Repolarization alternans reveals vulnerability to human atrial fibrillation.
Repolarization alternans reveals vulnerability to human atrial fibrillation.
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DOI：
10.1161/circulationaha.110.977827
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发表时间：
2011-06-28
期刊：
影响因子：
37.8
通讯作者：
Krummen DE
中科院分区：
文献类型：
--
作者：
Narayan SM;Franz MR;Clopton P;Pruvot EJ;Krummen DE
人类心房颤动（AF）的底物尚不清楚，但涉及异常复极化（动作电位持续时间，APD）。我们假设APD的搏动振荡可以解释AF底物，以及为什么对AF的易感形成了一个频谱，从无AF的对照组到阵发性和持续性AF患者。在33名受试者中（12名持续性AF， 13名阵发性AF， 8名无AF的对照组），我们记录了左心房APD （n=33）和右心房APD （n=6）从起搏周期长度（CL） 600-500 ms（100-120次/分钟）到AF。持续性AF患者的APD交替需要逐渐加快的速率。阵发性心房颤动与对照组（CL 411±94 vs 372±72 vs 218±33 ms; p<0.01）。在房颤患者中，APD交替发生率低至100-120次/分，与APD恢复无关（p=NS）。在这种情况下，自发性异位诱发房颤。在发生房颤的过程中，APD以较快的速度从无序转变为复杂振荡。在持续性房颤、阵发性房颤和对照组中，复杂振荡的发生速度也逐渐加快（CL: 316±99 ms vs 266±19 ms vs 177±16 ms; p=0.02）。在阵发性房颤中，APD振荡在房颤之前放大（p<0.001）。在对照组中，APD交替出现的速度非常快（CL < 250 ms；与AF组相比p<0.001），就在房颤之前。在n=4例快速起搏未引发房颤的AF患者中，APD交替出现短暂性，然后消失。心房APD交替显示房颤的动态底物，在持续性房颤中最容易发生（发生率较低，强度较高），然后是阵发性房颤，而在对照组中最不容易发生。APD交替出现在所有房颤发作之前，当房颤未发生时APD交替出现。在静息心率附近APD交替的细胞机制需要定义。
The substrates for human atrial fibrillation (AF) are poorly understood but involve abnormal repolarization (action potential duration, APD). We hypothesized that beat-to-beat oscillations in APD may explain AF substrates and why vulnerability to AF forms a spectrum from control subjects without AF to patients with paroxysmal then persistent AF. In 33 subjects (12 persistent AF, 13 paroxysmal AF, 8 controls without AF), we recorded left (n=33) and right (n=6) atrial APD on pacing from cycle lengths (CL) 600–500 ms (100–120 beats/min) to AF. APD alternans required progressively faster rates for patients with persistent AF, paroxysmal AF and controls (CL 411±94 vs 372±72 vs 218±33 ms; p<0.01). In AF patients, APD alternans occurred at rates as slow as 100–120 beats/min, unrelated to APD restitution (p=NS). In this milieu, spontaneous ectopy initiated AF. At fast rates, APD alternans disorganized to complex oscillations en route to AF. Complex oscillations also arose at progressively faster rates for persistent AF, paroxysmal AF and controls (CL: 316±99 vs 266±19 vs 177±16 ms; p=0.02). In paroxysmal AF, APD oscillations amplified prior to AF (p<0.001). In controls, APD alternans arose only at very fast rates (CL < 250 ms; p<0.001 vs AF groups) just prior to AF. In n=4 AF patients in whom rapid pacing did not initiate AF, APD alternans arose transiently then extinguished. Atrial APD alternans reveals dynamic substrates for AF, arising most readily (at lower rates and higher magnitudes) in persistent AF then paroxysmal AF, and least readily in controls. APD alternans preceded all AF episodes, and was absent when AF did not initiate. The cellular mechanisms for APD alternans near resting heart rates require definition.