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  • Another mechanism is that J waves represent a repolarization


    Another mechanism is that J waves represent a repolarization abnormality where J waves are created by the transmural voltage gradient [16]. During myocardial ischemia, the membrane ionic currents are known to be augmented, in turn augmenting the transient outward current (Ito). Augmented Ito would result in a deeper phase 1 notch of the action potential, which in turn, results in larger J waves in the surface ECG [17]. J waves and concomitant shortening of the folate analogue duration would result in ST elevation. In this case, the differences in QT interval between the acute and chronic phases were demonstrated, which might be related to the configuration of J waves; however, the precise mechanisms are still unknown. Furthermore, the normalization sequence of J waves and the ST segment suggests that J waves are more sensitive to ischemia. In fact, J waves were observed before ST-segment elevation when coronary spasms were induced in a provocation test [8,18]. However, the pathogenesis of ischemia-induced J waves is to be further elucidated.
    Introduction Micturition syncope is classified as situational syncope—a type of neurally mediated syncope (NMS). In this condition, a cardiopulmonary receptor and left ventricular mechanoreceptor is abnormally activated with decreased left ventricular dimensions, resulting in inappropriate peripheral blood pooling, blood pressure decrease, and bradycardia [1]. The effect of cardiac pacing therapy for NMS remains controversial because pacing therapy does not alter peripheral vasodilatation or prevent the occurrence of a reflex response [2,3]. Pacing therapy was not effective in a mixed group of NMS patients who were relatively young [1]. In contrast, a randomized trial showed that a DDD pacemaker with a rate-drop response function is more effective than the β-blocker treatment for recurrent vasovagal syncope [4]. A pacemaker with a closed-loop stimulation (CLS) function monitors myocardial contractile dynamics and translates intrinsic inotropic information into pacing rates. Occhetta et al. showed that CLS function is useful for the prevention of vasovagal syncope [5]. Kanjwal et al. demonstrated the effectiveness of the CLS function for the prevention of neurocardiogenic syncope as compared with the rate-drop or rate-hysteresis response [6]. The CLS function has long been used for the prevention of recurrent vasovagal syncope episodes [5,7]. However, the mechanism of how the CLS function prevents micturition syncope is not clear. We report a patient with micturition syncope in whom syncopal episodes could be prevented because of increased heart rates (HRs) caused by atrial pacing using the CLS function.
    Case report A 70-year-old man had been experiencing syncope approximately 3 times per year since 2006. These episodes generally occurred after micturition at midnight, after excess consumption of alcohol, after bathing, or during activities such as pruning. He had been advised to refrain from alcohol for approximately 3 years. In 2009, he was brought to our hospital because of a syncope episode that occurred after watching a bonfire. He experienced nausea and a cold sweat before the syncope. Holter electrocardiography (ECG) revealed an average HR of 53bpm, a maximum sinus arrest of 2.4s, and frequent sinoatrial block episodes. Electrophysiological assessment revealed a corrected sinus node recovery time of 778ms and a calculated sinoatrial conduction time of 223ms, indicating a mild sinus-node dysfunction. Although syncope was not elicited by an isoproterenol-infusion folate analogue head-up tilt test or a carotid sinus massage test, his syncopal episodes suggested situational syncope. Therefore, we implanted a DDD pacemaker with a CLS function (basal rate of 50ppm and a resting rate control of +20ppm) after he provided informed consent. Variations in HR and blood pressure (BP) were monitored during micturition during the day in both the DDD-R and DDD-CLS modes. In DDD-CLS, an increased atrial pacing ratio (79.3%) maintained his HR at approximately 70bpm during and after micturition (Fig. 1). In contrast, his intrinsic HR decreased from 67bpm to approximately 60bpm after micturition, but atrial pacing was not observed in the DDD-R mode. His systolic BP decreased by approximately 20mm Hg after micturition in both the DDD-CLS and DDD-R modes, but his systolic BP recovered within 1–2min; syncope did not occur in either mode.