Tavazzi L, Chimienti M, Salerno J A, Ray M, Bobba P
G Ital Cardiol. 1978;8(10):1072-89.
In 10 patients with supraventricular tachycardia who underwent an electrophysiological study the ectopic atrial origin of the tachycardia could be demonstrated by the intracavitary localization of the earliest depolarized point (six cases in the right atrium and four cases in the left). Vagal stimulation and/or the i.v. infection of ATP induced or increased the degree of AV block during tachycardia; in five cases ATP interrupted the tachycardia. On the basis of their clinical and electrophysiological behavior, the patients were divided into two groups. In the first one (6 patients) tachycardia was persistent, started following late atrial beats with the same morphology of the subsequent and showed a progressive initial rate increase (warm-up phenomenon); programmed atrial stimulation failed to start and interrupt it. In the second group (4 patients) tachycardia was paroxysmal or repetitive, started following early atrial beats and could be induced and interrupted by programmed atrial stimulation. With respect to the electrophysiological characteristics of each group the authors try to define the possible mechanism responsible for the tachycardia (automaticity and micro-reentry).
在10例接受电生理研究的室上性心动过速患者中，通过最早去极化点的腔内定位可证实心动过速的异位心房起源（6例起源于右心房，4例起源于左心房）。迷走神经刺激和/或静脉注射三磷酸腺苷（ATP）可诱发或加重心动过速时的房室传导阻滞程度；5例患者中ATP终止了心动过速。根据患者的临床和电生理表现，将其分为两组。第一组（6例患者）心动过速持续存在，起始于形态与后续心动过速相同的房性早搏晚期，并呈现初始心率逐渐增加（预热现象）；程控心房刺激不能诱发和终止心动过速。第二组（4例患者）心动过速为阵发性或反复性，起始于房性早搏早期，可被程控心房刺激诱发和终止。关于每组的电生理特征，作者试图确定导致心动过速的可能机制（自律性和微折返）。
