Wang K, Xiao H B, Fujimoto S, Gibson D G
Cardiac Department, Royal Brompton Hospital, London.
Br Heart J. 1995 Oct;74(4):403-7. doi: 10.1136/hrt.74.4.403.
To assess the effect of right atrial appendage pacing on atrial electromechanical interrelations in patients with DDD pacemakers.
Prospective study by M mode echocardiogram, Doppler echocardiogram, and apexcardiogram, along with electrocardiogram and phonocardiogram.
Tertiary cardiac referral centre.
20 patients with DDD pacemakers and 20 age matched normal controls.
Age, RR interval, atrial size, left ventricular size, and fractional shortening were similar in the two groups. Atrial electromechanical delay (the time from the onset of P wave or atrial pacing spike on ECG to the onset of atrial contraction on M mode echogram) was 68 (SD 7) ms at the lateral site of right atrium, 82 (9) ms at the central fibrous body, 93 (11) ms at the lateral site of left atrium in normals. In patients with DDD pacing, however, this delay increased to 85 (22) ms, 117 (23) ms, and 138 (25) ms respectively (all P < 0.01). Interatrial mechanical delay (the time from the onset of right atrial motion to the onset of the left) increased from 25 (6) ms in normal controls to 53 (18) ms in patients (P < 0.01). Intra-atrial mechanical dispersion (the time from the earliest to the latest onset of regional atrial motion around the atrioventricular ring) in the right atrium increased from 6 (2) ms in normals to 19 (2) ms in patients (P < 0.01), but it remained unchanged in the left atrium (6 (2) ms in normal controls v 7 (2) ms in patients, P > 0.05). Peak atrial shortening rate was not different between the two groups. Differences of atrial electromechanical activity between the two groups were also reflected on Doppler echocardiogram and apexcardiogram.
Right atrial appendage pacing disturbs the normal coordinate sequence of right atrial mechanical activity and leads to a striking and variable increase in intra-atrial conduction time as well as in interatrial conduction time. Left atrial contraction remains synchronous although the timing of the start of its contraction was delayed. These values can be determined in individual patients to allow optimal setting of DDD pacemakers.
评估右心耳起搏对植入DDD起搏器患者心房机电关系的影响。
采用M型超声心动图、多普勒超声心动图、心尖心动图,同时结合心电图和心音图进行前瞻性研究。
三级心脏转诊中心。
20例植入DDD起搏器的患者和20例年龄匹配的正常对照者。
两组患者的年龄、RR间期、心房大小、左心室大小和缩短分数相似。正常人心房机电延迟(心电图上P波或心房起搏信号开始至M型超声心动图上心房收缩开始的时间)在右心房外侧为68(标准差7)ms,在中心纤维体为82(9)ms,在左心房外侧为93(11)ms。然而,在DDD起搏患者中,该延迟分别增加至85(22)ms、117(23)ms和138(25)ms(均P<0.01)。房间机械延迟(右心房运动开始至左心房运动开始的时间)从正常对照者的25(6)ms增加至患者的53(18)ms(P<0.01)。右心房内机械离散度(房室环周围区域心房运动最早至最晚开始的时间)从正常者的6(2)ms增加至患者的19(2)ms(P<0.01),但左心房内机械离散度保持不变(正常对照者为6(2)ms,患者为7(2)ms,P>0.05)。两组之间心房缩短率峰值无差异。两组之间心房机电活动的差异也反映在多普勒超声心动图和心尖心动图上。
右心耳起搏扰乱了右心房机械活动的正常协调顺序,导致心房内传导时间以及房间传导时间显著且可变地增加。尽管左心房收缩开始时间延迟,但其收缩仍保持同步。这些数值可在个体患者中测定,以优化DDD起搏器的设置。