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与人类长期高血压相关的心房电和结构变化:对心房颤动基质的影响。

Atrial electrical and structural changes associated with longstanding hypertension in humans: implications for the substrate for atrial fibrillation.

机构信息

Department of Cardiology, Alfred Hospital and Baker IDI, Melbourne, Australia.

出版信息

J Cardiovasc Electrophysiol. 2011 Dec;22(12):1317-24. doi: 10.1111/j.1540-8167.2011.02125.x. Epub 2011 Jul 7.

DOI:10.1111/j.1540-8167.2011.02125.x
PMID:21736657
Abstract

UNLABELLED

INTRODUCTION

Hypertension (HT) is the most common modifiable risk factor for atrial fibrillation (AF), yet little is known of the atrial effects of chronic HT in humans. We aimed to characterize the electrophysiologic (EP) and electroanatomic (EA) remodeling of the right atrium (RA) in patients with chronically treated systemic HT and left ventricular hypertrophy (LVH) without a history of AF.

METHODS AND RESULTS

Twenty patients with (systolic BP 145 ± 10 mmHg) and without (BP 119 ± 11 mmHg, P < 0.01) systemic HT underwent detailed conventional EP and EA voltage and activation mapping. We measured RA refractoriness at the coronary sinus and high septum at cycle lengths (CLs) 600 and 450 ms, and RA conduction velocities, activation times, and voltages at a global and regional level at CLs 600 ms and 300 ms. HT was associated with slowing of global (73 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) and regional conduction velocity particularly in the posterior RA (70 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) at the crista terminalis (fractionation and double potentials in HT 72%± 4 vs 43%± 23 in controls, P = 0.04). Mean RA voltage was similar between the 2 groups, however HT was associated with an increase in areas of low voltage (<0.5 mV; HT 13% vs controls 9%, P = 0.04). Sustained AF was induced in 30% HT patients and no controls.

CONCLUSION

Chronically treated systemic HT with LVH is accompanied by atrial remodeling characterized by: (i) global conduction slowing, (ii) regional conduction delay particularly at the crista terminalis, and (iii) increased AF inducibility. These changes may in part be responsible for the increased propensity to AF associated with systemic HT.

摘要

目的

高血压(HT)是心房颤动(AF)最常见的可调节危险因素,但对于慢性 HT 患者的心房电生理(EP)和电解剖(EA)重构知之甚少。我们旨在描述患有慢性系统性 HT 和左心室肥厚(LVH)且无 AF 病史的患者的右心房(RA)的 EP 和 EA 重构。

方法和结果

20 例患者(收缩压 145 ± 10mmHg)和 20 例无系统性 HT 患者(血压 119 ± 11mmHg,P<0.01)接受了详细的常规 EP 和 EA 电压和激活映射。我们在窦房结和高位间隔的冠状窦处测量了 600ms 和 450ms 的 RA 不应期,并在 600ms 和 300ms 的 CL 时测量了 RA 传导速度、激活时间和全局及区域水平的电压。HT 与全球(73 ± 17cm/s 与对照组 96 ± 12cm/s,P<0.01)和区域传导速度(特别是在后部 RA 时)减慢相关(70 ± 17cm/s 与对照组 96 ± 12cm/s,P<0.01)在冠状窦末端的希氏束(HT 为 72%±4,对照组为 43%±23,P=0.04)。两组之间的平均 RA 电压相似,但 HT 与低电压区域(<0.5mV)的增加有关(HT 为 13%,对照组为 9%,P=0.04)。30%的 HT 患者和无对照组患者可诱发持续性 AF。

结论

慢性治疗性系统性 HT 伴 LVH 伴心房重构,其特征为:(i)全局传导减慢,(ii)局部传导延迟,特别是在冠状窦末端,(iii)AF 易感性增加。这些变化可能部分解释了与系统性 HT 相关的 AF 易感性增加。

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