Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany.
Heart Rhythm. 2013 Oct;10(10):1525-30. doi: 10.1016/j.hrthm.2013.07.015. Epub 2013 Jul 11.
Increased sympathetic activation during acute ventricular ischemia is involved in the occurrence of life-threatening arrhythmias.
To test the effect of sympathetic inhibition by renal denervation (RDN) on ventricular ischemia/reperfusion arrhythmias.
Anesthetized pigs, randomized to RDN or SHAM treatment, were subjected to 20 minutes of left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size, hemodynamics, premature ventricular contractions, and spontaneous ventricular tachyarrhythmias were analyzed. Monophasic action potentials were recorded with an epicardial probe at the ischemic area.
Ventricular ischemia resulted in an acute reduction of blood pressure (-29%) and peak left ventricular pressure rise (-40%), which were not significantly affected by RDN. However, elevation of left ventricular end-diastolic pressure (LVEDP) during LAD ligation was attenuated by RDN (ΔLVEDP: +1.8 ± 0.6 mm Hg vs +9.7 ± 1 mm Hg in the SHAM group; P = .046). Infarct size was not affected by RDN compared to SHAM. RDN significantly reduced spontaneous ventricular extrabeats (160 ± 15/10 min in the RDN group vs 422 ± 36/10 min in the SHAM group; P = .021) without affecting coupling intervals. In 5 of 6 SHAM-treated animals, ventricular fibrillation (VF) occurred during LAD occlusion. By contrast, only 1 of 7 RDN-treated animals experienced VF (P = .029). Beta-receptor blockade by atenolol showed comparable effects. Neither VF nor transient shortening of monophasic action potential duration during reperfusion was inhibited by RDN.
RDN reduced the occurrence of ventricular arrhythmias/fibrillation and attenuated the rise in LVEDP during left ventricular ischemia without affecting infarct size, changes in ventricular contractility, blood pressure, and reperfusion arrhythmias. Therefore, RDN may protect from ventricular arrhythmias during ischemic events.
急性心室缺血时交感神经激活增加与危及生命的心律失常的发生有关。
测试肾去神经支配（RDN）对心室缺血/再灌注心律失常的影响。
麻醉猪随机分为 RDN 或 SHAM 治疗组，进行左前降支冠状动脉（LAD）闭塞 20 分钟，然后再灌注。分析梗死面积、血流动力学、室性早搏和自发性室性心动过速。用心外膜探针在缺血区记录单相动作电位。
心室缺血导致血压急性下降（-29%）和左心室压力峰值升高（-40%），RDN 对其无明显影响。然而，RDN 减轻了 LAD 结扎时左心室舒张末期压（LVEDP）的升高（ΔLVEDP：+1.8±0.6mmHg 与 SHAM 组的+9.7±1mmHg；P=0.046）。与 SHAM 相比，RDN 对梗死面积无影响。RDN 显著减少自发性室性期外收缩（RDN 组 160±15/10min，SHAM 组 422±36/10min；P=0.021），而不影响偶联间期。在 6 只 SHAM 治疗动物中，5 只在 LAD 闭塞期间发生心室颤动（VF）。相比之下，只有 1 只 RDN 治疗动物发生 VF（P=0.029）。阿替洛尔的β受体阻断作用具有类似的效果。RDN 既不抑制再灌注期间 VF 也不抑制单相动作电位时程的短暂缩短。
RDN 减少了左心室缺血期间室性心律失常/颤动的发生和 LVEDP 的升高，而不影响梗死面积、心室收缩力、血压和再灌注心律失常。因此，RDN 可能在缺血事件中保护心室免受心律失常的影响。
