Promotion of atrial fibrillation by heart failure in dogs - Atrial remodeling of a different sort
Promotion of atrial fibrillation by heart failure in dogs - Atrial remodeling of a different sort
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DOI：
10.1161/01.cir.100.1.87
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发表时间：
1999-07-06
期刊：
影响因子：
37.8
通讯作者：
Nattel, S
中科院分区：
文献类型：
--
作者：
Li, DS;Fareh, S;Nattel, S
背景-对房性心动过速引起的心房颤动（AF）的研究提供了对“AF引起AF”的重构机制的见解，但尚未阐明在重构发生之前最初支持AF的底物。我们研究了充血性心力衰竭（CHF）对犬心房电生理的影响，并与快速心房起搏犬的结果进行了比较（RAP; 400 bpm），心室率受控（房室传导阻滞加心室起搏器，80 bpm）。方法和结果-快速心室起搏5周诱导CHF（220至240 bpm）增加了由短阵起搏诱导的AF持续时间（从对照犬的8 +/- 4秒增加到535 +/- 82秒; P < 0.01），与1周RAP的效果（713 +/- 300秒）相似。与RAP相比，CHF在360 ms时不改变心房不应期、不应期异质性和传导速度;然而，CHF犬在心房起搏期间的传导异质性显著增加（CHF犬的异质性指数为2.76 +/- 0.16，对照组为1.46 +/- 0.10，RAP犬为1.51 +/- 0.06; P < 0.01），这是由于离散的慢传导区域。组织学检查显示，广泛的间质纤维化（结缔组织占据12.8 +/- 1.9%的横截面积）在CHF狗与对照组（0.8 +/- 0.3%）和RAP（0.9 +/- 0.2%）dogs. Conclusions实验性CHF强烈促进诱导持续性AF引起间质纤维化，干扰局部传导。CHF中AF的基质与房性心动过速相关AF的基质非常不同，对于理解、治疗和预防CHF相关AF具有重要的潜在意义。
Background-Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus Ventricular pacemaker at 80 bpm).Methods and Results-CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8 +/- 4 seconds in control dogs to 535 +/- 82 seconds; P < 0.01), similar to the effect of 1 week of RAP (713 +/- 300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2.76 +/- 0.16 versus 1.46 +/- 0.10 for control and 1.51 +/- 0.06 for RAP dogs; P < 0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8 +/- 1.9% of the cross-sectional area) in CHF dogs compared with control (0.8 +/- 0.3%) and RAP (0.9 +/- 0.2%) dogs.Conclusions-Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia-related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.