Electrical remodeling of the human atrium: Similar effects in patients with chronic atrial fibrillation and atrial flutter
Electrical remodeling of the human atrium: Similar effects in patients with chronic atrial fibrillation and atrial flutter
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DOI：
10.1016/s0735-1097(97)00385-9
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发表时间：
1997-12-01
影响因子：
24
通讯作者：
Chavez, M
中科院分区：
文献类型：
--
作者：
Franz, MR;Karasik, PL;Chavez, M
目标。本研究旨在确定患者的慢性心房颤动 (AF) 和心房扑动是否会导致人类心房心肌的电重塑，表现为心房周期长度和动作电位持续时间 (APD) 之间的异常关系。背景。对山羊和离体人体心房组织的实验研究表明，长期房颤会导致心房不应期持续缩短，这种现象称为电重塑，有助于解释房颤为何会引发房颤。仍然缺乏关于人体原位心肌的直接数据。方法。我们同时使用两个右心房部位的单相动作电位记录，确定了 7 名慢性 AF 患者和 13 名慢性心房扑动患者（持续 3 周至 3 年）在转为窦性心律后 15 至 30 分钟起搏周期长度与 90% 复极 (APD90) 时的 APD 之间的关系。在规则节奏的周期长度（250 至 800 毫秒）期间测量 APD90，以确定稳态周期长度关系，并在 600 毫秒的基本周期长度的额外刺激间隔（从 800 毫秒到不应期）期间测量 APD90，以确定电恢复曲线。对九名窦性心律且无明显心房疾病的对照患者进行了相同的起搏方案和测量。结果。在对照患者中，稳态 APD90 随着周期长度从 250 毫秒增加到 800 毫秒而稳定增加，在周期长度为 800 毫秒时达到最大值 325 +/- 41 毫秒（平均值 +/- SD）。在心房扑动或房颤复律的患者中，稳态周期长度-APD90关系在周期长度>400 ms时向下移动并变平，在800 ms周期长度时分别仅达到219 +/- 44和245 +/- 39 ms（与对照相比，p < 0.005）。所有三组之间电恢复的早期时间进程（200 至 300 毫秒的额外刺激间隔）相似，但在额外刺激间隔 >350 毫秒时，AF 组和心房推杆组的 APD90 均比对照组短（p < 0.05）。房颤复律患者与房颤复律患者之间没有显着差异。稳态周期长度为 600 ms 时的 APD90 显示与既往 AF 或心房扑动的持续时间没有显着相关性。结论。 AF 和心房扑动导致右心房 APD 在稳态起搏和复律后相当长一段时间内的额外刺激期间出现明显的、定量相似的下降。这些数据证实，房颤和心房扑动都会导致人类心房的电重塑，并且在较长的周期长度中占主导地位。尽早中止两种类型的心律失常以防止电重构可能是谨慎的做法。 (C) 1997 年由美国心脏病学会发布。
Objectives. This study sought to determine whether chronic atrial fibrillation (AF) and atrial flutter in patients lead to electrical remodeling of the human atrial myocardium, manifested by an abnormal relation between atrial cycle length and action potential duration (APD).Background. Experimental studies in goats and isolated human atrial tissue have shown that prolonged AF leads to persistent shortening of atrial refractoriness, a phenomenon referred to as electrical remodeling and which helps to explain why AF begets AF. Direct data on human in situ myocardium are still lacking.Methods. Using monophasic action potential recordings at two right atrial sites simultaneously, we determined in 7 patients with chronic AF and 13 with chronic atrial flutter (3 weeks to 3 years in duration) the relation between paced cycle length and APD at 90% repolarization (APD90) 15 to 30 min after conversion to sinus rhythm. APD90 was measured during regularly paced cycle lengths (250 to 800 ms) to determine the steady state cycle length relation and during extrastimulus intervals (from 800 ms to refractoriness) at a basic cycle length of 600 ms to determine electrical restitution curves. The same pacing protocols and measurements were performed in nine control patients with sinus rhythm and no overt atrial disease.Results. In control patients, steady state APD90 increased steadily with increases in cycle length from 250 to 800 ms, reaching a maximal value of 325 +/- 41 ms (mean +/- SD) at a cycle length of 800 ms. In patients with cardioversion from atrial flutter or AF, the steady state cycle length-APD90 relation was shifted downward and flattened at cycle lengths >400 ms, reaching only 219 +/- 44 and 245 +/- 39 ms, respectively, at the 800 ms cycle length (p < 0.005 vs. control). The early time course of electrical restitution (200- to 300-ms extrastimulus intervals) was similar between all three groups, but at extrastimulus intervals >350 ms, APD90 was shorter in both the AF and atrial putter groups than in the control group (p < 0.05). There were no significant differences between patients with cardioversion from atrial putter and those with cardioversion from AF. APD90 at a steady state cycle length of 600 ms showed no significant correlation with the duration of previous AF or atrial flutter.Conclusions. AF and atrial flutter lead to marked, quantitatively similar decreases in the right atrial APD during steady state pacing and extrastimulation a considerable time after cardioversion. These data confirm that both AF and atrial flutter lead to electrical remodeling in the human atrium, with a preponderance at longer cycle lengths. It may be prudent to abort both types of arrhythmias early to prevent electrical remodeling. (C) 1997 by the American College of Cardiology.