. doi: 10.1007/s00395-005-0519-6. Epub 2005 Mar 9.
Increased proarrhythmia in dogs with chronic AV block (AVB) has been explained by ventricular remodeling causing a decrease in repolarization reserve. Beat-to-beat variability of repolarization (BVR) has been suggested to reflect repolarization reserve, in which high variability represents diminished reserve and larger propensity for repolarization-dependent ventricular arrhythmia. A subset of chronic AVB dogs (10%) suffers sudden cardiac death (SCD). With the assumption that repolarization defects constitute a potentially lethal proarrhythmic substrate, we hypothesized that BVR in SCD dogs are larger than in matched control chronic AVB dogs. From a population of 200 chronic AVB dogs, initially two groups were chosen retrospectively: 8 dogs that died suddenly (SCD) and 8 control dogs. Control dogs had a longer lifespan after AVB (10 to 18 weeks) than SCD dogs (5 to 10 weeks). All dogs had undergone electrophysiological testing under anesthesia where ECG, left and right ventricular endocardial monophasic action potentials (MAP) were recorded. BVR was assessed from 30 consecutive beats, illustrated by Poincare plots and was the only parameter discriminating between SCD and control group. All other electrophysiological parameters (RR, QT and MAP durations) were comparable for the two groups. Extending the number of animals and groups confirmed a larger BVR in the SCD group (SCD: 5.1 +/- 2.7; n = 11 versus control: 2.5 +/- 0.4 ms; n = 61; P < 0.05) and showed reverse-use dependence of BVR. In comparison, dogs with acute AVB had low variability (1.3 +/- 0.3 ms; n = 9; P < 0.05 versus chronic AVB). Cardiac electrical remodeling after AVB is associated with an increase in beat-to-beat variability of repolarization. Chronic AVB dogs displaying further elevated variability of repolarization are prone to arrhythmia-related SCD.
慢性房室传导阻滞(AVB)犬心律失常增加的原因是心室重构导致复极储备减少。复极逐搏变异性(BVR)被认为可反映复极储备,其中高变异性代表储备减少以及复极依赖性室性心律失常的更大倾向。一部分慢性AVB犬(10%)会发生心源性猝死(SCD)。假设复极缺陷构成潜在致命的致心律失常基质,我们推测SCD犬的BVR大于匹配的对照慢性AVB犬。在200只慢性AVB犬群体中,最初回顾性选择了两组:8只突然死亡的犬(SCD)和8只对照犬。对照犬在发生AVB后的寿命(10至18周)比SCD犬(5至10周)长。所有犬均在麻醉下接受了电生理测试,记录了心电图、左心室和右心室心内膜单相动作电位(MAP)。通过庞加莱图从连续30个搏动评估BVR,这是区分SCD组和对照组的唯一参数。两组的所有其他电生理参数(RR、QT和MAP持续时间)具有可比性。增加动物数量和分组后证实SCD组的BVR更大(SCD:5.1±2.7;n = 11,对照:2.5±0.4 ms;n = 61;P < 0.05),并显示BVR具有反向使用依赖性。相比之下,急性AVB犬的变异性较低(1.3±0.3 ms;n = 9;与慢性AVB相比,P < 0.05)。AVB后的心脏电重构与复极逐搏变异性增加有关。复极变异性进一步升高的慢性AVB犬易发生心律失常相关的SCD。