Zhao Qing-yan, Huang Cong-xin, Jiang Hong, Okello Emmy, Wang Xi, Tang Yan-hong, Li Geng-shan
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Can J Cardiol. 2009 Apr;25(4):e115-8. doi: 10.1016/s0828-282x(09)70069-8.
Atrial fibrillation (AF) is a common complication of myocardial infarction (MI). Angiotensin II receptor antagonists prevent the promotion and propagation of AF. However, the activation of the acetylcholine-regulated K(+) current (I(K,ACh)) in the atrium after MI and the effect of valsartan on I(K,ACh) are less understood.
Twenty-four adult rabbits were randomly divided into three groups: sham-operated, MI and MI plus valsartan administration (MI+valsartan). The sham-operated group received a median sternotomy without left ventricular coronary artery ligation. Both the MI group and the MI+valsartan group received a median sternotomy followed by ligation of the midpoint of the left ventricular coronary artery. The MI+valsartan group was administered oral valsartan for 12 weeks. After 12 weeks, the initiation of AF was measured by vagal stimulation followed by quick excision of the heart. I(K,ACh) in the left atrial myocardium was measured by the patch clamp technique.
AF was induced in four animals in the MI group, two in the sham-operated and two in the MI+valsartan groups, with the total AF duration expectedly longer in the MI group than in the sham-operated and MI+valsartan groups (38 s versus 9 s and 9 s, respectively). Furthermore, the mean (+/- SEM) density of I(K,ACh) increased significantly more in the left atrial myocardia of the MI group than in the sham-operated and the MI+valsartan groups (-13+/-0.42 pA/pF versus -9+/-0.38 pA/pF and -10+/-0.37 pA/pF, respectively at -100 mV; and 4.1+/-0.28 pA/pF versus 3.1+/-0.27 pA/pF and 3.3+/-0.27 pA/pF, respectively at 20 mV; P<0.05). However, there was no statistically significant difference in I(K,ACh) between the sham-operated group and the MI+valsartan group.
AF is associated with increased I(K,ACh) after MI. Inhibition of increased IK,ACh may be the mechanism by which valsartan prevents AF following MI.
心房颤动（AF）是心肌梗死（MI）的常见并发症。血管紧张素II受体拮抗剂可预防AF的发生和发展。然而，MI后心房中乙酰胆碱调节的钾电流（I(K,ACh)）的激活以及缬沙坦对I(K,ACh)的影响尚不清楚。
24只成年兔随机分为三组：假手术组、MI组和MI加缬沙坦给药组（MI+缬沙坦组）。假手术组接受正中胸骨切开术，但不结扎左心室冠状动脉。MI组和MI+缬沙坦组均接受正中胸骨切开术，随后结扎左心室冠状动脉中点。MI+缬沙坦组口服缬沙坦12周。12周后，通过迷走神经刺激诱发AF，随后迅速切除心脏，测量左心房心肌中的I(K,ACh)。
MI组有4只动物诱发AF，假手术组和MI+缬沙坦组各有2只，MI组的总AF持续时间预期比假手术组和MI+缬沙坦组长（分别为38秒、9秒和9秒）。此外，MI组左心房心肌中I(K,ACh)的平均（±SEM）密度比假手术组和MI+缬沙坦组显著增加更多（在-100 mV时分别为-13±0.42 pA/pF、-9±0.38 pA/pF和-10±0.37 pA/pF；在20 mV时分别为4.1±0.28 pA/pF、3.1±0.27 pA/pF和3.3±0.27 pA/pF；P<0.05）。然而，假手术组和MI+缬沙坦组之间的I(K,ACh)无统计学显著差异。
AF与MI后I(K,ACh)增加有关。抑制IK,ACh增加可能是缬沙坦预防MI后AF的机制。
