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人类大折返的功能特征:用额外刺激法对“预激”环路的研究

Functional characteristics of human macro-reentry: a study of "pre-excited" circuits by extrastimulus method.

作者信息

Mahmud R, Tchou P J, Denker S T, Lehmann M H, Akhtar M

出版信息

J Am Coll Cardiol. 1986 Nov;8(5):1073-81. doi: 10.1016/s0735-1097(86)80384-9.

Abstract

The effect of improved conduction in areas of delay was tested during macro-reentry within the His-Purkinje system, in an attempt to separate the role of conduction delay from that of prematurity of the extrastimulus as the key determinant of reentry. Using the right ventricular extrastimulus technique (S1S2 method), both the critical His-Purkinje system delays and the zone of S1S2 intervals causing His-Purkinje system reentry were determined. Then, using a previously described technique of atrioventricular (AV) sequential pacing during the basic drive, the potential site of His-Purkinje system conduction delay was (anterogradely) excited earlier (pre-excitation), as compared with the control S1S2 method. This produced a decrease in retrograde His-Purkinje system delay (S2H2), as compared with the same S1S2 interval during the control method. Changing the degree of pre-excitation at each S1S2 interval allowed for determination of the critical (or shortest) S2H2 delay necessary for His-Purkinje system reentry at each coupling interval. Of importance was the observation that the critical delay was not specific for each case but varied with the prematurity of S2. For example, the critical S2H2 delay required for reentry was actually less at shorter S1S2 intervals as compared with longer S1S2 intervals (from 206 +/- 25 to 187 +/- 20 ms, p less than 0.01). These data suggest that manifestation of reentry is a complex interplay between degree of prematurity and conduction delay. The so-called critical conduction delay can be readily modified by altering the site of block, which in turn may be dependent on prematurity of the extrastimulus.

摘要

在希氏 - 浦肯野系统内的大折返过程中,测试了延迟区域传导改善的效果,试图将传导延迟的作用与额外刺激的提前程度区分开来,因为后者是折返的关键决定因素。使用右心室额外刺激技术(S1S2法),确定了希氏 - 浦肯野系统的临界延迟以及导致希氏 - 浦肯野系统折返的S1S2间期范围。然后,在基础驱动期间使用先前描述的房室(AV)顺序起搏技术,与对照S1S2法相比,希氏 - 浦肯野系统传导延迟的潜在部位(顺行性)被更早地激动(预激)。与对照方法中相同的S1S2间期相比,这导致逆行希氏 - 浦肯野系统延迟(S2H2)减少。在每个S1S2间期改变预激程度,可确定每个耦合间期希氏 - 浦肯野系统折返所需的临界(或最短)S2H2延迟。重要的是观察到临界延迟并非每种情况都特定,而是随S2的提前程度而变化。例如,与较长的S1S2间期相比,较短的S1S2间期时折返所需的临界S2H2延迟实际上更小(从206±25到187±20毫秒,p小于0.01)。这些数据表明,折返的表现是提前程度和传导延迟之间复杂的相互作用。所谓的临界传导延迟可以通过改变阻滞部位轻易改变,而阻滞部位反过来可能取决于额外刺激的提前程度。

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