Syncope is a common clinical problem, but nevertheless is but one element of the broader issue of ‘transient loss of consciousness’ (TLOC). The first step is to ascertain whether the patient actually suffered a syncopal episode, and thereafter the goal must be to determine the basis of symptoms with sufficient confidence to assess prognosis and initiate an effective treatment strategy. The initial evaluation of these patients, which usually takes place in an emergency department (ED) or acute care facility, is challenging since patients are usually asymptomatic when they come for medical attention, may have little or no recall of the event, and witnesses, if any, often cannot provide reliable information. Given these circumstances, it is understandable that frontline physicians often tend to take a seemingly ‘safe’ approach, and admit both high-risk and intermediate-risk syncope patients to hospital. This strategy has many implications, including life-style and economic concerns for the patient, and health care management issues for physicians, hospital administrators and the overall health care system. The European Society of Cardiology (ESC) guidelines and several clinical studies provide helpful advice regarding “risk stratification” to help guide physicians in selecting patients for either early hospital admission or later oupatient subspeciality evaluation. The utility of syncope management units in the ED, and a guideline-based approach to the syncope patient, has tended to both diminish the number of undiagnosed cases and reduce the hospital admission rate. In this review, we have attempted to both highlight a cost-effective diagnostic pathway beginning with the initial evaluation of the patient with suspected syncope, and to provide criteria which may help frontline physicians better base their decisions regarding need for in-hospital versus outpatient clinic evaluation of syncope patients.

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Understanding the role played by autonomic tone changes in the initiation of paroxysmal atrial fibrillation (PAF) may be helpful in preventing the occurrence of the arrhythmia. The purpose of this review article is to discuss the relationship between sympathovagal imbalance and the initiation of PAF from past literature and our data regarding circadian distribution and heart rate variability (HRV) analysis in PAF. PAF in non-structural heart disease (NHD) frequently occurs during evening and night hours with a longer duration of each episode, and its initiation is directly associated with an increase in vagal tone. According to our data of HRV analysis in NHD, HF power (indicator of vagal tone) showed a reduction 15 to 30 minutes before PAF, followed by a sharp increase immediately before the onset, suggesting a primary increase in sympathetic tone followed by a marked changes toward vagal predominance. Very few studies have been reported on PAF onset or the modulation of autonomic tone in structural heart disease (SHD). Some studies showed no significant differences in the circadian variation of the onset between NHD and SHD. However, we demonstrated a triphasic circadian pattern with maximum peaks in early morning, late afternoon, and night in SHD, suggesting an association with not only a vagally induced origin but also a sympathecally induced or stress triggered origin in PAF onset in SHD. The occurrence of PAF greatly depends on modulation of autonomic tone and is extremely complicated. Further studies are required to clarify the relationship between the occurrence of PAF and autonomic modulation.

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Background: The current status of the efficacy of implantable cardioverter-defibrillator (ICD) and cardiac-resynchronization therapy with implantable defibrillator (CRT-D) in patients with left ventricular dysfunction needs to be clarified.
Methods and Results: From the Japanese Cardiac Device Treatment Registry database, a total of 1,584 patients who had an LVEF≤40% and had an ICD or CRT-D were selected as subjects in this study. The difference in the clinical characteristics between the primary and secondary prevention groups and the transition of the indications for device implantation over time were examined. Primary prevention gradually increased up to about 50% in all patients. The implantations of ICD/CRT-D for primary prevention in ischemic hear disease was significantly lower than that in dilated cardiomyopathy (33% vs 51%; p<0.0001). The number of implantations for CRT-D for primary prevention increased dramatically over a one-year period.
Conclusions: In Japan, the implantable defibrillator devices for primary prevention was significantly lower in ischemic heart disease compared with dilated cardiomyopathy. Further, an extension of the indications for ICD/CRT-D implantations has recently been occurring, especially with CRT-D devices for primary prevention.

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Background: Nifekalant is a unique class III anti-arrhythmic agent with a strong effect on prolonging the myocardial refractoriness, but its clinical effect is still unclear. In this study, we evaluated the effect of nifekalant on life-threatening ventricular arrhythmias and compared the clinical background between the effective and non-effective patients in order to clarify the clinical factors which may have an influence on the efficacy of nifekalant.
Methods: The study population consisted of 47 consecutive patients who underwent nifekalant administration for life-threatening ventricular arrhythmias (VT/VF). Their clinical characteristics and ECG parameters were retrospectively compared between patients with and without an effective result with the nifekalant administration.
Results: Nifekalant was effective for refractory VT/VF in 26/47 patients. There was no significant difference in the age, gender or left ventricular ejection fraction, but the incidence of ischemic heart disease was higher in the effective group (17/26) than non-effective group (9/21, p=0.004). The incidence of in-hospital events was higher in the effective group than non-effective group (20/26 vs 10/21, p=0.037). A significant prolongation in the QTc interval was observed in all patients and the degree of QTc prolongation was greater in the effective group than in the non-effective group (0.46±0.04 vs 0.43±0.02 sec^1⁄2, p=0.026).
Conclusion: Nifekalant was effective in 55% of the patients for refractory VT/VF. It was considered that nifekalant was more effective for patients with ischemic heart disease, during the perioperative period or in those experiencing in-hospital events. The prolongation of the QTc interval might also be useful as an index for the efficacy of nifekelant administration.

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This case report describes a patient with incessant atrial tachycardia (AT) who underwent catheter ablation. During electrophysiological study, the stable AT circuit spontaneously shifted to unstable AT due to intermittent frequent firing from the right inferior pulmonary vein (PV) after termination of cavo-tricuspid isthmus dependent atrial flutter. A macro-reentrant AT circuit was observed after electrical isolation of right inferior PV potentials. These findings suggest that the presence of rapid activated firing is likely to be associated with the development of instability in the AT circuit. This may lead to a greater understanding of the physiology of atrial tachyarrhythmia as a simple clinical model.

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A 29-year-old male who underwent a complete tetralogy of Fallot repair at 2 years of age was referred to our hospital for treatment of sustained ventricular tachycardia (VT). The bipolar voltage map using an electroanatomical mapping system (CARTO, Biosense-Webster) during sinus rhythm revealed a low voltage area identical to the site of the right ventricular outflow tract (RVOT) patch on the anterior wall of the RVOT. During the tachycardia, the activation wavefront was found to revolve in a counterclockwise manner around the patch in the RVOT. Two radiofrequency catheter ablation (RFCA) sessions creating a line between the patch in the RVOT and pulmonary artery achieved only transient success. He underwent a pulmonary valve replacement and reconstruction of the RVOT with a transannular patch to treat the VT refractory to RFCA and severe pressure gradient in the RVOT. In postoperative electrophysiological study, a low voltage area in the RVOT connected to the pulmonary artery with the patch was observed, and produced conduction block in the reentry circuit of the VT. The patient has been free from any VT recurrence during 6 months of follow up.

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Recently, cardiac resynchronization therapy (CRT) has been established as an effective treatment for drug-resistant heart failure with left ventricular dyssynchrony in patients with a New York Heart Association class (NYHA) of III-IV. Many cases have already been treated with CRT in Japan, however, some challenges still remains, such as difficult placement of the left ventricular (LV) lead at the target site, high threshold values even after successful placement of the LV lead, and the need to reposition of the LV lead due to diaphragmatic stimulation regardless of an appropriate threshold value. In particular, those cases with high threshold values at a distal site or those in which the lead is placed at a proximal site because of diaphragmatic stimulation are prone to lead dislodgement, and re-operation may be required. We report on a patient in whom stabilization of the LV lead was obtained by placing a coronary stent in the coronary sinus wall which resulted in an improved clinical course.

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We report a case of ventricular fibrillation (VF) which an automated external defibrillator (AED) could not detect. A 13-year-old girl collapsed just after playing basketball. Cardio pulmonary resuscitation (CPR) was started immediately and 5 minutes later an AED was applied by a rescue team. The monitor of the AED displayed typical VF, but the AED did not detect it as VF. The VF was not detected during 2 more attempts. Detection occurred on the fourth attempt, and counter-shock was successfully delivered, but the process took an extra 9 minutes. After the event, the girl was diagnosed with a latent type of prolonged QT syndrome. We analyzed the reason why the VF was not detected by the AED and found that the ECG detected by the AED fell outside the device’s parameters for ventricular tachycardia (VT) or VF. We emphasize that the AED is an excellent device, but we should also be aware of its limitations.

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