Quintanilla Jorge G, Moreno Javier, Archondo Tamara, Alfonso-Almazán José Manuel, Lillo-Castellano José María, Usandizaga Elena, García-Torrent María Jesús, Rodríguez-Bobada Cruz, González Pablo, Borrego Luis, Cañadas-Godoy Victoria, González-Ferrer Juan J, Pérez-Castellano Nicasio, Pérez-Villacastín Julián, Filgueiras-Rama David
Fundación Centro Nacional de Investigaciones Cardiovasculares, Carlos III (CNIC), Myocardial Pathophysiology Area, Madrid, Spain; Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Department of Cardiology, Madrid, Spain; CIBER de Enfermedades Cardiovasculares, Spain.
CIBER de Enfermedades Cardiovasculares, Spain; Hospital Universitario Ramón y Cajal, Department of Cardiology, Madrid, Spain.
Prog Biophys Mol Biol. 2017 Nov;130(Pt B):394-403. doi: 10.1016/j.pbiomolbio.2017.08.003. Epub 2017 Aug 9.
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 (LV) afterload in-vivo. HF-ER was induced in 7 pigs by high-rate ventricular pacing. Seven weight-matched animals 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 LV afterload by partially clamping the ascending aorta, while measuring QRS complex duration during sinus rhythm (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 ECG during ventricular pacing. Increased myocardial wall stress also widens the QRS complex during SR in-vivo.
猪的压力超负荷和心力衰竭电生理重构（HF-ER）与传导速度（CV）降低和复极离散有关，这会导致室性心律失常风险增加。本研究旨在建立体外心室压力（IVP）升高和/或HF-ER期间QRS波群时限与CV潜在变化之间的相关性，并确定QRS时限是否对体内左心室（LV）后负荷的急性增加敏感。通过高速心室起搏在7头猪中诱导HF-ER。7头体重匹配的动物用作对照。使用离体Langendorff灌注心脏进行程序性心室刺激，分别使用容积传导心电图和心外膜光学标测，研究低/高IVP下的QRS波群时限和CV。另外4头猪接受开胸手术，通过部分夹闭升主动脉增加LV后负荷，同时测量窦性心律（SR）期间的QRS波群时限。在纳入分析的13颗心脏中，HF-ER和IVP升高均显示心外膜CV显著减慢（分别为-40%和-15%，p<0.001和p=0.004），这与QRS波群类似程度的增宽相关（分别为+41%和+17%，p=0.005和p<0.001）。在增加IVP时，HF-ER心脏的QRS波群延长幅度大于对照组（分别为+21%对+12%。HF-ER*IVP相互作用：p=0.004）。体内增加LV后负荷后QRS波群增宽（n=3），QRS时限与主动脉舒张压之间存在相关性（R=0.58，p<0.001）。总之，高IVP和/或HF-ER显著降低CV，这与心室起搏期间心电图上的QRS增宽相关。增加的心肌壁应力在体内SR期间也会使QRS波群增宽。
