Panagides D, Bory M, Bonnet J L, Yvorra S, Desfossez L, Savin B, Ebagosti A, Van de Walle J P
Service de cardiologie A, CHU Timone, Marseille.
Arch Mal Coeur Vaiss. 1994 Jan;87(1):111-4.
Ischaemia has been the suggested mechanism of simultaneous left bundle branch block and chest pain on effort with normal coronary angiography. This hypothesis is very controversial and was not the mechanism in the two new cases of this syndrome. The two patients in whom effort pain and left bundle branch block were observed had been treated for paroxysmal supraventricular tachycardia with flecaine. Withdrawal of the anti-arrhtymic resulted in the disappearance of this syndrome. In these cases, the ischaemic mechanism could be excluded without ambiguity. The flecaine was the only cause of rate-related LBBB by slowing conduction in the left bundle branch with no effects on coronary reserve. It would seem that LBBB alone was the cause of chest pain. The absence of coronary artery disease was confirmed in the first patient and the diagnosis was highly improbable in the second.
缺血一直被认为是在冠状动脉造影正常的情况下,运动时同时出现左束支传导阻滞和胸痛的机制。这一假说极具争议性,并非这两例该综合征新病例的发病机制。观察到运动性疼痛和左束支传导阻滞的两名患者曾用氟卡尼治疗阵发性室上性心动过速。停用抗心律失常药物后,该综合征消失。在这些病例中,可以明确排除缺血机制。氟卡尼是与心率相关的左束支传导阻滞的唯一原因,它通过减慢左束支的传导而不影响冠状动脉储备。似乎仅左束支传导阻滞就是胸痛的原因。首例患者经证实无冠状动脉疾病,第二例患者患此病的可能性极小。