Obel O A, Camm A J
Department of Cardiological Sciences, St George's Hospital Medical School, London, U.K.
Eur Heart J. 1998 May;19 Suppl E:E13-24, E50-1.
Patients who have an accessory pathway (AP) of atrioventricular (AV) conduction may develop circus movement tachycardia otherwise known as atrioventricular re-entrant tachycardia (AVRT). Orthodromic AVRT is the most common form. It occurs as a result of antegrade conduction through the normal AV conduction system and retrograde conduction to the atria via the AP. Less commonly, conduction occurs in the opposite direction resulting in antidromic AVRT. Tachycardia may also involve multiple APs which may provide both antegrade and retrograde conduction and may alternate antegradely or retrogradely. Tachycardia may occur in which the AP simply acts as a bystander, and does not participate in the tachycardia mechanism. When atrial fibrillation is conducted to the ventricles via and AP, the resultant ventricular rate may be extremely rapid, placing the patient at risk of developing ventricular fibrillation and cardiac arrest. This paper reviews the anatomical and physiological substrates involved in the pathogenesis of AVRT. The acute and long-term management of patients who suffer from these arrhythmias will then be discussed. The normal AV annulus is composed exclusively of electrically inert fibrous tissue. The AV node and His bundle normally act as the sole route of electrical conduction. Accessory pathways occur at all points along the AV ring, and usually occur as isolated abnormalities, although a proportion of patients have associated congenital abnormalities. This is particularly true of right-sided APs. Most APs exhibit non-decremental conduction properties, and conduct faster than normal AV conduction tissue. In many patients with APs the surface ECG reveals clear evidence of pre-excitation, and a good idea of pathway localization is possible using one or more of several algorithms which have been developed. Patients with latent pre-excitation, intermittent pre-excitation, and patients with concealed APs have not evidence of pre-excitation on a proportion or all of Their surface ECGs. Patients present with a history of paroxysmal palpitations, often with associated symptoms such as chest discomfort Syncope is a rare presenting symptom. Unless bundle branch block is present, patients with orthodromic AVRT exhibit a narrow complex tachycardia on the surface ECG. Patients with pre-excited tachycardia including antidromic AVRT, and other forms of SVT in which the AP conducts to the ventricles as a bystander but does not participate in the tachycardias mechanism, present as broad complex tachycardias on the surface ECG which may be difficult to distinguish from ventricular tachycardia. Adenosine is increasingly used for this purpose since it is highly efficacious and has an extremely short half-life. Adenosine is also very useful in the diagnosis of broad-complex tachycardia, and in unmasking latent pre-excitation during sinus rhythm. Electrophysiology study in these patients is frequently performed at the same time as an attempt at catheter ablation; it aims to diagnose, localize and determine the functional characteristics of an AP, and to characterize the role of the pathway in tachycardia. AVRT can be reliably terminated by effective AV nodal blockade. Drug therapy for the prevention of AVRT is useful for temporary control whilst awaiting more definitive measures and in certain cases as long-term management. No class of drug stands out as 'therapy of choice', and physician preference, pro-arrhythmic effects and associated conditions need to be taken into account such that an individual choice can be made in each patient. The management of patients with AVRT has been revolutionized in recent years with the advent of catheter-based techniques for their cure. Whilst this method of treatment is highly effective and has low complication rates, pathways in particular locations such as the septal region remain challenging.
具有房室(AV)传导旁路(AP)的患者可能会发生环形运动性心动过速,即房室折返性心动过速(AVRT)。顺向型AVRT是最常见的形式。它是由于通过正常AV传导系统的前向传导以及经AP逆向传导至心房而发生的。较少见的情况是,传导方向相反,导致逆向型AVRT。心动过速也可能涉及多个AP,这些AP可提供前向和逆向传导,并且可能交替进行前向或逆向传导。心动过速可能发生在AP仅作为旁观者而不参与心动过速机制的情况下。当房颤通过AP传导至心室时,所产生的心室率可能极快,使患者有发生心室颤动和心脏骤停的风险。本文回顾了AVRT发病机制中涉及的解剖和生理基础。然后将讨论这些心律失常患者的急性和长期管理。正常的房室环仅由电惰性纤维组织组成。房室结和希氏束通常作为唯一的电传导途径。AP沿房室环的所有部位均可出现,通常作为孤立的异常出现,尽管一部分患者伴有先天性异常。右侧AP尤其如此。大多数AP表现出非递减传导特性,并且比正常AV传导组织传导更快。在许多有AP的患者中,体表心电图显示有明确的预激证据,使用已开发的几种算法中的一种或多种可以很好地定位旁路。隐匿性预激、间歇性预激患者以及隐匿性AP患者在其部分或全部体表心电图上没有预激证据。患者有阵发性心悸病史,常伴有胸痛等相关症状。晕厥是一种罕见的首发症状。除非存在束支阻滞,顺向型AVRT患者在体表心电图上表现为窄QRS波心动过速。预激性心动过速患者,包括逆向型AVRT,以及其他形式的室上性心动过速(SVT),其中AP作为旁观者传导至心室但不参与心动过速机制,在体表心电图上表现为宽QRS波心动过速,可能难以与室性心动过速区分。腺苷越来越多地用于此目的,因为它非常有效且半衰期极短。腺苷在宽QRS波心动过速的诊断以及在窦性心律期间揭示隐匿性预激方面也非常有用。这些患者的电生理检查通常与导管消融尝试同时进行;其目的是诊断、定位并确定AP的功能特征,以及确定该旁路在心动过速中的作用。有效的房室结阻滞可以可靠地终止AVRT。预防AVRT的药物治疗对于等待更明确措施期间的临时控制以及在某些情况下作为长期管理是有用的。没有哪一类药物脱颖而出成为“首选治疗”,需要考虑医生的偏好、促心律失常作用和相关情况,以便为每个患者做出个体化选择。近年来,随着基于导管技术用于治愈AVRT,AVRT患者的管理发生了变革。虽然这种治疗方法非常有效且并发症发生率低,但在某些特定部位(如间隔区域)的旁路消融仍具有挑战性。