Massumi R A, Udhoji V N
Department of Medicine, Sepulveda VA Medical Center, California.
J Electrocardiol. 1988 Jan;21(1):83-8. doi: 10.1016/s0022-0736(88)80028-1.
In a 67-year-old man with multiple myocardial infarctions in the past, the use of oral verapamil for control of angina pectoris was followed by the appearance of two previously undiagnosed abnormalities, namely, a dual-pathway AV node conduction pattern, and paroxysms of AV nodal reentrant tachycardia precipitated by premature ventricular beats (PVB). It is probable that the differential effects of verapamil on the fast and slow AV node pathways, and the interplay of PVB with its concealment within the AV node, created the necessary circumstances in the AV node to precipitate the tachycardia. Observed off verapamil over several months, the patient remained in normal sinus rhythm but continued to have numerous premature ventricular beats (PVB's). Nevertheless, neither the clinical electrocardiographic features of dual-pathway AV node conduction nor the AV nodal reentrant tachycardia could be found. The proarrhythmic effect of verapamil and its ability to provoke the very arrhythmia against which it is most effective are of particular interest in view of a similar behavior exhibited by the Class I antiarrhythmic agents.
一名67岁男性，既往有多次心肌梗死病史，在使用口服维拉帕米控制心绞痛后，出现了两个先前未被诊断出的异常情况，即双径路房室结传导模式，以及室性早搏（PVB）诱发的房室结折返性心动过速发作。维拉帕米对房室结快径路和慢径路的不同作用，以及室性早搏与其在房室结内隐匿性的相互作用，可能在房室结内创造了引发心动过速的必要条件。在停用维拉帕米几个月的观察期内，患者维持正常窦性心律，但仍有大量室性早搏。然而，未发现双径路房室结传导的临床心电图特征，也未出现房室结折返性心动过速。鉴于I类抗心律失常药物也表现出类似行为，维拉帕米的促心律失常作用及其引发自身最有效的心律失常的能力尤其值得关注。
