Li Yue, Li Weimin, Yang Baofeng, Han Wei, Dong Deli, Xue Jingyi, Li Baoxin, Yang Shusen, Sheng Li
Cardiovascular Department, the First Clinical Hospital, Harbin Medical University, Harbin, PR China.
J Electrocardiol. 2007 Jan;40(1):100.e1-6. doi: 10.1016/j.jelectrocard.2006.04.001. Epub 2006 Oct 25.
The effects of angiotensin-converting enzyme inhibitor on long-term atrial electrophysiologic and structural remodeling are still unclear. The purpose of this study is to investigate the effects of Cilazapril on atrial electrical, structural, and functional remodeling in atrial fibrillation (AF) dogs induced by chronic rapid atrial pacing.
Twenty dogs were randomly divided into sham-operated group (n = 6), control group (n = 7), and Cilazapril group (n = 7). One thin silicon plaque containing 4 pairs of electrodes was sutured to each atrium. A pacemaker was implanted in a subcutaneous pocket and attached to a screw-in epicardial lead in the right atrial appendage. The dogs in control group and Cilazapril group were paced at 400 beats per minute for 6 weeks. The dogs in Cilazapril group received Cilazapril (0.5 mg x kg(-1) x d(-1)) 1 week before rapid atrial pacing until pacing stop. Before and after 6-week rapid atrial pacing, atrial effective refractory period (AERP) at 8 sites, AERP dispersion, intraatrium conduction time, inducibility, and duration of AF were measured. Transthoracic and transesophageal echocardiographic examinations included left atrium (LA) maximal volume, LA minimal volume, LA ejection fraction, left atrial appendage (LAA) maximal volume, LAA minimal volume, LAA ejection fraction, LAA maximal forward flow velocity, and LAA minimal backward flow velocity were performed. Atrial collagen volume fraction was analyzed by Masson staining.
After 6-week rapid atrial pacing, although there was no significant difference in AERP shortening and AERP rate adaptation reduction between the control group and the Cilazapril group, the inducibility and duration of AF were found to be dramatically lower in the Cilazapril group than those in the control group (AF inducibility, 65.7% vs 95.7%, P < .05; AF duration, 531.5 +/- 301.2 vs 1432.2 +/- 526.5 s, P < .01). The post-tachycardia intraatrium conduction times after 6 weeks with Cilazapril were significantly shorter than those in the control group. Cliazapril could partially prevent AERP dispersion increase induced by chronic rapid atrial pacing. Compared with the control group, the LA and LAA volumes were significantly smaller; LA ejection fraction, LAA ejection fraction, LAA maximal forward flow velocity, and LAA minimal backward flow velocity were dramatically higher in the Cilazapril group. The Cilazapril group had a significantly lower percentage of interstitial fibrosis than the control group.
Cilazapril can suppress structural and functional remodeling and prevent the induction and promotion of AF in chronic rapid atrial pacing dogs.
血管紧张素转换酶抑制剂对长期心房电生理及结构重塑的影响仍不明确。本研究旨在探讨西拉普利对慢性快速心房起搏诱导的房颤犬心房电活动、结构及功能重塑的影响。
20只犬随机分为假手术组（n = 6）、对照组（n = 7）和西拉普利组（n = 7）。每只犬的每个心房均缝合一块含有4对电极的薄硅片。将起搏器植入皮下囊袋，并连接至右心耳的螺旋式心外膜导线。对照组和西拉普利组的犬以每分钟400次的频率起搏6周。西拉普利组的犬在快速心房起搏前1周开始接受西拉普利（0.5 mg·kg⁻¹·d⁻¹）治疗，直至起搏结束。在6周快速心房起搏前后，测量8个部位的心房有效不应期（AERP）、AERP离散度、心房内传导时间、房颤的诱发率及持续时间。进行经胸和经食管超声心动图检查，包括左心房（LA）最大容积、LA最小容积、LA射血分数、左心耳（LAA）最大容积、LAA最小容积、LAA射血分数、LAA最大前向流速和LAA最小反向流速。采用Masson染色分析心房胶原容积分数。
6周快速心房起搏后，虽然对照组和西拉普利组在AERP缩短及AERP频率适应性降低方面无显著差异，但发现西拉普利组的房颤诱发率和持续时间显著低于对照组（房颤诱发率，65.7%对95.7%，P <.05；房颤持续时间，531.5±301.2对1432.2±526.5 s，P <.01）。西拉普利治疗6周后的心动过速后心房内传导时间显著短于对照组。西拉普利可部分预防慢性快速心房起搏引起的AERP离散度增加。与对照组相比，西拉普利组的LA和LAA容积显著较小；LA射血分数、LAA射血分数、LAA最大前向流速和LAA最小反向流速显著较高。西拉普利组的间质纤维化百分比显著低于对照组。
西拉普利可抑制慢性快速心房起搏犬的结构和功能重塑，并预防房颤的诱发和进展。
