Takekuni Hayashi

Prophylactic catheter ablation for induced monomorphic ventricular tachycardia in patients with implantable cardioverter defibrillators as primary prevention.

AIMS Prophylactic catheter ablation (CA) has been established to reduce the incidence of appropriate implantable cardioverter-defibrillator (ICD) therapy (anti-tachycardia pacing or shock) in secondary prevention patients. The aim of this study was to determine whether prophylactic CA for induced ventricular tachycardia (VT) reduces the incidence of appropriate ICD therapy in primary prevention patients. METHODS AND RESULTS We retrospectively investigated 66 consecutive patients with structural heart disease who had undergone ICD implantation as primary prevention and electrophysiological study. Patients with hypertrophic cardiomyopathy or no inducible monomorphic VT had been excluded, and the remaining 38 patients were divided into two groups; those who had undergone prophylactic CA for induced monomorphic VT (the CA group, n = 18), and those who had not undergone CA (the non-CA group, n = 20). During a mean follow-up of 50 ± 38 months, 1 patient (5%) received appropriate ICD therapy in the CA group and 13 (65%) in the non-CA group. Kaplan-Meier survival analysis revealed a significantly higher event-free survival rates for appropriate ICD therapy in the CA group compared with the non-CA group (P = 0.003). Among the patients, one patient (5%) in the CA group and nine patients (45%) in the non-CA group suffered appropriate shock (P = 0.018). CONCLUSIONS Prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy including shock in primary prevention patients. These results indicate that prophylactic CA may be considered for structural heart disease patients who are candidates for ICD implantation as primary prevention.

Prevalence and electrophysiological characteristics of typical atrial flutter in patients with atrial fibrillation and chronic obstructive pulmonary disease.

AIMS Chronic obstructive pulmonary disease (COPD) is one of the important underlying diseases of atrial fibrillation (AF). However, the prevalence and electrophysiological characteristics of typical atrial flutter (AFL) in patients with AF and COPD remain unknown. The purpose of the present study was to investigate those characteristics. METHODS AND RESULTS We investigated 181 consecutive patients who underwent catheter ablation of AF. Twenty-eight patients were diagnosed with COPD according to the Global Initiatives for Chronic Obstructive Lung Disease (GOLD) criteria. Forty patients with no lung disease served as a control group. We analysed the electrophysiological characteristics in these groups. Typical AFL was more common in the COPD group (19/28, 68%) than in the non-COPD group (13/40, 33%; P = 0.006). The prevalence of AFL increased with the severity of COPD: 4 (50%) of 8 patients with GOLD1, 13 (72%) of 18 patients with GOLD2, and 2 (100%) of 2 patients with GOLD3. Atrial flutter cycle length and conduction time from the coronary sinus (CS) ostium to the low lateral right atrium (RA) during CS ostium pacing before and after the cavotricuspid isthmus ablation were significantly longer in the COPD group than in the non-COPD group (285 vs. 236, 71 vs. 53, 164 vs. 134 ms; P = 0.009, 0.03, 0.002, respectively). CONCLUSION In COPD patients with AF, conduction time of RA was prolonged and typical AFL was commonly observed.

Mitral Isthmus Ablation: Is the Conduction Block Completed? The Importance of the Marshall Bundle Epicardial Connections.

A 66-year-old man underwent electrophysiological study and catheter ablation for persistent atrial fibrillation. At the beginning of the procedure, sinus rhythm was restored by internal cardioversion. Circumferential pulmonary vein isolation was performed, and the electric isolation of all 4 pulmonary veins was confirmed. Subsequently, linear ablation of a left atrial roof and the mitral isthmus (MI) was performed. The MI ablation was applied from the 4 o’clock direction of the mitral annulus (MA) to the left-side pulmonary vein bottoms, and further radiofrequency applications were delivered within the coronary sinus (CS) opposite of the endocardial MI line. We confirmed the complete conduction block of the roof line, and the activation sequence of the CS during the left atrial appendage (LAA) pacing was changed from distal to proximal (Figure 1A) to proximal to distal (Figure 1B) while the MI ablation was being performed. Furthermore, the conduction time from the distal CS electrodes (CS 1–2) to the LAA during CS 1 to 2 pacing was longer than the conduction time from the proximal CS electrodes (CS 7–8) to the LAA during CS 7 to 8 pacing after the MI ablation (Figure 1C and 1D). Was the conduction block of the MI completed? Figure 1. Intracardiac electrograms before and after the mitral isthmus (MI) ablation. A , Before the MI ablation, the activation sequence of the coronary sinus (CS) was distal to proximal. B , After the MI ablation, the activation sequence of the CS was changed to proximal to distal. C , After the MI ablation, the conduction time from CS 1 to 2 to the left atrial appendage (LAA) was 106 ms during CS 1 to 2 pacing. D , After the MI ablation, the conduction time from CS 7 to 8 to the LAA was 87 ms during CS 7 to 8 pacing. …

Ablation of swallowing-induced atrial tachycardia affects heart rate variability: a case report.

A 47-year-old man underwent slow pathway ablation for slow-fast atrioventricular nodal reentrant tachycardia. Following the procedure, he felt palpitations while swallowing, and swallowing-induced atrial tachycardia was diagnosed. Swallowing-induced atrial tachycardia arose from the right atrium-superior vena cava junction and was cured by catheter ablation. After the procedure, the patient’s heart rate variability changed significantly, indicating suppression of parasympathetic nerve activity. In this case, swallowing-induced atrial tachycardia was related to the vagal nerve reflex. Analysis of heart rate variability may be helpful in elucidating the mechanism of swallowing-induced atrial tachycardia.

Identical Atrio-His Interval and A-A Intervals During Long RP Tachycardia What Is the Mechanism?

A 46-year-old woman with frequent palpitations underwent electrophysiological study. The findings of transthoracic echocardiography were normal, and a 12-lead ECG showed no ventricular pre-excitation. Four catheters were placed in standard locations: high right atrium, His bundle, coronary sinus (CS), and right ventricular apex. All the recorded baseline intervals were within normal limits. Retrograde ventriculoatrial (VA) conduction showed decremental and dual pathways during ventricular pacing and single extrastimulus testing. Antegrade atrioventricular (AV) nodal conduction showed decremental and triple pathways during atrial single extrastimulus testing. Narrow-complex supraventricular tachycardia (SVT) was reliably induced with a V–A–V sequence by a single ventricular extrastimulus (Figure 1). Ventricular premature depolarization (VPD) during tachycardia, when the His bundle was refractory, did not reset the atrial cycle. Retrograde Wenckebach periodicity occurred during right ventricular overdrive pacing at a cycle length (CL) of 500 ms. The tachycardia was terminated with atrio–His (A–H) and VA block during atrial and ventricular entrainment pacing. Figure 2 shows progressive prolongation and abrupt shortening of the A–A interval with block during SVT. In addition, the A–H interval was identical to the A–A interval during SVT. On the basis of these findings, what is the mechanism of the tachycardia? Figure 1. Intracardiac electrogram showing that narrow-complex supraventricular tachycardia was induced with a V–A–V sequence by a single ventricular extrastimulus (600/370 ms). CS indicates coronary sinus; HBE, His bundle electrogram; HRA, high right atrium; and RVA, right ventricular apex. Figure 2. Intracardiac electrogram showing progressive prolongation and abrupt shortening …

Alcohol-induced Ventricular Fibrillation in Brugada Syndrome

A 37‐year‐old man lost consciousness suddenly due to ventricular fibrillation (VF). After cardioversion, twelve‐lead ECG showed a pattern characteristic of type 1 Brugada. An implantable cardioverter defibrillator (ICD) was implanted for Brugada syndrome. In the following three years, VF occurred eight times after consumption of alcohol. Association between the Brugada syndrome and alcohol consumption has rarely been reported. Recently, it was reported that alcohol has inhibitory effect on single cardiac sodium channel gating and it may be that alcohol acted as a sodium channel blocker in this patient. Here we report a case of alcohol‐induced VF in Brugada syndrome.

Mitral isthmus ablation: the importance of epicardial connections between the coronary sinus and Marshall bundle

The ligament of Marshall is an epicardial vestigial fold that contains the vein of Marshall (VOM) and a myocardial sleeve called the Marshall bundle (MB). Marshall bundle epicardial connections bypassing the endocardial mitral isthmus (MI) should be blocked to achieve complete MI block. …

Termination of peri-mitral atrial flutter involving coronary sinus by single extrastimulus with non-global atrial capture

A 62-year-old man with dilated cardiomyopathy was admitted for catheter ablation of recurrent uncommon atrial tachycardia (AT). The baseline tachycardia cycle length was 260 ms. Counter-clockwise peri-mitral atrial flutter (PMAFL) involving the coronary sinus (CS) was diagnosed using entrainment and three-dimensional electroanatomical …

Automatic switching between the AAI and the DDD algorithm can prevent repetitive non-reentrant ventriculoatrial synchrony

A 67‐year‐old man with non‐obstructive hypertrophic cardiomyopathy had received an implantable cardioverter‐defibrillator (ICD) for an unstable, sustained ventricular tachycardia (VT) induced by programmed stimulation during an electrophysiological study 5 years earlier. An intracardiac electrogram recorded by the ICD revealed repetitive, non‐reentrant ventriculoatrial synchrony (RNRVAS) associated with hypotension. Electrophysiologic and hemodynamic studies indicated that RNRVAS was induced and reproducibly termed by a single ventricular extrastimulus from the right ventricular apex. Following attainment of the elective replacement indicator, we replaced the ICD with another having managed ventricular pacing, which automatically switched AAI and DDD, thereby avoiding unnecessary ventricular pacing. Thus far, the patient has not experienced further RNRVAS. Thus, we believe that automatic switching between AAI and DDD can prevent RNRVAS.

Identical atrio-His interval and A-A intervals during long RP tachycardia: what is the mechanism? Diagnosis: Atypical AVNRT.

A 46-year-old woman with frequent palpitations underwent electrophysiological study. The findings of transthoracic echocardiography were normal, and a 12-lead ECG showed no ventricular pre-excitation. Four catheters were placed in standard locations: high right atrium, His bundle, coronary sinus (CS), and right ventricular apex. All the recorded baseline intervals were within normal limits. Retrograde ventriculoatrial (VA) conduction showed decremental and dual pathways during ventricular pacing and single extrastimulus testing. Antegrade atrioventricular (AV) nodal conduction showed decremental and triple pathways during atrial single extrastimulus testing. Narrow-complex supraventricular tachycardia (SVT) was reliably induced with a V–A–V sequence by a single ventricular extrastimulus (Figure 1). Ventricular premature depolarization (VPD) during tachycardia, when the His bundle was refractory, did not reset the atrial cycle. Retrograde Wenckebach periodicity occurred during right ventricular overdrive pacing at a cycle length (CL) of 500 ms. The tachycardia was terminated with atrio–His (A–H) and VA block during atrial and ventricular entrainment pacing. Figure 2 shows progressive prolongation and abrupt shortening of the A–A interval with block during SVT. In addition, the A–H interval was identical to the A–A interval during SVT. On the basis of these findings, what is the mechanism of the tachycardia? Figure 1. Intracardiac electrogram showing that narrow-complex supraventricular tachycardia was induced with a V–A–V sequence by a single ventricular extrastimulus (600/370 ms). CS indicates coronary sinus; HBE, His bundle electrogram; HRA, high right atrium; and RVA, right ventricular apex. Figure 2. Intracardiac electrogram showing progressive prolongation and abrupt shortening …