Recent advances in invasive electrocardiology dramatically revealed the unique nature of atrial fibrillation originating from the pulmonary veins. By the same invasive technique, the origin of ventricular premature contraction (VPC) has been clarified as being located in the pulmonary outflow tract, ventricular Purkinje fibers or coronary cusps. Despite these clarifications, the essential mechanism of VPCs still remains uncertain. In addition to automaticity, the possible contribution of reentrant pathway cannot be fully ruled out. To analyze the mechanism, we previously reported on a two dimensional color display of interectopic intervals in VPC patients. This display could estimate the fundamental mechanism of VPC for a full day and clearly differentiate parasystole from fixed coupling interval VPCs.
In this review, first we briefly document the historical background. In order to explain the mechanism of the much more frequently observed fixed coupling interval VPCs, we introduced a new version of color display. Using this modified version, a unique electrocardiogram associated with heart rate doubling during interpolated VPC bigeminy was depicted. The role of interpolated VPCs applied to phase analysis was stressed. From the findings, we developed a strong modulation hypothesis.
Clinical significance of interpolated VPC together with heart rate doubling and harmonic feature was illustrated. Our hypothesis can be applied not only to specific form of parasystole with various coupling intervals but also to fixed coupling interval VPCs. The modified display can roughly discriminate the relative ratio of parasystole cycle length from sinus cycle length. Furthermore, simple estimation of the intrinsic automaticity cycle length together with the heart rate dependence in individual patients was possible.

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Background: We investigated the efficacy and safety of strict voltage-based substrate mapping and radiofrequency catheter ablation (SV-substrate-map ablation) in patients with electrical storm.
Methods and Results: SV-substrate-map ablation was performed in 15 patients suffering from multiple appropriate shocks (6.0±3.8/day) from implantable cardioverter defibrillators (ICDs). Strict voltage criteria were defined as: non-arrhythmogenic areas, >0.6 mV; low voltage areas, >0.1 to ≤0.6 mV; and scar, ≤0.1 mV. Using an electroanatomic mapping system, catheter ablation was performed at every possible arrhythmogenic region inside the low voltage areas. Further, we presented a review of the literature and investigated the published data on substrate-mapping guided ablation for electrical storm. After repeat endocardial ablation procedures in 4 patients and an epicardial approach in one, the targeted ventricular tachycardias (VTs) were successfully ablated, and the electrical storms were completely controlled in all. During a mean follow-up period of 801±409 days, only one VT followed by an appropriate ICD shock was observed. No potential complications occurred during the procedure or follow-up. Our results were comparable or better than that of previous substrate-mapping guided ablation studies.
Conclusion: SV-substrate-mapping ablation may be effective and safe for resolving serious clinical situations and prolonging the longevity of ICD devices in patients with electrical storms.

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A 57-year-old woman with chronic renal failure due to the thrombotic thrombocytopenic purpura complained of palpitation. A 12-lead ECG showed supraventricular tachycardia with a cycle length of 375 ms. During the electrophysiological study, a tachycardia with a cycle length of 375 ms was reproducibly induced and terminated by atrial extrastimulation. The tachycardia exhibited an inverse relationship between the coupling interval of extrastimulus initiating the tachycardia, and the first postpacing return cycle, as well as an increasing pattern of resetting the tachycardia with an atrial extrastimulus. Ventricular burst pacing during tachycardia produced AV dissociation. Intravenous injections of a low dose (4 mg) of adenosine triphosphate (ATP) terminated the tachycardia without a preceding atrio-His bundle block. The tachycardia was diagnosed as an ATP-sensitive micro-reentrant atrial tachycardia. Real-time endocardial activation mapping using an electroanatomical mapping system revealed that the earliest activation site of the tachycardia was located at the mid-lateral portion of the crista terminalis. The tachycardia was abolished by focal ablation targeting the earliest activation site during tachycardia. This is the first reported case of an ATP-sensitive micro-reentrant atrial tachycardia associated with thrombotic thrombocytopenic purpura.

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In May 2005 a 68-year-old woman received a VDD pacemaker implantation in the right pectoral region at our hospital for the treatment of complete atrioventricular block. In July 2008, she was diagnosed with dilated cardiomyopathy based on histological testing. In November 2008, she developed syncope due to ventricular tachycardia while at another hospital. She underwent external electrical cardioversion with an anterior-lateral paddle position using a single shock of 100 J. This shock led to severe bradycardia resulting in a transfer to our hospital. The physician who provided the shock could not have been aware that the patient had an implanted pacemaker. The skin above the pulse generator was burned. The electrocardiogram showed no pacing spikes or ventricular escape rhythm. Investigation of the pacemaker 3 hours after cardioversion revealed reprogramming of the device and a marked rise in the lead impedance (>3,000 ohm). Removal of the generator and implantation of a biventricular cardioverter defibrillator were required. The emergency situation, the small size of the generator, the small incision made using the buried suture method, and the patient’s obesity all probably contributed to the physician’s not noticing the implanted pacemaker. It is important to increase awareness of the severe consequences that may follow if the physician administering external defibrillation does not know about the patient’s implanted pacemaker.

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A 43-year-old male was transferred to our institute. His heart rhythm on admission was ventricular fibrillation (VF) which was successfully defibrillated with a direct current shock (DC). A diagnosis of short QT syndrome (SQTS) was made on the basis of an abnormally short QT interval of 280 ms during the sinus rhythm. During treatment for mild total hypothermia, VF recurred repeatedly necessitating DCs. Nifekalant at a dose of 0.3 mg/kg was intravenously administered, the QT interval was prolonged from 280 to 370 ms and VF no longer recurred. Subsequently the patient underwent implantation of an implantable cardioverter defibrillator.

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An 83-year-old woman was admitted to our hospital because of palpitation. She had hypertension and paroxysmal atrial fibrillation, treated with digoxin and cibenzoline, and took dipyridamole for microalbuminuria. Before admission, she had taken pilsicainide pills in addition. On admission, electrocardiogram showed regular tachycardia with mildly prolonged QRS width. For the purpose of terminating tachycardia, 10 mg of adenosine triphosphate (ATP) was rapidly injected. About 20 sec later, atrioventricular block and ventricular standstill occurred. She presented loss of consciousness and convulsion, and chest compression was performed. About 30 sec later, the QRS complex reappeared, and she became alert. Serum concentration of digoxin, cibenzoline and pilsicainide was within therapeutic level, respectively. We should be cautious in using ATP for a patient taking dipyridamole and antiarrhythmic agents.

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Introduction: We have sometimes experienced difficulty in crossing two or more sheath through one septal puncture for catheter based pulmonary vein isolation.
Methods: Subjects were 32 consecutive patients (25 men and 7 women) ranging from age 43 to 76 with paroxysmal or sustained atrial fibrillation, who underwent extensive pulmonary vein isolation. After the Brockenbrough puncture using a Daig SL0 dilator sheath system, the sheath dilator was pulled back into the right atrium leaving the 0.035 inch guide wire in the left atrium. In the initial 19 patients, we attempted to put the second Daig SL0 sheath in the left atrium using the electrode catheter. In the 13 subsequent patients, we used the SL0 sheath dilator in 6 and a newly developed steerable introducer in 7 patients. The sheath dilator was aligned with the anchored first guide wire under the guidance of biplane fluoroscopy. After advancing the second dilator system in the left atrium, the system was pulled back leaving the second guide wire in the left atrium. The third sheath system was positioned in the same manner.
Results: In the two of the 19 conventional cases, the second sheath with electrode did not pass the septum and needed another Brokenbrough puncture. In the 13 subsequent cases using the new method, the sheath dilator systems were successfully positioned in all cases with no major complications. The steerable sheath was very useful for aiming at the puncture site.
In conclusion, the new technique was very useful and simple for crossing two or more sheaths through a single trans-septal puncture.

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