Recently, the effects of QT interval prolongation have received more attention among clinicians, industry, and official regulatory agencies. Some have advocated the total elimination or discontinuing development of drugs which prolong the QT interval. In this review, we will give a brief overview of the pathophysiology and the dynamic variability and morphology of the QT interval. From the view point of arrhythmogenesis, QT interval prolongation with increased heterogeneity of ventricular repolarization is critical. The problem is how to detect such an abnormal repolarization. To detect heterogeneity, a new index should be developed and validated, and it must incorporate QT variability and morphology of the T wave. The heart rate correction of the QT interval is also an important issue, and disclosing conflict-corrected QT intervals depend on the formulae used.
Not just QT interval prolongation is important; what also matters is the heterogeneity of ventricular repolarization.

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This report was an overview of pacing therapy for heart failure to explain the usefulness and problems of CRT in broad terms. It is not an exaggeration to say that pacemakers were originally developed to improve cardiac function in patients with heart failure. However, it must be understood that pacing itself is unphysiological, and we should know what pacing does to the heart. Concerning the simple issue of pacing, it is true that there are a lot of matters that we think we understand but actually we do not, such as the effects of the differences in site, output, and frequency. At least, it seems clear that the currently available CRT devices are effective for patients with heart failure and for improving survival. Further improvement in their effectiveness is an important issue we must continue to address.

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Introduction: Radiofrequency catheter ablation (RFCA) that targets pulmonary veins (PV) is an established treatment for paroxysmal atrial fibrillation (PAF). Recent studies have demonstrated that RFCA can eliminate PAF in over 90% of patients. However, the effectiveness for persistent or permanent AF has not been clarified.
Methods and Results: 27 patients (29%) had persistent or permanent AF. RFCA including PV antrum isolation (PVAI) was performed using a circular mapping catheter in the patients with persistent or permanent AF. Four patients (15%) underwent only PVAI. Thirteen patients (48%) underwent PVAI and left atrium roof and/or mitral isthmus linear ablation. Ten patients (37%) underwent PVAI and RFCA to an area with complex fractionated atrial electrograms. All patients were observed for over a year. After repeat ablation at mean follow-up of 16±5 months, 23 patients (85%) had normal sinus rhythm and were free of symptomatic AF or atrial flutter. Three patients required antiarrhythmic drugs to maintain sinus rhythm during follow-up period. One patient had a transient phrenic nerve injury. Two patients were documented with sustained atrial tachycardia (AT). Mapping in 2 patients showed a macro reentry AT due to gaps in the ablation lines and further ablation was needed. No other complications including PV stenosis occurred.
Conclusions: The present study demonstrated that RFCA is an effective and feasible treatment for persistent or permanent AF.

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A 35-year-old man experienced chest pain and a subsequent syncope attack at during the night. Ventricular fibrillation (VF) was documented, which was successfully defibrillated. The ST-segment of his 12-lead electrocardiogram (ECG) showed day-by-day variation, sometimes showing spontaneous coved-type elevation in V1 and V2. He was diagnosed as having Brugada syndrome, and an implantable cardioverter defibrillator was implanted. A coronary angiography was performed. During the procedure, the catheter was selectively inserted to the right ventricular (RV) branch of the right coronary artery (RCA) whereupon the ST-segment in V1 and V2 elevated rapidly, manifesting a coved-type Brugada ECG. The main RCA angiogram revealed the conus branch running to the RV outflow tract area, indicating that the ST-segment elevation was due to ischemia of the RV outflow tract area by transient occlusion of conus branch. The findings indicate that some patients with Brugada syndrome are specifically sensitive to ischemia in the RV outflow tract area, leading to manifestation of the ST-segment elevation in precordial ECG leads.

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A 75-year-old man with a prior myocardial infarction, who underwent a coronary artery bypass graft, suffered from typical atrial flutter. He underwent a cavotricuspid linear catheter ablation. Eighteen days after the ablation, he suddenly died. A transmural ablation line was created between the inferior vena cava and tricuspid annulus. Transmural loss of the cardiomyocytes and small clusters of coagulative necrosis were observed. Evidence of edema and a patchy hemorrage remained in the extracellular space.

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We treated a patient with hypertrophic obstructive cardiomyopathy (HOCM) who underwent DDD pacing therapy. He suffered from attacks of paroxysmal atrial fibrillation (PAF) complicated by sick sinus syndrome. Initially, we were unable to decrease the left ventricular outflow tract (LVOT) gradient by pacing from the mid-distal portion of the right ventricular (RV) septum. However, by changing the pacing site to the apical portion guided by right ventriculography, it was possible to decrease the LVOT gradient and at the same time reduce the mitral regurgitation. Tissue Doppler imaging (TDI) revealed a marked motion delay of the ventricular septum during DDD pacing. The mechanism of the therapy for HOCM provided by the DDD pacing was clearly confirmed by TDI. Furthermore, a dramatic effect of preventing symptomatic PAF with the use of overdrive pacing in the region of Bachmann’s bundle was also observed. This case report provides new insight into DDD pacing therapy for patients with HOCM.

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A 78-year-old man with a permanent pacemaker (PM) implanted in his left prepectoral area reported twitches in his left lateral abdominal region. Chest X-rays revealed a broken right atrial (RA) lead and a fracture of the right ventricular (RV) lead at the left costoclavicular ligament. The electrocardiogram (ECG) and the Holter ECG revealed atrial fibrillation (AF) and an improperly functioning PM. We observed that the twitching seemed to correspond with each pacing beat and that it did not appear with his own beat. We suspected that the twitching was due to electric current leakage from the broken RV lead. We performed a PM re-implantation with a screw-in RV lead using the extrathoracic approach. After re-implantation the twitching disappeared. Costoclavicular ligament related electrode lead fractures are not uncommon and electric current leaks can be a source of problems in cardiac pacing. In this case, the electric current leak from the broken RV lead at the costoclavicular ligament stimulated the left phrenic nerve.

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