REENTRY AS A CAUSE OF VENTRICULAR-TACHYCARDIA IN PATIENTS WITH CHRONIC ISCHEMIC HEART-DISEASE - ELECTROPHYSIOLOGIC AND ANATOMIC CORRELATION
REENTRY AS A CAUSE OF VENTRICULAR-TACHYCARDIA IN PATIENTS WITH CHRONIC ISCHEMIC HEART-DISEASE - ELECTROPHYSIOLOGIC AND ANATOMIC CORRELATION
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DOI：
10.1161/01.cir.77.3.589
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发表时间：
1988-03-01
期刊：
影响因子：
37.8
通讯作者：
HAUER, RNW
中科院分区：
文献类型：
--
作者：
DEBAKKER, JMT;VANCAPELLE, FJL;HAUER, RNW
在这份报告中，我们描述了心肌梗死慢性期持续性室性心动过速患者的心脏和心内膜切除标本的电生理和组织学结果。我们同时记录了72例因药物难治性室性心动过速而接受手术的患者心动过速期间的64个内分泌部位。另外两名患者接受了心脏移植，并在连接到Langendorff灌注装置的分离的心脏上进行标测。术中可诱发不同形态心动过速139例。尽管大多数证据支持这些心动过速的折返机制的概念，但我们发现105例心动过速似乎出现在小于1.4 cm 2的病灶区域。只有三例病例可以检测到梗死疤痕周围的大折返。在21例“起源”似乎是局灶性的心动过速中，最早的内膜下激活之前是低振幅的离散电描记图（收缩前活动）。在三个心动过速收缩前活动检测到在几个网站，允许重建其路线。在这些病例中，其中一例的内膜切除标本的组织学检查显示，在记录到收缩前活动的区域中存在独立的存活心肌纤维区。这些区域位于壁内和心内膜下，支持通过在梗死边缘和较大的内膜下肌肉质量处的孤立的存活肌细胞束发生折返的概念。通过孤立的管道的传导速度是在25厘米/秒的数量级。在两个离体心脏中发现了类似的折返通路。细胞外和细胞内的记录，从20内皮细胞的准备工作，切除的地区，其中心动过速起源。在组织浴中灌注制剂。这些实验表明，动作电位通常接近正常，但偶尔也会发现振幅降低和缓慢上升的动作电位，此外，根据波前的方向，有些细胞会同时表现出快速和缓慢的上升。七个切除的制剂和离体心脏的组织学显示，心内膜下以及壁内位于区的存活心肌。在存活的肌纤维和纤维组织股交织的区域，以及肌纤维平行取向但被结缔组织股隔离的区域，发现细胞外电描记图的分级和缓慢传导。（400字处截断摘要）
In this report we describe electrophysiologic and histologic findings in hearts and endocardially resected preparations from patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction. We recorded simultaneously from 64 endocardial sites during tachycardia in 72 patients that were operated on for medically intractable ventricular tachycardias. Two other patients underwent heart transplantation, and mapping was performed on the explanted isolated heart connected to a Langendorff perfusion set-up. During operation 139 tachycardias with different morphologies could be induced. Although the majority of evidence supports the concept of a reentrant mechanism for these tachycardias, we found that 105 tachycardias appeared to arise at a focal area of less than 1.4 cm2. In only three cases macroreentry around the infarction scar could be detected. Of 21 tachycardias in which the "origin" appeared to be focal, earliest subendocardial activation was preceded by discrete electrograms of low amplitude (presystolic activity). In three tachycardias presystolic activity was detected at several sites, permitting reconstruction of its route. Histology of the endocardial resected preparation in one of these cases revealed separate zones of viable myocardial fibers in areas in which presystolic activity was recorded. These zones were located intramurally and subendocardially, supporting the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass. Conduction velocity through the isolated tracts was on the order of 25 cm/sec. Similar reentrant pathways were found in the two isolated hearts. Extracellular and intracellular recordings were made from 20 endocardial preparations that were excised from areas in which tachycardia originated. Preparations were superfused in a tissue bath. These experiments showed that action potentials were usually close to normal, but occasionally action potentials with reduced amplitude and slow upstrokes were found. In addition, there were cells that exhibited both fast and slow upstrokes, depending on the direction of the wavefront. Histology of seven resected preparations and the isolated hearts showed subendocardially as well as intramurally located zones of viable myocardium. Fractionation of extracellular electrograms and slow conduction were found in areas where surviving muscle fibers and strands of fibrous tissue were interwoven, and in zones where muscle fibers were oriented in parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED AT 400 WORDS)