A 58-year-old male with a history of type 2 diabetes, hypertension, chronic kidney disease, a severe ischemic cardiomyopathy (left ventricular [LV] ejection fraction 19%), paroxysmal atrial fibrillation, and ventricular tachycardia (VT) which had been treated with amiodarone and a defibrillator, was admitted with worsening heart failure and palpitations. He was found to be volume overloaded with acute kidney injury and hypokalemia. Diuresis and potassium repletion were started. That evening telemetry revealed a wide complex tachycardia (Figure 1). The cardiac resynchronization defibrillator (CRT-D) was programmed to DDDR mode of 60 to 130 beats/min, with a ventricular tachycardia zone of 190 to 220 beats/min and a ventricular fibrillation zone starting at 220 beats/min. What is the tachycardia mechanism?

Figure 1. ECG during tachycardia.

Please turn the page to read the diagnosis.

The ECG shows regular, wide complex tachycardia at a rate of 120 beats/min with an inferior rightward axis and right bundle branch morphology transitioning at V6, associated with a pacing spike. This QRS morphology is markedly different from that seen during the atrial-sensed, ventricular-paced rhythm of 85 beats/min recorded on admission (Figure 2A). Given the patient’s history of ventricular tachycardia, a CRT-D, and amiodarone therapy, as well as the possibility of slow ventricular tachycardia with ventricular-sensed response—pacing into a sensed ventricular event—a CRT-D algorithm designed to optimize ventricular resynchronization was considered.

Figure 2. Baseline and presenting ECGs, intracardiac electrograms, and confirmation ECGs. A, Baseline ECG showing atrial-sensed, biventricular-paced rhythm during preferential left ventricular pacing. Significant and optimal narrowing of the patient’s underlying left bundle-branch block was seen with this pacing configuration. B, Presenting ECG. B, inset, Lead II. Red arrows show retrograde P waves. C, Intracardiac electrograms from device interrogation confirming an atrial-sensed, left ventricular–paced rhythm during tachycardia. D, ECG strip showing atrial-sensed, left ventricular pacing at 75 beats/min producing a QRS morphology identical to the patient’s baseline ECG. E, Left ventricular pacing at 120 beats/min resulting in a QRS morphology identical to that of the clinical tachycardia. A indicates atrial; AS, atrial sensed; LVP, left ventricular pace; and RV, right ventricle.

However, closer inspection revealed both that the pacer spike initiates the QRS and that there is a 1:1 relationship between the P waves and the paced QRS. Further, the P waves have a negative axis (Figure 2B), consistent with either retrograde conduction or atrial tachycardia. Interrogation of the CRT-D confirmed an atrial-sensed, ventricular-paced rhythm (Figure 2C), an upper atrial tracking rate of 130 beats/min and that LV preferential pacing was programmed on, suggesting the diagnoses of atrial tachycardia with ventricular tracking or pacemaker-mediated tachycardia (PMT) as the QRS morphology of the clinical tachycardia suggests pacing from the anterolateral base of the LV.

Further investigation of the patient’s telemetry demonstrated that a ventricular premature contraction (Figure 3) initiated the tachycardia, making PMT the most likely diagnosis. This was confirmed by performing LV-only pacing at the tachycardia rate (120 beats/min) (Figure 2E), producing a QRS morphology identical to the wide complex tachycardia, likely because of a lack of native conduction and loss of fusion at this rate.

Figure 3. Ladder diagram of tachycardia initiation. A, Rhythm strip demonstrating the initiation of the clinical tachycardia by a ventricular premature contraction. B, Cardiac implantable electronic device marker channel. C, Same strip with a superimposed ladder diagram. A sensed ventricular event (ventricular premature contraction) leads to AV block, permitting retrograde conduction (arrow) which results in atrial sensing after PVARP and initiates tachycardia. AS indicates atrial sense; PVARP, post–ventricular atrial refractory period; PVB, post–ventricular blanking period; rP, retrograde P wave; SAV, sensed atrio-ventricular interval; and VP, ventricular paced.

PMT has been recognized since the early days of dual chamber pacemakers.¹ It requires (1) a cardiac implantable electronic device programmed to a pacing configuration (DDD) that permits atrial sensing and ventricular pacing; (2) a sensed ventricular event not preceded by an atrial event that penetrates the AV node, triggering the tachycardia; and (3) ventriculoatrial (retrograde) conduction through the intrinsic conduction system slow enough to evade the programmed post–ventricular atrial refractory period (PVARP), which is designed to prevent tracking of events early after the QRS. The tachycardia is typically initiated by a ventricular premature contraction, as in our case, atrial ectopy, loss of atrial capture, or, in newer devices, an algorithm that produces PR prolongation designed to minimize ventricular pacing.² Identifying retrograde conduction, measuring the ventriculoatrial conduction time and, if possible, programming a PVARP sufficiently long to prevent sensing of retrograde P waves is critical to preventing initiation of PMT in the first place. However, this may limit the upper tracking rate of the device (PVARP + AV delay), and thus auto AV delay, allowing preprogrammed shortening of the AV delay at faster heart rates, PVARP extension after a sensed ventricular premature contraction, as well as specific PMT termination algorithms have been developed to help overcome this difficulty.² In a patient with a pacemaker, placing a magnet over the device converts it to an asynchronous mode (DOO) and can be used to manually interrupt the tachycardia, an option not available for defibrillators.

The PMT rate is determined by the sum of the ventriculoatrial conduction time plus the programmed AV delay and is usually close to the programmed maximal atrial tracking rate. In our patient, LV-only pacing may have contributed to an extremely long ventriculoatrial conduction time, facilitating sensing of retrograde P waves and slowing the PMT rate to 120 beats/min, less than the programmed maximal atrial tracking rate of 130 beats/min.³ Although our patient’s cardiac implantable electronic device was programmed with a specific PMT termination algorithm, it required detection of 16 paced cycles at the maximal atrial tracking rate to trigger prolongation of the programmed PVARP to 500 ms, with the goal of preventing atrial tracking for 1 cycle and thus interrupting the tachycardia. It therefore made no attempts at tachycardia termination.

Our patient’s PVARP was lengthened and his upper tracking rate was decreased to 110 beats/min. On follow-up he had no further palpitations and cardiac implantable electronic device interrogation did not identify any additional PMT.

None.

Disclosures None.

For Sources of Funding and Disclosures, see page 1869.

Circulation is available at www.ahajournals.org/journal/circ

一名 58 岁男性，有 2 型糖尿病、高血压、慢性肾病、严重缺血性心肌病（左心室 [LV] 射血分数 19%）、阵发性心房颤动和室性心动过速 (VT) 病史。用胺碘酮和除颤器治疗，因心力衰竭和心悸恶化入院。他被发现因急性肾损伤和低钾血症而容量超负荷。开始利尿和补钾。那天晚上的遥测显示广泛复杂的心动过速（图 1）。心脏再同步除颤器 (CRT-D) 被编程为 60 至 130 次/分钟的 DDDR 模式，室性心动过速区为 190 至 220 次/分钟，心室颤动区从 220 次/分钟开始。心动过速的机制是什么？

图 1. 心动过速期间的心电图。

请翻页阅读诊断。

心电图显示规则的、广泛的复杂性心动过速，速率为 120 次/分钟，右下轴和右束支形态在 V6 处过渡，与起搏尖峰相关。这种 QRS 形态与入院时记录的 85 次/分钟的心房感应、心室起搏节律明显不同（图 2A）。鉴于患者的室性心动过速、CRT-D 和胺碘酮治疗史，以及伴随心室感知反应的缓慢室性心动过速的可能性——起搏进入感知到的心室事件——设计用于优化心室再同步化的 CRT-D 算法是经过考虑的。

图 2. 基线和呈现心电图、心内电图和确认心电图。A，基线心电图显示在优先左心室起搏期间心房感应的双心室起搏节律。使用这种起搏配置可以看到患者潜在的左束支传导阻滞显着和最佳变窄。B、呈现心电图。B，插图，铅 II。红色箭头显示逆行 P 波。C，来自设备询问的心内电图，确认心动过速期间心房感应的左心室起搏节律。D，心电图条显示心房感应的左心室起搏频率为 75 次/分钟，产生与患者基线心电图相同的 QRS 形态。E，左心室以 120 次/分钟起搏，导致 QRS 形态与临床心动过速相同。A表示心房；AS，心房感应；LVP，左心室起搏；和 RV，右心室。

然而，更仔细的检查显示，起搏器尖峰启动 QRS，并且 P 波和起搏 QRS 之间存在 1:1 的关系。此外，P 波具有负轴（图 2B），与逆行传导或房性心动过速一致。对 CRT-D 的询问证实了心房感应的心室起搏节律（图 2C），上心房跟踪速率为 130 次/分钟，并且 LV 优先起搏已编程，提示通过心室跟踪或心室跟踪诊断房性心动过速或起搏器介导的心动过速 (PMT) 作为临床心动过速的 QRS 形态表明从 LV 前外侧基部起搏。

对患者遥测的进一步调查表明，室性早搏（图 3）引发了心动过速，使 PMT 成为最可能的诊断。这通过以心动过速率（120 次/分钟）执行仅 LV 起搏得到证实（图 2E），产生与广泛复杂性心动过速相同的 QRS 形态，可能是由于缺乏本机传导和以该速率失去融合.

图 3. 心动过速开始的梯形图。A，节律条显示由室性早搏引起的临床心动过速。B、心脏植入式电子设备标记通道。C , 同一条带叠加梯形图。感知到的心室事件（室性早搏）导致 AV 传导阻滞，允许逆行传导（箭头），这导致 PVARP 后心房感知并引发心动过速。AS表示心房感；PVARP，心室后心房不应期；PVB，心室后空白期；rP，逆行 P 波；SAV，感测的房室间期；和 VP，心室起搏。

PMT 自双腔起搏器诞生之初就已得到认可。¹它需要 (1) 一个心脏植入式电子设备，其编程为允许心房感应和心室起搏的起搏配置 (DDD)；(2) 感测到的心室事件之前没有穿透 AV 结的心房事件，触发心动过速；(3) 通过内在传导系统的心室心房（逆行）传导速度足够慢，可以避开程序化的心室后心房不应期 (PVARP)，PVARP 旨在防止在 QRS 后早期跟踪事件。心动过速通常由室性早搏引发，如在我们的案例中，心房异位、心房夺获丧失，或者在较新的设备中，一种产生 PR 延长的算法，旨在最大限度地减少心室起搏。²识别逆行传导，测量心室心房传导时间，如果可能的话，编程足够长的 PVARP 以防止感应到逆行 P 波，这对于首先防止 PMT 的启动至关重要。然而，这可能会限制设备的上限跟踪速率（PVARP + AV 延迟），从而限制自动 AV 延迟，允许在更快的心率下预编程缩短 AV 延迟、感知室性早搏后的 PVARP 延长，以及特定的已经开发了 PMT 终止算法来帮助克服这个困难。²对于有心脏起搏器的患者，将磁铁置于设备上方可将其转换为异步模式 (DOO)，并可用于手动中断心动过速，该选项不适用于除颤器。

PMT 率由心室心房传导时间加上程序化 AV 延迟的总和决定，通常接近程序化最大心房跟踪率。在我们的患者中，仅 LV 起搏可能导致了极长的心室心房传导时间，有助于感知逆行 P 波并将 PMT 速率减慢至 120 次/分钟，低于 130 次/分钟的程序化最大心房跟踪率。³尽管我们患者的心脏植入式电子设备采用特定的 PMT 终止算法进行编程，但它需要以最大心房跟踪速率检测 16 个起搏周期，以触发将编程的 PVARP 延长至 500 ms，目标是阻止心房跟踪 1 个周期从而中断心动过速。因此，它没有尝试终止心动过速。

我们的患者的 PVARP 延长，他的上追踪率降低到 110 次/分钟。在随访中，他没有进一步的心悸，心脏植入电子设备的询问没有发现任何额外的 PMT。

没有任何。

披露无。

有关资金来源和披露信息，请参见第 1869 页。

流通可在 www.ahajournals.org/journal/circ