Markowitz Steven M, Brodman Richard F, Stein Kenneth M, Mittal Suneet, Slotwiner David J, Iwai Sei, Das Mithilesh K, Lerman Bruce B
Division of Cardiology, The New York Hospital-Cornell University Medical Center, New York, New York 10021, USA.
J Am Coll Cardiol. 2002 Jun 19;39(12):1973-83. doi: 10.1016/s0735-1097(02)01905-8.
The purpose of this study was to define the anatomic distribution of electrically abnormal atrial tissue and mechanisms of atrial tachycardia (AT) after mitral valve (MV) surgery.
Atrial tachycardia is a well-recognized long-term complication of MV surgery. Because atrial incisions from repair of congenital heart defects provide a substrate for re-entrant arrhythmias in the late postoperative setting, we hypothesized that atriotomies or cannulation sites during MV surgery also contributed to postoperative arrhythmias.
In 10 patients with prior MV surgery, electroanatomic maps were constructed of 11 tachycardias (6 right atrium [RA], 4 left atrium [LA] and 1 biatrial). Activation and voltage maps were used to identify areas of low voltage, double potentials and conduction block.
Lesions were present in the lateral wall of the RA (six of seven maps) and in the LA along the septum adjacent to the right pulmonary veins (four of five maps). In 8 of 10 patients, these findings corresponded to atrial incisions or cannulation sites. Arrhythmia mechanisms were identified for 9 of 11 tachycardias. A macro-re-entrant circuit was mapped in six cases, three involving lesions in the lateral wall of the RA and three involving the LA septum and right pulmonary veins. In three of these cases figure-of-eight re-entry was demonstrated, and in the other three a single macro-re-entrant circuit was observed. In three other cases, a focal origin was identified adjacent to abnormal tissue in the RA (two cases) or within a pulmonary vein (one case).
Surgical incisions for MV surgery provide a substrate for atrial arrhythmias. Both macro-re-entrant and focal mechanisms contribute to AT after MV surgery.
本研究旨在明确二尖瓣手术(MV)后电活动异常心房组织的解剖分布及房性心动过速(AT)的机制。
房性心动过速是MV手术公认的长期并发症。由于先天性心脏缺陷修复时的心房切口为术后晚期折返性心律失常提供了基质,我们推测MV手术期间的心房切开或插管部位也会导致术后心律失常。
对10例曾接受MV手术的患者,构建了11次心动过速的电解剖图(6次右心房[RA]、4次左心房[LA]和1次双房)。利用激动图和电压图识别低电压、双电位和传导阻滞区域。
病变存在于RA侧壁(7张图中的6张)以及LA中与右肺静脉相邻的间隔处(5张图中的4张)。10例患者中有8例,这些发现与心房切口或插管部位相符。确定了11次心动过速中9次的心律失常机制。6例绘制出大折返环,3例涉及RA侧壁病变,3例涉及LA间隔和右肺静脉。其中3例证实为8字形折返,另外3例观察到单一的大折返环。其他3例中,确定1例起源于RA异常组织附近(2例)或肺静脉内(1例)。
MV手术的手术切口为房性心律失常提供了基质。大折返机制和局灶机制均促成MV手术后的AT。