Ventricular fibrillation (VF) storm is a life-threatening condition that is particularly challenging to manage when resistant to conventional therapies such as antiarrhythmic drugs, deep sedation, overdrive pacing, and hemodynamic support. We report a case of a 55-year-old male with ischemic heart disease and recurrent VF storm unresponsive to initial treatments, requiring percutaneous cardiopulmonary support to stabilize hemodynamics. A left ventricular inferoseptal Purkinje-related premature ventricular contraction (PVC) was identified as the VF trigger, with continuous propagating activity involving Purkinje and myocardial substrates as the driver. Targeted radiofrequency catheter ablation (RFCA) at the earliest activation site of the triggering PVC and continuous propagating activity effectively suppressed VF and maintained stable sinus rhythm. The patient was successfully weaned off support devices and was discharged with an implantable cardioverter-defibrillator. This case highlights the importance of accurately localizing triggers and drivers in refractory VF management and suggests the efficacy of RFCA in managing VF storm associated with structural heart disease. Learning objective 1. The origin and exit of the Purkinje-related triggering premature ventricular contraction (PVC) differed. 2. During initiation of ventricular fibrillation (VF), the Purkinje and myocardial potentials fused, exhibiting continuous propagating activity in the limited area surrounding the origin and exit of the triggering PVC. 3. Radiofrequency catheter ablation targeting both the triggering PVC and continuous propagating activity demonstrated notable efficacy in the suppression of the VF storms.

A 70-year-old man presented with regular wide QRS complex tachycardia (WCT) at a rate of 185 beats/min, characterized by left bundle branch block morphology. WCT termination was achieved through electrical cardioversion. A subsequent 12-lead electrocardiogram revealed sinus rhythm with complete right bundle branch block (CRBBB) morphology. Echocardiography showed normal left ventricular function without structural heart disease. An electrophysiological study was then conducted, followed by catheter ablation. At baseline, the atrio-His and His-ventricular intervals were normal. Fractionated ventricular potentials were observed in the para-Hisian region during sinus rhythm. Neither dual atrioventricular (AV) nodal physiology nor ventriculoatrial conduction was observed during programmed pacing. Clinical WCT was induced by ventricular extra-stimulation with concurrent AV dissociation and no visual His bundle potential, confirming the diagnosis of ventricular tachycardia (VT). Figure 1 illustrates 12-lead electrocardiograms recorded during overdrive pacing from the right ventricular apex (RVA) and right atrial septum during VT. The electroanatomical activation map revealed a distinctive focal breakout pattern with fractionated potentials originating from the para-Hisian region. In the noncoronary cusp (NCC), corresponding to the opposite side of the para-Hisian region, prolonged and fractionated ventricular potentials preceding QRS onset by 56 ms were recorded (Figure 2A). Figure 2B shows the intracardiac electrogram recorded during ventricular overdrive pacing from the NCC during VT. Based on these observations, what is the mechanisms underlying the tachycardia?

Atrial fibrillation (AF) is mainly initiated by arrhythmogenic triggers originating from the pulmonary veins, and ganglion plexus often plays a crucial role in the induction and maintenance of AF. In this report, we describe a case of successful cryoballoon ablation of focal atrial tachycardia originating from the left inferior pulmonary, in which vagal response was observed, and discuss its tachycardia mechanism.

A 77-year-old woman with palpitations was referred for a second radiofrequency ablation for persistent atrial tachycardia (AT). She previously underwent pulmonary vein (PV) isolation for paroxysmal atrial fibrillation, linear ablation between the 3’o clock position of the mitral annulus (MA) and left PV from the endocardium, and ablation inside the coronary sinus (CS) for perimitral atrial tachycardia (PMAT) in the first procedure. A baseline 12-lead electrocardiogram in the second procedure showed stable AT with a cycle length (CL) of 250 ms. No PV reconnection was observed. The CS catheter was placed from 3:30 to 5:00 on the MA, and a proximal-to-distal pattern of CS activation during AT was observed. Activation mapping in the left atrial (LA) endocardium using a three-dimensional mapping system (CARTO3, Biosense Webster, Diamond Bar, CA, USA) revealed a sequence of counterclockwise rotations of the MA. Figures 1A and 1B show the intracardiac electrograms during high-output (20 V) and low-output (5 V) atrial entrainment pacing at a pacing CL of 240ms from CS 3,4, which corresponds to the 4’o clock position of the MA. Dose residual conduction occur across the mitral isthmus (MI) endocardium, epicardium, or both? What is the electrophysiological mechanism during high- and low-output entrainment pacing?

A 72-year-old female with frequent palpitation was referred for radiofrequency ablation. The baseline 12-lead electrocardiogram and echocardiography results were normal. At baseline, the atrio-His (AH) and His-ventricular (HV) intervals were 90 and 41 ms, respectively. Dual atrioventricular (AV) nodal physiology or ventriculoatrial (VA) conduction was not observed during programmed atrial and ventricular stimulation. After isoproterenol infusion, VA conduction became decremental and concentric, with the earliest atrial activation seen at the His bundle (HB) region during ventricular pacing. A supraventricular tachycardia with a long RP interval (SVT) was induced by atrial extra-stimulation, without any jump-up in the AH interval. During the SVT, the AH and HV intervals were 180 and 180 ms, respectively, and the earliest atrial activation was recorded in the HB region (Figure 1A). During the SVT, transient 2:1AV conduction was observed (Figure 1B). Ventricular overdrive pacing at a pacing cycle length (CL) of 360 ms was performed during the SVT with a CL of 390ms (Figures 2A and B). Based on these observations, what is the mechanism of this tachycardia?

The treatment of digital ulcer (DU) in systemic sclerosis (SSc) has not been established. A 77-year-old female with a refractory DU in SSc on the right foot was transferred to our hospital. Wound healing had not been achieved despite several endovascular treatments (EVT) and minor amputations. We started Waon therapy 5 days per week as an adjunct therapy. She was placed in a far-infrared-ray dry sauna maintained at 45 °C for 15 min, and was subsequently kept to rest with soothing warmth using a blanket for additional 30 min outside the room. Gradually, the wound had become smaller and the skin perfusion pressure (SPP) had increased. The increase of the blood flow to the wound could be observed in the angiogram on day 109. An additional EVT on day 109 also accelerated wound healing. Finally, wound healing was completely achieved without additional amputations on day 173. In this presented case, Waon therapy contributed to increase of the blood flow to the wound, evidenced by SPP value. Waon therapy may serve as an effective adjunct therapy of DU in SSc.

It is still difficult to treat acute limb ischemia (ALI) in the non-stenting zone such as the popliteal artery. We describe a temporary endoluminal bypass technique for ALI in the non-stenting zone using a guide extension catheter. An 83-year-old female was admitted and diagnosed with ALI in her left leg. The angiogram showed a thrombotic obstruction of the left popliteal artery. Aspiration and dilation by angioplasty could not revascularize. Although Fogarty thrombectomy can be applicable, we avoided it because of its risk of complications and performed a temporary endoluminal bypass technique. After evaluating the occluded lesion by intravascular ultrasound, we delivered a guide extension catheter to fully cover it. Because it played the role of an endoluminal bypass, the blood flow to the distal tibial arteries could be confirmed in the angiogram. A thrombolytic drug was administered intra-arterially for the whole day, and the angiogram showed a reduction of the thrombus on postoperative day (POD) 1. On POD 2, the blood flow was maintained without flow limitation even after removing the catheter. Finally, she was discharged without any complications. This technique might be an alternative in cases of failed conventional treatments for ALI although further investigation needs to be undertaken.

A 39-year-old woman was referred for radiofrequency ablation of narrow QRS supraventricular tachycardia (SVT) with occasional absence of retrograde P waves (Figure 1A ). A baseline 12-lead electrocardiogram showed normal sinus rhythm. At baseline, atrio-His (AH) and His-ventricular intervals were 80 and 45 ms, respectively. Dual atrioventricular (AV) nodal physiology was observed during programmed atrial extrastimulation. Programmed ventricular stimulation showed concentric decremental retrograde conduction, and ventriculoatrial conduction was intermittent at a paced cycle length (CL) of 545 ms. Para-Hisian pacing showed an AV nodal pattern. After infusion of isoproterenol, SVT with a fixed 1:1 AV relationship was induced by atrial extra stimulation with a finding of an AH jump (Figure 1B). During SVT, the atrial activation sequence was identical to that during ventricular pacing. A ventricular extrastimulus delivered during SVT when the His bundle (HB) was refractory did not reset the atrial cycle. Figure 2 shows the response to overdrive pacing with 2 pacing trains from the right ventricle (RV). What is the mechanism of this tachycardia? Figure 2Intracardiac electrograms of the response to overdrive pacing with 2 pacing trains from the right ventricle during the tachycardia. A: A ventricular-ventricular-atrial response was observed upon resumption of the tachycardia on cessation of ventricular entrainment pacing. B: During RV pacing at a pacing cycle length of 400 ms, 2 consecutive His bundle potentials occur at the pacing cycle length shortly after the fourth and fifth pacing stimuli, but there was no change in the AA intervals of 432 ms after those pacing stimuli. rH = retrograde His bundle potential; other abbreviations as in Figure 1. View Large Image Figure Viewer Download Hi-res image

Irregular narrow QRS complex tachycardia with intermittent atrioventricular dissociation: What is the mechanism?Atsushi Doi, MD, PhD; Naoko Miyazaki, MD; Tomohiko Goda, MD; Haruya Yamane, MD; Kei Tanaka, MD; Ryo Araki, MD,PhD; Fumi Sato, MD, PhD; Takayuki Yamada, MD.Department of Cardiovascular Medicine, Otemae Hospital, 1-5-34 Otemae, Chuo-ku, Osaka, 540-0008, Japan.Correspondence to Atsushi Doi, MD, PhD. Department of Cardiovascular Medicine, Otemae Hospital, 1-5-34 Otemae, Chuo-ku, Osaka, 540-0008, Japan.Tel: 81-6-6941-0484, Fax: 81-6-6942-2848E-mail; m1410001@med.osaka-cu.ac.jp