Fagundes M L, Cruz Filho F E, Boghossian S, Ribeiro J C, Vanheusden L, Maia I G
Hospital de Cardiologia de laranjeiras e Hospital Pró-Cardíaco, Rio de Janeiro.
Arq Bras Cardiol. 1995 May;64(5):447-53.
To evaluate the mechanisms and dynamics of episodes of progression to high degree (HD) atrioventricular (AV) block (B) analyzed during incremental atrial pacing (St), in patients with previous 2:1 His-Purkinje (HP) AVB.
Data from 4 patients were analyzed. All of them with history of syncope and ECG exhibiting 2:1 AVB with wide QRS pattern. The AVB was in the HP system (HPS) in all. Every patient was submitted to electrophysiologic study with incremental atrial pacing, by which the conduction sequences and the AV conduction ratios (AVR) were analyzed. The basal (B) cycle length (CL) was defined as the shortest interval between two conducted beats (spontaneous or pacing-induced). The incremental atrial stimulation was performed beginning with CL 10 msec shorter than BCL until reaching 250 msec.
Nineteen episodes of progression to HD-AVB were seen. A) With StCL between 31 and 26% of BCL, AVR were 3:1, 4:1 and 5:1, with only one blocking zone (BZ) in the HPS; B) with StCL between 24 and 22% of BCL, AVR were 5:1, 7:2, 9:2e11:3. In this situation a 2nd BZ ensues-on proximal, site of a decremental conduction, situated in the AV node (AVN) or in the HPS, and the other (distal level) always in HPS; C) with StCL between 24 and 16% of BCL, AVR were 5:1, 6:1, 10:2, 11:2 and 12:3. Here, these AVR were explained by postulating 3 BZ where 2 were in AVN and 1 in HPS, or inversely with 1 in AVN and 2 in HPS. The decremental conduction occurred in 1 or 2 out 3 BZ and an integral conduction (like 2:1 or 3:1) in the others.
The BCL is the determinant of the AVR observed. As the StCL is shortened (< 26% BCL) a 2nd or 3rd BZ in the AVN or in the HPS ensues. These observations suggest that the mechanisms and dynamics of progression to HD-AVB apply only during incremental atrial pacing and there is a clear difference with what has been observed with the progression occurring exclusively at AV node.
评估既往有2∶1希氏-浦肯野(HP)房室传导阻滞(AVB)的患者在递增性心房起搏(St)期间分析的进展为高度(HD)房室传导阻滞(B)发作的机制和动态变化。
分析4例患者的数据。所有患者均有晕厥病史,心电图显示2∶1 AVB伴宽QRS波型。所有患者的AVB均位于HP系统(HPS)。每位患者均接受递增性心房起搏的电生理研究,分析传导序列和房室传导比(AVR)。基础(B)周期长度(CL)定义为两次传导搏动(自发或起搏诱发)之间的最短间隔。递增性心房刺激从比基础周期长度(BCL)短10毫秒的CL开始,直至达到250毫秒。
观察到19次进展为HD-AVB的发作。A)当StCL在BCL的31%至26%之间时,AVR为3∶1、4∶1和5∶1,HPS中只有一个阻滞区(BZ);B)当StCL在BCL的24%至22%之间时,AVR为5∶1、7∶2、9∶2至11∶3。在这种情况下,第二个BZ出现在近端,即递减传导的部位,位于房室结(AVN)或HPS中,另一个(远端水平)总是在HPS中;C)当StCL在BCL的24%至16%之间时,AVR为5∶1、6∶1、10∶2、11∶2和12∶3。在这里,这些AVR通过假设有3个BZ来解释,其中2个在AVN中,1个在HPS中,或者相反,1个在AVN中,2个在HPS中。递减传导发生在3个BZ中的1个或2个中,其他BZ为整体传导(如2∶1或3∶1)。
BCL是观察到的AVR的决定因素。随着StCL缩短(<26% BCL),AVN或HPS中会出现第二个或第三个BZ。这些观察结果表明,进展为HD-AVB的机制和动态变化仅在递增性心房起搏期间适用,与仅在房室结发生进展时所观察到的情况有明显差异。