QRS波时程反映了左心室内压力升高和心力衰竭时传导速度的潜在变化
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QRS duration reflects underlying changes in conduction velocity during increased intraventricular pressure and heart failure
背景与目的
猪的血压超负荷和心力衰竭电生理重塑（HF-ER）与传导速度（CV）和复极离散度有关，可导致心室性心律失常的风险增高。本研究的目的是明确在离体心脏心室内压力（IVP）和/或HF-ER增加时QRS波时程和CV潜在变化之间的关系，以及明确QRS时程是否对在体心脏左心室后负荷急性增加敏感。
方 法
通过高频心室起博对7头猪诱导HF-ER模型。同时采用7头同等重量的猪作为对照组。制作Lanendorff离体心脏灌注后采用程序性心室刺激，分别使用体积-传导ECG和心外膜光学图谱来采集低/高IVP下的QRS波时程和CV。另外4只猪采用胸外科手术通过钳夹部分升主动脉来增加左心室后负荷，SR时测量QRS波时程。
结 果
对13只心脏进行分析，HF-ER和IVP增高时显示出心外膜的CV明显减慢（-40％和-15％，分别为p <0.001和p = 0.004），这与QRS波增宽似乎有关系（+ 41％和+ 17％，p = 0.005和p <0.001）。在增加IVP时，HF-ER心脏比对照组的QRS波明显延长（+ 21％对+ 12％，HF-ER * IVP相互作用：p = 0.004）。当在体心脏的LV增大时，QRS波增宽（n=3），这与QRS波 时程和主动脉舒张压之间有关系（R = 0.58，p <0.001）
结 论
总之，高IVP和/或HF-ER可显著降低CV，这与心室起博时体表ECG上的QRS波增宽有关。心肌室壁压力的增加也增宽了在体心脏SR时的QRS波。
原始文献摘要
Svjetlana Dosenovic, MD,* Antonia Jelicic Kadic, MD, PhD,† Maja Miljanovic, MA, et al. Interventions for Neuropathic Pain: An Overview of Systematic Reviews.[J]. Anesth Analg 2017;125:643–52
Abstract
Pressure overload and heart failure electrophysiological remodeling (HF-ER) in pigs are associated with decreased conduction velocity (CV) and dispersion of repolarization, which lead to higher risk of ventricular arrhythmia. This work aimed to establish the correlation between QRS complex duration and underlying changes in CV during increased intraventricular pressure (IVP) and/or HF-ER ex-vivo, and to determine whether QRS duration could be sensitive to an acute increase in left ventricular afterload in-vivo. HF-ER was induced in 7 pigs by high-rate ventricular pacing. Seven weight-matched controls were used as controls. Isolated Langendorff-perfused hearts underwent programmed ventricular stimulation to study QRS complex duration and CV under low/high IVP, using volume-conducted ECG and epicardial optical mapping, respectively. Four additional pigs underwent open-chest surgery to increase left ventricular afterload by partially clamping the ascending aorta, while measuring QRS complex duration during SR. In 13 hearts included for analysis, both HF-ER and increased IVP showed significantly slower epicardial CV (-40% and -15%, p < 0.001 and p = 0.004, respectively), which correlated with similar widening of the QRS complex (+41% and +17%, p = 0.005 and p < 0.001, respectively). HF-ER hearts shower larger prolongation of the QRS complex than controls upon increasing the IVP (+21% vs. +12%, respectively. HF-ER*IVP interaction: p = 0.004). QRS complex widened after increasing LV afterload in-vivo (n=3), with correlation between QRS duration and aortic diastolic pressures (R = 0.58, p < 0.001). In conclusion, high IVP and/or HF-ER significantly decrease CV, which correlates with QRS widening on the surface ECG during ventricular pacing. Increased myocardial wall stress also widens the QRS complex during SR in-vivo.
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