Díez José Luis, Hernandiz Amparo, Cosín-Aguilar Juan, Aguilar Amparo, Portolés Manuel
Servicio de Cardiología, Hospital Dr. Peset Aleixandre, Valencia, Spain.
Med Sci Monit Basic Res. 2013 May 31;19:153-62. doi: 10.12659/MSMBR.889115.
The alteration of contractile function after tachyarrhythmia ceases is influenced by the type of prior ischemia (acute coronary syndrome or ischemia inherent in a coronary revascularization procedure). We aimed to analyze cardiac dysfunction in an acute experimental model of supraphysiological heart rate preceded by different durations and types of ischemia.
Twenty-four pigs were included in: (S1) series of ventricular pacing; (S2, A and B) series with 10 or 20 min, respectively, of coronary occlusion previous to ventricular pacing; S3 with 20 brief, repeated ischemia/reperfusion processes prior to ventricular pacing and; (S4) control series. Overall cardiac function parameters and regional myocardial contractility at the apex and base of the left ventricle were recorded, as were oxidative stress markers (glutathione and lipid peroxide serum levels). Left ventricular pacing at 60% over baseline heart rate was performed for 2 h followed by 1 h of recovery.
High ventricular pacing rates preceded by short, repeated periods of coronary ischemia/reperfusion resulted in worse impairment of overall cardiac and regional function that continued to be altered 1 h after tachycardia ceased. There was significant reduction of stroke volume (26.9 ± 5.3 basal vs. 16 ± 6.2 ml; p<0.05), LVP; dP/dt and LAD flow (13.1 ± 1.5 basal vs. 8.4 ± 1.6 ml/min; p<0.05); the base contractility remained altered when recovering compared to baseline (base SF: 5.6 ± 2.8 vs. 2.2 ± 0.7%; p<0.05); and LPO levels were higher than less aggressive series at the end of recovery.
Ischemia and tachycardia accumulate their effects, with increased cardiac involvement depending on the type of ischemia.
快速性心律失常终止后收缩功能的改变受先前缺血类型（急性冠状动脉综合征或冠状动脉血运重建术中固有的缺血）影响。我们旨在分析在不同持续时间和类型的缺血之前的超生理心率急性实验模型中的心脏功能障碍。
24头猪被纳入：（S1）心室起搏系列；（S2、A和B）分别在心室起搏前进行10或20分钟冠状动脉闭塞的系列；S3在心室起搏前进行20次短暂、重复的缺血/再灌注过程；以及（S4）对照系列。记录了整体心脏功能参数以及左心室心尖和心底的局部心肌收缩力，还记录了氧化应激标志物（谷胱甘肽和脂质过氧化物血清水平）。以超过基线心率60%的频率进行左心室起搏2小时，随后恢复1小时。
在短暂、重复的冠状动脉缺血/再灌注期后出现的高心室起搏率导致整体心脏和局部功能的更严重损害，在心动过速终止1小时后仍持续改变。每搏输出量显著降低（基础值26.9±5.3 vs. 16±6.2 ml；p<0.05），左心室压力；dp/dt和左心房血流（基础值13.1±1.5 vs. 8.4±1.6 ml/min；p<0.05）；与基线相比，恢复时心底收缩力仍发生改变（心底缩短分数：5.6±2.8 vs. 2.2±0.7%；p<0.05）；并且恢复结束时脂质过氧化物水平高于侵袭性较小的系列。
缺血和心动过速会累积它们的影响，心脏受累程度增加取决于缺血类型。
