Langer Frank, Tibayan Frederick A, Rodriguez Filiberto, Timek Tomasz, Zasio Mary K, Liang David, Daughters George T, Ingels Neil B, Miller D Craig
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
J Heart Valve Dis. 2005 May;14(3):286-94; discussion 294.
Pacing-induced mitral regurgitation contributes to the 'pacemaker syndrome', which usually is observed with ventricular (V) pacing, but has also been reported with atrioventricular (AV) sequential pacing. Effects of different pacing modes on 3-D kinematics of the mitral apparatus are incompletely understood.
Radio-opaque markers were placed on the left ventricular (LV) and mitral apparatus including the annulus, leaflets and papillary muscles of eight sheep. Hemodynamic and 3-D dynamic marker geometry were obtained one week later with biplane videofluoroscopy (60 Hz) during atrial (pacing site = left atrium), AV-sequential (140 ms interval) and (anterolateral LV epicardial) ventricular pacing.
Compared with A-pacing (p <0.05): 1) The regurgitant fraction increased with both AV- and V-pacing (A: 6 +/- 3%, AV: 13 +/- 3%, V: 15 +/- 2%); 2) AV and V-pacing delayed closure at the leaflet center (A: 21 +/- 10 ms, AV: 52 + 5 ms, V: 92 +/- 6 ms*) and posterior commissure (A: 17 +/- 10 ms, AV: 46 +/- 8 ms*, V: 94 +/- 6 ms*). V-pacing delayed valve closure at the anterior commissure (A: 27 +/- 9 ms, V: 94 +/- 6 ms*); 3) The end-diastolic leaflet opening angle was greater with AV- and V-pacing (anterior mitral leaflet (AML): A: 32 +/- 2 degrees, AV: 41 +/- 4 degrees*, V: 46 +/- 4 degrees*; posterior mitral leaflet (PML): A: 56 +/- 4 degrees, AV: 62 +/- 3 degrees*, V: 68 +/- 3 degrees*); 4) 'Effective' end-diastolic PML midline length was reduced with AV- and V-pacing (A: 11.2 +/- 0.7 mm, AV: 10.0 +/- 0.4 mm*, V: 10.2 +/- 0.3 mm*), as was the distance from each papillary muscle (PM) tip to the AML edge ('effective' chordal length) close to the commissures (anterior PM-AML: A: 31.5 +/-1.8 mm, AV: 30.5 +/- 1.9 mm*, V: 29.7 +/- 1.8 mm*; posterior PM-AML: A: 33.7 +/- 1.8 mm, AV: 33.1 +/- 1.9 mm*, V: 32.8 +/- 1.9 mm*).
Both ventricular and AV-sequential-pacing resulted in a more widely opened valve at end-diastole and leaflet dyssynchrony with delayed mitral valve closure and early systolic mitral regurgitation. These alterations which result in pacing-induced mitral regurgitation may be clinically important in patients with impaired LV function.
起搏诱发的二尖瓣反流会导致“起搏器综合征”，通常在心室（V）起搏时出现，但也有报道称在房室（AV）顺序起搏时也会出现。不同起搏模式对二尖瓣装置三维运动学的影响尚未完全明确。
在八只绵羊的左心室（LV）和二尖瓣装置（包括瓣环、瓣叶和乳头肌）上放置不透射线的标记物。一周后，通过双平面视频荧光透视法（60Hz）在心房起搏（起搏部位 = 左心房）、房室顺序起搏（间期140ms）和（左心室前外侧心外膜）心室起搏过程中获取血流动力学和三维动态标记物几何形状。
与心房起搏相比（p <0.05）：1）房室起搏和心室起搏时反流分数均增加（心房起搏：6±3%，房室起搏：13±3%，心室起搏：15±2%）；2）房室起搏和心室起搏延迟瓣叶中心（心房起搏：21±10ms，房室起搏：52±5ms*，心室起搏：92±6ms*）和后联合处（心房起搏：17±10ms，房室起搏：46±8ms*，心室起搏：94±6ms*）的关闭。心室起搏延迟前联合处瓣膜关闭（心房起搏：27±9ms，心室起搏：94±6ms*）；3）房室起搏和心室起搏时舒张末期瓣叶开口角度更大（前二尖瓣叶（AML）：心房起搏：32±2°，房室起搏：41±4°，心室起搏：46±4°；后二尖瓣叶（PML）：心房起搏：56±4°，房室起搏：62±3°，心室起搏：68±3°）；4）房室起搏和心室起搏时舒张末期“有效”PML中线长度缩短（心房起搏：11.2±0.7mm，房室起搏：10.0±0.4mm*，心室起搏：10.2±0.3mm*），靠近联合处的每个乳头肌（PM）尖端到AML边缘的距离（“有效”腱索长度）也缩短（前PM-AML：心房起搏：31.5±1.8mm，房室起搏：30.5±1.9mm*，心室起搏：29.7±1.8mm*；后PM-AML：心房起搏：33.7±1.8mm，房室起搏：33.
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