A 40-year-old man was referred to a tertiary center for consideration of ablation of a symptomatic supraventricular tachycardia resistant to oral bisoprolol (Figure 1). What is the underlying mechanism of arrhythmia, and what are the differential diagnostic considerations?

Figure 1. Twelve-lead ECG.

Please turn the page to read the diagnosis.

The ECG reveals a narrow complex tachycardia with a ventricular rate of 108 beats/min and nonspecific ST-T wave changes. P waves are upright in lead V₁ and inverted in leads II, III, and aVF, suggesting retrograde atrial activation. There is a short R-P interval (85 ms), and the P waves are mainly conducted with a 2:1 ratio (Figure 2).

Figure 2. Annotated 12-lead ECG. The ECG reveals a narrow complex tachycardia with a ventricular rate of 108 beats/min and nonspecific ST-T wave changes. P waves consistent with retrograde atrial activation are seen (labeled with arrow), along with a short R-P interval (85 ms) and intermittent 2:1 ventriculoatrial conduction.

The differential diagnosis for a narrow complex tachycardia with ventriculoatrial dissociation includes (1) atrioventricular nodal reentrant tachycardia with retrograde block in the upper common pathway, (2) junctional tachycardia with retrograde block to the atrium, and (3) orthodromic reciprocating nodofascicular or nodoventricular tachycardia with block to the atrium (Figure 3). The presence of atrioventricular dissociation rules out the possibility of conventional orthodromic atrioventricular reentrant tachycardia because the atrium is a required part of this circuit.

Figure 3. Differential diagnosis of supraventricular tachycardia with ventriculoatrial block. Schematic of mechanisms of supraventricular tachycardia with ventriculoatrial dissociation. The main differential includes: atrioventricular nodal reentrant tachycardia with retrograde block in the upper common pathway (A), junctional tachycardia with retrograde block to the atrium (B), orthodromic reciprocating nodofascicular tachycardia with block to the atrium (C), and orthodromic reciprocating nodoventricular tachycardia with block to the atrium (D). AVN indicates atrioventricular node; FP, fast pathway; NF, nodofascicular; NV, nodoventricular; and SP, slow pathway.

He underwent an electrophysiology study, which was consistent with a diagnosis of junctional tachycardia: premature atrial beats timed to septal refractoriness had no effect on the tachycardia cycle length; scanning premature atrial beats early in the diastolic interval would advance the immediate His potential with subsequent continuation of tachycardia; and ventricular extrastimuli timed to His refractoriness did not affect the timing of the next His activation.¹ It is interesting to note that during the study, there were periods of marked sinus bradycardia with complete atrioventricular dissociation and a narrow complex tachycardia (Figure 4).

Figure 4. Twelve-lead ECG on day of electrophysiology study. The ECG reveals sinus bradycardia with atrioventricular dissociation and a narrow complex tachycardia at a rate of 118 beats/min.

Given that the junctional tachycardia focus typically lies in close anatomic proximity to the compact atrioventricular node, radiofrequency ablation was not attempted during the procedure because of the high risk of iatrogenic atrioventricular block. He was started on sotalol 120 mg twice daily with good response and maintained normal sinus rhythm on a follow-up 48-hour Holter monitor.

Junctional tachycardia is an arrhythmia, well-described in pediatric patients, that can occur spontaneously or as a postoperative sequela of congenital heart surgery. In adults, junctional tachycardia is uncommon but may occur transiently after slow pathway modification in the electrophysiology laboratory or after cardiopulmonary bypass as a result of ischemic injury to the conduction system and postoperative inotropic agents. In addition, junctional tachycardia may be observed in the setting of myocardial ischemia or digoxin toxicity.² In some patients, junctional tachycardia presents nearly continuously (also known as incessant junctional tachycardia). The mechanism of arrhythmia is likely enhanced automaticity, although triggered activity may contribute in some patients.³

Differentiation of junctional tachycardia from atrioventricular nodal reentrant tachycardia is clinically important, because ablation of junctional tachycardia is associated with a higher risk of atrioventricular block and reserved for cases where medical therapy is ineffective or contraindicated.² Features that increase the likelihood of a diagnosis of junctional tachycardia include incessant tachycardia and the presence of atrioventricular dissociation. The onset of tachycardia is spontaneous, does not require initiation with a premature atrial or ventricular beat (unlike atrioventricular nodal reentrant tachycardia), and has a gradual onset (ie, warm-up phenomenon). During tachycardia, this arrhythmia may have varying degrees of cycle length irregularity or variation in heart rate. Last, overdrive pacing or electrical cardioversion does not reliably terminate the tachycardia.² Confirmation of a diagnosis can be made during an invasive electrophysiology study.¹

Dr Chew is supported by a Canadian Institutes of Health Research Banting Fellowship and an Arthur JE Child Cardiology Fellowship.

None.

https://www.ahajournals.org/journal/circ

一名40岁的男子因消融对口服比索洛尔耐药的症状性室上性心动过速而被转诊至三级中心（图1）。心律不齐的潜在机制是什么，鉴别诊断要考虑什么？

图1. 十二导联心电图。

请翻页阅读诊断。

ECG显示狭窄的复杂性心动过速，心室速率为108次/分钟，且ST-T波无特异性变化。P波在V ₁导线中直立，而在II，III和aVF导线中倒置，表明心房逆行激活。RP间隔很短（85 ms），P波主要以2：1的比率传导（图2）。

图2.带 注释的12导联心电图。ECG显示狭窄的复杂性心动过速，心室速率为108次/分钟，且ST-T波无特异性变化。观察到与逆行性心房激活一致的P波（用箭头标记），以及短的RP间隔（85毫秒）和间断的2：1心室心房传导。

狭窄性复杂性心动过速伴室性心房分离的鉴别诊断包括：（1）房室结折返性心动过速，在上共同通路中具有逆行性阻滞；（2）交界性心动过速伴有心房逆行性阻滞；以及（3）正畸往复性十二指肠或心室性心动过速与心房阻滞（图3）。房室解离的存在排除了常规正畸性房室折返性心动过速的可能性，因为心房是该回路必不可少的部分。

图3. 房室传导阻滞与室上性心动过速的鉴别诊断。室上性心动过速与室性心房分离的机制示意图。主要区别包括：房室结折返性心动过速，在上共同通路中逆行阻滞（A），交界性心动过速至心房逆行阻滞（B），正向往复性十二指肠性心动过速而对心房阻滞（C），以及正向往复性窦性心动过速心动过速，心房阻塞（D）。AVN表示房室结；FP，快速通道；NF，结节性；NV，结节性脑室；和SP，缓慢的路径。

他进行了电生理学研究，与结节性心动过速的诊断相符。在舒张期间隔早期扫描过早的心房搏动，将立即提高他的潜力，并随后持续心动过速；定时至他的顽固性的心室刺激未影响下一次激活他的时间。¹有趣的是，在研究过程中，存在明显的窦性心动过缓，房室完全分离和狭窄的复杂性心动过速（图4）。

图4. 电生理研究当天的十二导联心电图。心电图显示窦性心动过缓伴房室解离和狭窄的复杂心动过速，搏动速度为118次/分钟。

考虑到交界性心动过速的焦点通常位于紧密的房室结解剖附近，因此在手术过程中未尝试进行射频消融，原因是医源性房室传导阻滞的风险很高。他开始服用索他洛尔120 mg，每天两次，反应良好，并在后续的48小时动态心电图监护仪上维持正常的窦性心律。

结节性心动过速是一种心律不齐，在小儿患者中已有描述，可以自发发生或作为先天性心脏病手术的后遗症。在成年人中，结节性心动过速并不常见，但在电生理实验室中缓慢的路径修饰后或由于对传导系统和术后正性肌力药物的缺血性损伤而在体外循环后可能会短暂发生。此外，在心肌缺血或地高辛毒性的情况下可能会观察到连接性心动过速。²在某些患者中，结节性心动过速几乎连续出现（也称为持续性结节性心动过速）。心律失常的机制很可能会增强自动化程度，尽管某些患者可能会触发活动。³

结节性心动过速与房室结折返性心动过速的区别在临床上很重要，因为结节性心动过速的消融与房室传导阻滞的风险较高有关，并且保留用于无效或禁忌药物治疗的情况。^2个增加诊断结节性心动过速的可能性的特征包括持续性心动过速和房室解离的存在。心动过速的发作是自发的，不需要过早的心房或心室搏动（不同于房室结折返性心动过速），并且具有逐渐发作的现象（即热身现象）。在心动过速期间，这种心律失常可能具有不同程度的周期长度不规则或心率变化。最后，超速起搏或心脏电复律不能可靠地终止心动过速。²可以在侵入性电生理研究中确定诊断。^1个

周博士获得了加拿大卫生研究院禁止研究金和Arthur JE儿童心脏病学研究金的支持。

没有。

https://www.ahajournals.org/journal/circ