Zarzoso M, Mironov S, Guerrero-Serna G, Willis B Cicero, Pandit S V
Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI, USA; Department of Physiotherapy, Universitat de València, Valencia, Spain.
Acta Physiol (Oxf). 2014 May;211(1):36-47. doi: 10.1111/apha.12185. Epub 2013 Dec 5.
Excess weight gain and obesity are one of the most serious health problems in the western societies. These conditions enhance risk of cardiac disease and have been linked with increased prevalence for cardiac arrhythmias and sudden death. Our goal was to study the ventricular remodelling occurring in rabbits fed with high-fat diet (HFD) and its potential arrhythmogenic mechanisms.
We used 15 NZW rabbits that were randomly assigned to a control (n = 7) or HFD group (n = 8) for 18 weeks. In vivo studies included blood glucose, electrocardiographic, and echocardiographic measurements. Optical mapping was performed in Langendorff-perfused isolated hearts.
Body weight (3.69 ± 0.31 vs. 2.94 ± 0.18 kg, P < 0.001) and blood glucose levels (230 ± 61 vs. 141 ± 14 mg dL(-1) , P < 0.05) were higher in the HFD group vs. controls. The rate-corrected QT interval and its dispersion were increased in HFD rabbits vs. controls (169 ± 10 vs. 146 ± 13 ms and 37 ± 11 vs. 9 ± 2 ms, respectively; P < 0.05). Echocardiographic analysis showed morphological and functional alterations in HFD rabbits indicative of left ventricle (LV) hypertrophy. Isolated heart studies revealed no changes in repolarization and propagation properties under conditions of normal extracellular K(+) , suggesting that extrinsic factors could underlie those electrocardiographic modifications. There were no differences in the dynamics of ventricular fibrillation (frequency, wave breaks) in the presence of isoproterenol. However, HFD rabbits showed a small reduction in action potential duration and an increased incidence of arrhythmias during hyperkalaemia.
High-fat feeding during 18 weeks in rabbits induced a type II diabetes phenotype, LV hypertrophy, abnormalities in repolarization and susceptibility to arrhythmias during hyperkalaemia.
体重过度增加和肥胖是西方社会最严重的健康问题之一。这些情况会增加心脏病风险，并与心律失常和猝死的患病率增加有关。我们的目标是研究高脂饮食（HFD）喂养的兔子发生的心室重构及其潜在的致心律失常机制。
我们使用15只新西兰白兔，随机分为对照组（n = 7）或高脂饮食组（n = 8），为期18周。体内研究包括血糖、心电图和超声心动图测量。在Langendorff灌注的离体心脏上进行光学标测。
高脂饮食组的体重（3.69±0.31 vs. 2.94±0.18 kg，P < 0.001）和血糖水平（230±61 vs. 141±14 mg dL⁻¹，P < 0.05）高于对照组。与对照组相比，高脂饮食组兔子的心率校正QT间期及其离散度增加（分别为169±10 vs. 146±13 ms和37±11 vs. 9±2 ms；P < 0.05）。超声心动图分析显示高脂饮食组兔子存在形态和功能改变，提示左心室（LV）肥厚。离体心脏研究显示，在正常细胞外钾离子条件下，复极化和传导特性无变化，表明外在因素可能是这些心电图改变的基础。在异丙肾上腺素存在的情况下，心室颤动的动力学（频率、波破碎）没有差异。然而，高脂饮食组兔子在高钾血症期间动作电位时程略有缩短，心律失常发生率增加。
兔子18周的高脂喂养诱导了II型糖尿病表型、左心室肥厚、复极化异常以及高钾血症期间对心律失常的易感性。
