A 39-year-old woman with a nonischemic dilated car-diomyopathy was admitted for an exacerbation of congestive heart failure. During her hospitalization, she had a witnessed cardiac arrest. Telemetry findings (Fig. 1) demonstrated a baseline normal sinus rhythm transitioning to atrial fibrillation (AF) with rapid ventricular rates that subsequently initiated polymorphous ventricular tachycardia (PMVT) and degenerated into ventricular fibrillation. The same finding is noted on the intracardiac electrogram from her single chamber defibrillator (Fig. 2). Normal sinus rhythm was restored with a shock by the patient's internal defibrillator. Her AF was more aggressively rate controlled to minimize the risks of further defibrillator shocks. It is a well-known electro-physiological phenomenon that arrhythmias can beget other arrhythmias, such as supraventricular tachycardias initiating AF. In this situation, an atrial arrhythmia induced a ventricular arrhythmia. Ischemia caused by rapid AF is one possible mechanism for the resulting PMVT. Another explanation is that the irregularity of AF led to closely coupled ventricular depolarizations falling into a vulnerable period (R on T), thus initiating PMVT. Although AF is not typically considered a lethal arrhythmia, clinicians should be aware of this ability to initiate fatal arrhythmias.
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机译：一名患有非缺血性扩张型心肌病的39岁妇女因充血性心力衰竭加重而入院。在住院期间，她目击了心脏骤停。遥测结果（图1）表明基线正常窦性心律以快速心室率向心房纤颤（AF）过渡，随后开始多形性室性心动过速（PMVT），并退化为心室纤颤。她的单室除颤器在心内电描记图上也发现了相同的发现（图2）。病人的内部除颤器在电击后恢复了正常的窦性心律。她的房颤被更积极地控制了速度，以最大程度地降低除颤器进一步电击的风险。心律失常可引起其他心律不齐，例如引发房颤的室上性心动过速是一种众所周知的电生理现象。在这种情况下，房性心律失常引起室性心律失常。快速房颤引起的缺血是导致PMVT的一种可能机制。另一个解释是，房颤的不规则性导致紧密耦合的心室去极化进入脆弱期（R on T），从而启动了PMVT。尽管通常不认为房颤为致命性心律失常，但临床医生应意识到这种引发致命性心律失常的能力。
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