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A 60-year-old woman with dilated cardiomyopathy was referred to our hospital due to recurrent syncope. The electrocardiogram recorded by an implantable loop recorder during a syncopal episode revealed an episode of ventricular fibrillation lasting almost 3 min that terminated spontaneously. A detailed analysis of the rhythm strip showed that the chaotic rhythm became an organized ventricular rhythm with a cycle length of 220 ms for the last 14 s before it terminated.
<Learning objective: Ventricular tachyarrhythmias are one of the causes of syncope and have been observed in 1–3% of syncopal patients using an implantable loop recorder (ILR). However, long-lasting ventricular fibrillation (VF) as a cause of syncope is rare in clinical practice, because VF seldom terminates spontaneously. The long-lasting VF became an organized ventricular rhythm, and finally self-terminated as sinus rhythm was restored and this entire sequence of the arrhythmic events was recorded by an ILR.>
Ventricular fibrillation (VF) is a life-threatening arrhythmia that requires immediate defibrillation. In general, it is rare for long-lasting VF to terminate spontaneously. However, we encountered an interesting case in which long-lasting VF became an organized ventricular rhythm, and finally self-terminated as sinus rhythm was restored. The electrocardiogram (ECG) during this arrhythmic episode was recorded by an implantable loop recorder (ILR).
A 60-year-old woman was referred to our hospital with recurrent syncopal episodes. A 12-lead ECG revealed a sinus rhythm without any evidence of an old myocardial infarction, J waves, or QT-interval abnormalities (Fig. 1). The head-up tilt test and Schellong test were negative. A Holter ECG showed only frequently isolated premature ventricular contractions (16,709/day), without any episodes of ventricular tachycardia (VT), VF, or bradycardia. The coronary angiogram was normal. She had no signs of heart failure; however, an echocardiogram revealed a reduced left ventricular ejection fraction (LVEF = 27%) without any local asynergy or valvular heart disease, and the findings of the endomyocardial biopsy specimens were compatible with dilated cardiomyopathy. Therefore, an oral administration of carvedilol was started.
While 1-year carvedilol therapy improved the patient's LVEF significantly (to 54%), she experienced a loss of consciousness at rest, without any preceding symptoms. Bystander cardiopulmonary resuscitation was initiated immediately. On arrival of the medical team, she had already regained consciousness and was free of symptoms. In the electrophysiological study, no ventricular tachyarrhythmias were induced even with three extrastimuli delivered from the right ventricular apex and right ventricular outflow tract, with or without isoproterenol. Sinus node function and atrioventricular nodal conduction were also normal. Considering her current cardiac function and the noninducibility of ventricular tachyarrhythmias in the electrophysiological study, and in view of the patient's recurrent unexplained syncopal episodes, she underwent an implantation of an ILR.
Two months later, she experienced a recurrent syncopal episode that occurred without any preceding symptoms while she was preparing dinner. The ECG during the syncope recorded by the ILR revealed a self-terminating VF episode lasting almost 3 min. First, the VF episode was initiated, which then became an organized ventricular rhythm with a cycle length of 220 ms for the last 14 s before terminating spontaneously (Fig. 2). Since VF was the cause of this syncopal episode, the mechanism of the patient's previous syncopal episodes could also have been self-terminating VF. Accordingly, an implantable cardioverter-defibrillator was implanted to prevent sudden cardiac death.
Syncope is defined as a transient loss of consciousness and postural tone due to transient global cerebral hypoperfusion. Unexplained syncope often requires a variety of investigations to elucidate the cause. The ILR was developed as a means of long-term monitoring to capture the cardiac rhythm during an episode of syncope. In this case, considering her current cardiac function after the medical therapy (LVEF 54%) and the noninducibility of ventricular tachyarrhythmias in the electrophysiological study, initially an ILR was implanted instead of an ICD. Consequently, the sequential arrhythmic events could be confirmed during a syncopal episode in which long-lasting VF converted to an organized ventricular rhythm and finally self-terminated. Ventricular tachyarrhythmias are one of the causes of syncope and are observed in 1–3% of syncopal patients when detected by an ILR [
]; however, long-lasting VF as a cause of syncope is rare in clinical practice. One of the reasons why the long-lasting VF in this case could terminate spontaneously was the ability to organize from VF, before returning to sinus rhythm. Spontaneous reversion to sinus rhythm typically occurs when the localized chaotic activity is confined to a small area of the heart and gradually becomes regular. Mäkikallio et al. [
] found that spontaneously terminating VF displays more organized local activation dynamics than sustained VF terminated only by electric shocks, suggesting that the dynamic behavior of the local cardiac activation might be related to the maintenance of ventricular tachyarrhythmias. Chest compressions also may relieve the ischemia and the local excitability may recover from fibrillatory conduction, which could facilitate the VF changing to a relatively organized ventricular rhythm. Such slowing and organization of the VF activity 1–2 min after the VF onset are widely known as Wiggers’ stage III. However, the occurrence of self-terminating long-lasting VF is clinically rare.
This organization may be explained by the three possible mechanisms. The first is that the underlying structural heart disease in this patient was dilated cardiomyopathy. The thin ventricular walls of the patients with dilated cardiomyopathy restrain the intramural reentry due to the tissue boundary effect (electrotonic influence of ventricular surfaces on VF wavefronts), resulting in both organization of the VF activity and lowering of the excitation frequency [
]. Spatiotemporal dispersion of refractoriness within the ventricular wall may also in part contribute to the VF organization. Indeed, pharmacologically attenuating the spatiotemporal heterogeneity of the refractoriness during early VF promotes VF organization, causing spontaneous VF termination [
VF-induced myocardial ischemia is the second possible mechanism of the VF organization. In an experimental study, two types of VF were demonstrated. Type 1 VF is characterized by the presence of multiple, wandering wavelets, whereas type 2 VF exhibits a local spatiotemporal periodicity and a single mother rotor with fibrillatory conduction [
]. The underlying mechanism of VF may be explained by a condition in which the action potential duration (APD) restitution is steep and the excitability is normal just after the initiation of VF. However, global cardiac ischemia usually occurs during sustained VF, which flattens the APD restitution curve and induces a conduction delay leading to type 2 VF (reduced excitability and a flat APD restitution). This patient might have had type 2 VF just before the VF termination. Mandapati et al. [
] also showed that ischemia (low perfusion of the myocardium) during VF reduces the tissue excitability, resulting in the prolongation of the spiral wave reentrant cycle length, enlargement of the spiral wave core, and a decrease in the number of spiral wavefronts. The reduced tissue excitability can be explained by ischemia-dependent hyperkalemia, because the hyperkalemia depolarizes the reversal potential of IK1, causing a reduction in the tissue excitability [
] showed that the ischemia-related hyperkalemia restrains the spiral wave breakup by flattening the restitution curve of the APD.
The third possible mechanism for the self-termination of the VF is that high cardiac catecholamine concentrations improve the electrotonic spatial interaction between the myocytes, leading to the organization of the VF activity. However, this idea is based only on the experimental studies [
Decreasing the number of VF wavefronts, regardless of the mechanism of the organization of the VF activity, increases the probability of restoring sinus rhythm by the collision of all meandering spiral waves with anatomical blocklines and/or tissue borders. Uncovering the precise mechanism of VF self-termination could open new avenues to the avoidance of cardiac sudden death via spiral wave control.
Conflict of interest
The authors declare no conflict of interest.
The authors express their gratitude to Mr. John Martin for his linguistic revision of the manuscript.
Jose Olalla J.
Utility of implantable loop recorders for diagnosing unexplained syncope in clinical practice.