Kyriacou Andreas, Rajkumar Christopher A, Pabari Punam A, Sohaib S M Afzal, Willson Keith, Peters Nicholas S, Lim Phang B, Kanagaratnam Prapa, Hughes Alun D, Mayet Jamil, Whinnett Zachary I, Francis Darrel P
The Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK.
International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College London, London, W12 0HS, UK.
Pacing Clin Electrophysiol. 2018 Jun 1;41(8):959-66. doi: 10.1111/pace.13401.
Controversy exists regarding how atrial activation mode and heart rate affect optimal atrioventricular (AV) delay in cardiac resynchronization therapy. We studied these questions using high-reproducibility hemodynamic and echocardiographic measurements.
Twenty patients were hemodynamically optimized using noninvasive beat-to-beat blood pressure at rest (62 ± 11 beats/min), during exercise (80 ± 6 beats/min), and at three atrially paced rates: 5, 25, and 45 beats/min above rest, denoted as A , A , and A , respectively. Left atrial myocardial motion and transmitral flow were timed echocardiographically.
During atrial sensing, raising heart rate shortened optimal AV delay by 25 ± 6 ms (P < 0.001). During atrial pacing, raising heart rate from A to A shortened it by 16 ± 6 ms; A shortened it 17 ± 6 ms further (P < 0.001). In comparison to atrial-sensed activation, atrial pacing lengthened optimal AV delay by 76 ± 6 ms (P < 0.0001) at rest, and at ∼20 beats/min faster, by 85 ± 7 ms (P < 0.0001), 9 ± 4 ms more (P = 0.017). Mechanically, atrial pacing delayed left atrial contraction by 63 ± 5 ms at rest and by 73 ± 5 ms (i.e., by 10 ± 5 ms more, P < 0.05) at ∼20 beats/min faster. Raising atrial rate by exercise advanced left atrial contraction by 7 ± 2 ms (P = 0.001). Raising it by atrial pacing did not (P = 0.2).
Hemodynamic optimal AV delay shortens with elevation of heart rate. It lengthens on switching from atrial-sensed to atrial-paced at the same rate, and echocardiography shows this sensed-paced difference in optima results from a sensed-paced difference in atrial electromechanical delay. The reason for the widening of the sensed-paced difference in AV optimum may be physiological stimuli (e.g., adrenergic drive) advancing left atrial contraction during exercise but not with fast atrial pacing.
关于心房激动模式和心率如何影响心脏再同步治疗中最佳房室(AV)间期,目前存在争议。我们使用高重复性的血流动力学和超声心动图测量方法对这些问题进行了研究。
对20例患者在静息状态(62±11次/分钟)、运动状态(80±6次/分钟)以及三种心房起搏频率下进行血流动力学优化,这三种心房起搏频率分别比静息时高5、25和45次/分钟,分别记为A₁、A₂和A₃。通过超声心动图对左心房心肌运动和二尖瓣血流进行计时。
在心房感知期间,心率升高使最佳AV间期缩短25±6毫秒(P<0.001)。在心房起搏期间,心率从A₁升至A₂时,最佳AV间期缩短16±6毫秒;从A₂升至A₃时进一步缩短17±6毫秒(P<0.001)。与心房感知激动相比,心房起搏在静息时使最佳AV间期延长76±6毫秒(P<0.0001),在心率快约20次/分钟时延长85±7毫秒(P<0.0001),延长幅度多9±4毫秒(P=0.017)。从机械角度来看,心房起搏在静息时使左心房收缩延迟63±5毫秒,在心率快约20次/分钟时延迟73±5毫秒(即多延迟10±5毫秒,P<0.05)。运动使心房率升高时,左心房收缩提前7±2毫秒(P=0.001)。心房起搏使心房率升高时则没有这种情况(P=0.2)。
血流动力学最佳AV间期随心率升高而缩短。在相同心率下从心房感知转换为心房起搏时,最佳AV间期延长,并且超声心动图显示这种感知起搏在最佳值上的差异是由心房机电延迟的感知起搏差异导致的。AV最佳值中感知起搏差异扩大的原因可能是生理刺激(如肾上腺素能驱动)在运动时使左心房收缩提前,但快速心房起搏时则不然。