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Background: A 70‐year‐old man revealed a rare type of atrioventricular nodal re‐entrant tachycardia (AVNRT) involving distinct retrograde pathways, superior slow pathway, and inferolateral left atrial slow pathway. Result: Radiofrequency ablation was successfully performed on the noncoronary cusp and in the left atrium, respectively, to eliminate the tachycardias. Discussion and Conclusion: Due to the anomalous electrical conduction patterns, careful diagnosis and ablation strategies were necessary to avoid the risk of atrioventricular block. These findings underscore the diversity and complexity of AVNRT and highlight the importance of tailored therapeutic approaches. [ABSTRACT FROM AUTHOR]

Aims Patients with particular mutations of type-2 long QT syndrome (LQT2) are at an increased risk for malignant arrhythmia during fever. This study aimed to determine the mechanism by which KCNH2 mutations cause fever-induced QT prolongation and torsades de pointes (TdP). Methods and results We evaluated three KCNH2 mutations, G584S, D609G, and T613M, in the Kv11.1 S5-pore region, identified in patients with marked QT prolongation and TdP during fever. We also evaluated KCNH2 M124T and R269W, which are not associated with fever-induced QT prolongation. We characterized the temperature-dependent changes in the electrophysiological properties of the mutant Kv11.1 channels by patch-clamp recording and computer simulation. The average tail current densities (TCDs) at 35°C for G584S, WT+D609G, and WT+T613M were significantly smaller and less increased with rising temperature from 35°C to 40°C than those for WT, M124T, and R269W. The ratios of the TCDs at 40°C to 35°C for G584S, WT+D609G, and WT+T613M were significantly smaller than for WT, M124T, and R269W. The voltage dependence of the steady-state inactivation curve for WT, M124T, and R269W showed a significant positive shift with increasing temperature; however, that for G584S, WT+D609G, and WT+T613M showed no significant change. Computer simulation demonstrated that G584S, WT+D609G, and WT+T613M caused prolonged action potential durations and early afterdepolarization formation at 40°C. Conclusion These findings indicate that KCNH2 G584S, D609G, and T613M in the S5-pore region reduce the temperature-dependent increase in TCDs through an enhanced inactivation, resulting in QT prolongation and TdP at a febrile state in patients with LQT2. [ABSTRACT FROM AUTHOR]

Background: Gain-of-function mutations in CACNA1C encoding Cav1.2 cause syndromic or non-syndromic type-8 long QT syndrome (LQTS) (sLQT8 or nsLQT8). The cytoplasmic domain (D)Ⅰ-Ⅱ linker in Cav1.2 plays a pivotal role in calcium channel inactivation, and mutations in this site have been associated with sLQT8 (such as Timothy syndrome) but not nsLQT8. Objective: Since we identified a novel CACNA1C mutation, located in the DⅠ-Ⅱ linker, associated with nsLQTS, we sought to reveal its biophysical defects. Methods: Target panel sequencing was employed in 24 genotype-negative nsLQTS probands (after Sanger sequencing) and three family members. Wild-type (WT) or R511Q Cav1.2 was transiently expressed in tsA201 cells, then whole-cell Ca2+ or Ba2+ currents (ICa or IBa) were recorded using whole-cell patch-clamp techniques. Results: We identified two CACNA1C mutations, a previously reported R858H mutation and a novel R511Q mutation located in the DⅠ-Ⅱ linker. Four members of one nsLQTS family harbored the CACNA1C R511Q mutation. The current density and steady-state activation were comparable to those of WT-ICa. However, persistent currents in R511Q-ICa were significantly larger than those of WT-ICa (WT at +20 mV: 3.3±0.3%, R511Q: 10.8±0.8%, P<0.01). The steady-state inactivation of R511Q-ICa was weak in comparison to that of WT-ICa at higher prepulse potentials, resulting in increased window currents in R511Q-ICa. Slow component of inactivation of R511Q-ICa was significantly delayed compared to that of WT-ICa (WT-tau at +20 mV: 81.3±3.3 ms, R511Q-tau: 125.1±5.0 ms, P<0.01). Inactivation of R511Q-IBa was still slower than that of WT-IBa, indicating that voltage-dependent inactivation (VDI) of R511Q-ICa was predominantly delayed. Conclusions: Delayed VDI, increased persistent currents, and increased window currents of R511Q-ICa cause nsLQT8. Our data provide novel insights into the structure-function relationships of Cav1.2 and the pathophysiological roles of the DⅠ-Ⅱ linker in phenotypic manifestations. [ABSTRACT FROM AUTHOR]

Introduction: The electrophysiological discrimination between fast‐slow (F/S‐) atrioventricular (AV) nodal reentrant tachycardia (NRT) and atrial tachycardia (AT) originating from the interatrial septum remains challenging. While a V‐A‐A‐V response may occur immediately after ventricular induction or entrainment of either tachycardia, the electrophysiological dissimilarities in that response between the two tachycardias remain unclear. The purpose of this study was to identify a diagnostic indicator discriminating F/S‐AVNRT from AT by examining the difference in the V‐A‐A‐V response between the two tachycardias. Methods: This retrospective study included 17 patients with F/S‐AVNRT [seven with common‐form F/S‐AVNRT using a typical slow pathway (SP) and 10 with superior type F/S‐AVNRT using a superior SP] and 10 patients with reentrant AT. All 27 patients presented with long RP supraventricular tachycardia and an initial V‐A‐A‐V response upon ventricular induction or entrainment. The V‐A‐A‐V response in patients with F/S‐AVNRT was due to dual atrial responses. We measured the interval between the first (A1) and second atrial electrogram (A2) of V‐A‐A‐V and calculated ΔAA by subtracting A1‐A2 from the tachycardia cycle length. Results: V‐A‐A‐V responses were observed most often upon ventricular induction of F/S‐AVNRT (6 ± 5 times) as well as AT (6 ± 6 times; p =.87). The V‐A‐A‐V response upon ventricular entrainment was observed in a single patient with F/S‐AVNRT versus 10 all patients with AT (p <.001). ΔAA ranged between −80 and 228 ms in F/S‐AVNRT and between −184 and 26 ms in AT. A ΔAA > 26 ms predicted a diagnosis of F/S‐AVNRT with a 76% sensitivity and 100% specificity, while a ΔAA <−80 ms predicted a diagnosis of AT with a 50% sensitivity and 100% specificity. Conclusions: ΔAA is a useful, confirmatory, diagnostic indicator of F/S‐AVNRT versus AT associated with the V‐A‐A‐V response. [ABSTRACT FROM AUTHOR]

A case study of 53-year-old woman with a history of multiple episodes of narrow QRS tachycardia underwent electrophysiological study and catheter ablation. Topics include Tachycardia with concentric atrial activation and simultaneous ventricular activation a sudden increase in the atrio-His (AH) interval during premature atrial stimulation; and diagnosis of junctional tachycardia (JT) was excluded by atrial entrainment pacing.

According to guidelines, carbon-ion beam therapy is considered to carry a high safety risk for patients with cardiac implantable electronic devices (CIEDs), although the actual impacts remain unclear. In this study, we investigated the safety of carbon-ion beam therapy in patients with CIEDs. Patients with CIEDs who underwent carbon-ion therapy at Gunma University Heavy Ion Medical Center between June 2010 and December 2019 were identified and investigated for abnormalities in the operation of their CIEDs, such as oversensing and resetting during irradiation, and abnormalities in operation after treatment. In addition, the risk of irradiation from carbon-ion beam therapy was evaluated by model simulations. Twenty patients (22 sites) with CIEDs were identified, 19 with pacemakers and one with an implantable cardioverter-defibrillator (ICD). Treatments were completed without any problems, except for one case in which the treatment was discontinued because of worsening of the primary disease. Monte Carlo simulation indicated that the carbon beam irradiation produced neutrons at a constant and high level in the irradiation field. Nevertheless, with the distances between the CIEDs and the irradiation fields in the analyzed cases, the quantity of neutrons at the CIEDs was lower than that within the irradiation. Although carbon-ion beam therapy can be safely administered to patients with CIEDs, it is advisable to perform the therapy with sufficient preparation and backup devices because of the risks involved. [ABSTRACT FROM AUTHOR]

Introduction: We tested our hypothesis that atrial entrainment pacing (EP) of a) the common‐type (com‐) fast‐slow (F/S‐) atypical atrioventricular nodal reentrant tachycardia (AVNRT) using a typical slow pathway (SP), or b) the superior‐type (sup‐) F/S‐AVNRT using a superior SP, both modify the retrograde conduction time across the SP immediately after termination of EP (retro‐SP‐time). Methods: We measured the difference in the His‐atrial interval (HA difference) immediately after cessation of EP, performed at 2 ± 2 rates from the high right atrium (HA[1]‐HRA) versus from the proximal coronary sinus (HA[1]‐CS) in 17 patients with com‐F/S‐AVNRT and 11 patients with sup‐F/S‐AVNRT. We also measured the atrial‐His and HA intervals of the first and second cycles immediately after cessation of EP and during stable tachycardia. Results: Unequal responses, defined as a ≥ 20‐ms HA difference at ≥1 EP rates, were observed in 16 patients (57%), including 7 with com‐ and 9 with sup‐F/S‐AVNRT. Irrespective of the EP rate, all unequal responses of com‐F/S‐AVNRT were due to a shorter HA[1]‐CS than HA[1]‐HRA, with a mean 34 ± 11 ms HA difference, whereas all unequal responses of sup‐F/S‐AVNRT were due to a longer HA[1]‐CS than HA[1]‐HRA, with a mean 49 ± 25 ms HA difference. The unequal responses resolved within two cycles after the cessation of EP. Conclusions: We have identified a little‐known pacing site‐ and pacing rate‐dependent shortening of the retro‐SP‐time. [ABSTRACT FROM AUTHOR]

Background: SCN5A‐related Brugada syndrome (BrS) can be caused by multiple mechanisms including trafficking defects and altered channel gating properties. Most SCN5A mutations at pore region cause trafficking defects, and some of them can be rescued by mexiletine (MEX). Objective: We recently encountered symptomatic siblings with BrS and sought to identify a responsible mutation and reveal its biophysical defects. Methods: Target panel sequencing was performed. Wild‐type (WT) or identified mutant SCN5A was transfected into tsA201 cells. After incubation of transfected cells with or without 0.1 mM MEX for 24–36 hr, whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques. Results: The proband was 29‐year‐old male who experienced cardiopulmonary arrest. Later, his 36‐year‐old sister, who had been suffering from recurrent episodes of syncope since 12 years, was diagnosed with BrS. An SCN5A W374G mutation, located at pore region of domain 1 (D1 pore), was identified in both. The peak density of W374G‐INa was markedly reduced (WT: 521 ± 38 pA/pF, W374G: 60 ± 10 pA/pF, p <.01), and steady‐state activation (SSA) was shifted to depolarizing potentials compared with WT‐INa (V1/2‐WT: −39.1 ± 0.8 mV, W374G: −30.9 ± 1.1 mV, p <.01). Incubation of W374G‐transfected cells with MEX (W374G‐MEX) increased INa density, but it was still reduced compared with WT‐INa (W374G‐MEX: 174 ± 19 pA/pF, p <.01 versus W374G, p <.01 versus WT). The SSA of W374G‐MEX‐INa was comparable to W374G‐INa (V1/2‐W374G‐MEX: −31.6 ± 0.7 mV, P = NS). Conclusions: Reduced current density, possibly due to a trafficking defect, and depolarizing shift in activation of SCN5A W374G are underlying biophysical defects in this severe form of BrS. Trafficking defects of SCN5A mutations at D1 pore may be commonly rescued by MEX. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 76‐year‐old woman with a history of multiple episodes of a long RP tachycardia with biphasic P waves in inferior leads underwent electrophysiological studies and a catheter ablation procedure. Topics include premature ventricular extrastimuli on His bundle refractoriness has not reset atrial cycles; and an injection of adenosine triphosphate of a dose of 2mg terminated the tachycardia with an end of ventricular deflection.

Background: The epinephrine infusion test (EIT) typically induces marked QT prolongation in LQT1, but not LQT3, while the efficacy of β‐blocker therapy is established in LQT1, but not LQT3. We encountered an LQT3 family, with an SCN5A V1667I mutation, that exhibited epinephrine‐induced marked QT prolongation. Methods: Wild‐type (WT) or V1667I‐SCN5A was transiently expressed into tsA‐201 cells, and whole‐cell sodium currents (INa) were recorded using patch‐clamp techniques. To mimic the effects of epinephrine, INa was recorded after the application of protein kinase A (PKA) activator, 8‐CPT‐cAMP (200 μM), for 10 minutes. Results: The peak density of V1667I‐INa was significantly larger than WT‐INa (WT: 469 ± 48 pA/pF, n = 20; V1667I: 690 ± 62 pA/pF, n = 19, P <.01). The steady‐state activation (SSA) and fast inactivation rate of V1667I‐INa were comparable to WT‐INa. V1667I‐INa displayed a significant depolarizing shift in steady‐state inactivation (SSI) in comparison to WT‐INa (V1/2‐WT: −88.1 ± 0.8 mV, n = 17; V1667I: −82.5 ± 1.1 mV, n = 17, P <.01), which increases window currents. Tetrodotoxin (30 μM)‐sensitive persistent V1667I‐INa was comparable to WT‐INa. However, the ramp pulse protocol (RPP) displayed an increased hump in V1667I‐INa in comparison to WT‐INa. Although 8‐CPT‐cAMP shifted SSA to hyperpolarizing potentials in WT‐INa and V1667I‐INa to the same extent, it shifted SSI to hyperpolarizing potentials much less in V1667I‐INa than in WT‐INa (V1/2‐WT: −92.7 ± 1.3 mV, n = 6; V1667I: −85.3 ± 1.6 mV, n = 6, P <.01). Concordantly, the RPP displayed an increased hump in V1667I‐INa, but not in WT‐INa. Conclusions: We demonstrated an increase of V1667I‐INa by PKA activation, which may provide a rationale for the efficacy of β‐blocker therapy in some cases of LQT3. [ABSTRACT FROM AUTHOR]

Background: Ablation of slow‐fast atrioventricular nodal reentrant tachycardia (S/F‐AVNRT) is occasionally refractory. We hypothesized that the site of ablation for curing S/F‐AVNRT can be screened by simple differential atrial entrainment pacing (EP) from the high right atrium (HRA) and proximal coronary sinus (prox‐CS). Methods: We enrolled 43 patients with S/F‐AVNRT who underwent successful differential atrial EP followed by successful ablation of slow pathway (SP) using step‐wise approach, and compared the atrio‐His (A‐H) interval at the recording of His bundle immediately after EP from the HRA [A‐H(HRA)], with the interval between atrial deflection at the prox‐CS and His bundle electrogram after EP at an identical cycle length from the prox‐CS [A‐H (prox‐CS)]. Results: A typical A‐H(CS) shorter than A‐H(HRA), consistent with typical SP conduction, was observed in 39 patients (91%), and an atypical A‐H(HRA) shorter than A‐H(CS) was observed in 4 patients (9%). Successful ablation was obtained at the posteroseptum/midseptum in 32/7 patients with typical responses but only at the midseptum in all 4 patients with atypical responses (P =.0027). The atypical responses predicted a necessity for ablation at the midseptum, with positive and negative predictive values of 100% and 82%, respectively. The mechanism of an atypical response remains unclear but may involve an anatomical variation of Koch's triangle and/or the participation of a variant of the SP, including the superior SP, over which retrograde conduction was observed more frequently in patients with atypical responses (P =.0013). Conclusions: Differential atrial EP predicts the ablation site for successfully curing S/F‐AVNRT. [ABSTRACT FROM AUTHOR]

Introduction: Electrophysiological properties of reentry circuits of fast‐slow atrioventricular nodal reentrant tachycardia (F/S‐AVNRT) may contribute to cyclic variability after atrial induction. Methods: In 156 atrial inductions of 33 patients with F/S‐AVNRT, we measured the atrio‐His (AH) and His‐atrial (HA) intervals in the first cycle after the induction (AH[1] and HA[1], respectively), those in the second cycle (AH [2] and HA [2], respectively), and those during tachycardia that maintained a stable cycle length AH[T] and HA[T], respectively), and calculated the value of AH(1) minus AH(T) [ΔAH] and the value of HA(1) minus HA(T) [ΔHA] in each induction. According to the sum of ΔAH and ΔHA, tachycardia variability was classified as incremental (<−20), balanced (−20 to 20), or decremental (>20). Results: ΔAH and ΔHA were significantly different between the three responses: 6 ± 28 and −67 ± 39 in 55 inductions (35%) with an incremental response, 20 ± 10 and −23 ± 28 in 59 (38%) with a balanced response, and 54 ± 44 and 4 ± 50 in 42 (27%) with a decremental response, respectively. Incremental response was reproducibly and consistently observed in 33% of patients. HA(2) was similar to HA(T) in inductions with an incremental response. These results suggest that incremental response can be manifested only in the first cycle when HA(1) is excessively shortened, approximating a retrograde conduction time over a slow pathway, in contrast, and far superior to a decremental delay of AH(1). Conclusion: In specific patients with F/S‐AVNRT, poorly recognized, electrophysiological properties of shortening a retrograde conduction time over a slow pathway was manifested during atrial induction. [ABSTRACT FROM AUTHOR]

A case study of a 71‐year‐old woman who is diagnosed with Atrioventricular nodal reentry tachycardia (AVNRT) is presented. It reports that the retrograde depolarization of the His bundle (HB) by the ventricular stimulus eliminated the long‐short activation sequence in the HB. It also mentions that the injection of adenosine triphosphate (ATP), and atrial and ventricular entrainment during the tachycardia were not attempted owing to the poor inducibility of the sustained tachycardia.

The article focuses on knowing the mechanism of QRS tachycardia. Topics discussed include chart of the Intracardiac electrograms of an induction of the tachycardia with burst stimulation from the high right atrium (HRA), analysis of the AV relationship and QRS morphology during atrial overdrive pacing, and manifestation of ventricularpre-excitation via the nodoventricular (NV) fiber.

Background Although a ventriculoatrial interval (VAI) of ≤70 ms is used to distinguish atrioventricular nodal reentrant tachycardia from orthodromic atrioventricular reciprocating tachycardia (AVRT), a VAI of ≤70 ms is sometimes observed in cases of AVRT. The study aimed to evaluate the short VAI that is seen in AVRT and to understand its underlying mechanism. Methods Electrophysiologic studies of 46 consecutive patients with AVRT involving an accessory pathway (AP) were examined retrospectively. Results AP was right sided in seven patients and left sided in 39. A VAI (interval from QRS onset to the earliest intracardiac atrial electrogram recorded by any mapping catheter during AVRT) ≤70 ms during AVRT (short VAI) was observed in eight patients: six with a left lateral AP and two with a left posteroseptal AP. During AVRT involving a left-sided AP, the QRS-V interval (from the earliest QRS onset to the local ventricular electrogram at a site which showed earliest atrial electrogram recorded from the coronary sinus catheter) was significantly shorter (37 ± 7 ms vs 54 ± 13 ms, P = 0.001) and supernormal conduction (QRS duration or the QRS-V interval shortening by ≥10 ms during AVRT) was more frequently seen (63% vs 6%, P = 0.02) in the short VAI group than in the normal VAI group. Furthermore, these parameters were shown to be determinants for short VAI. Conclusions A short VAI is sometimes observed during AVRT involving a left-sided AP. The short VAI may be caused by rapid propagation or supernormal conduction between the proximal Purkinje-muscle junction and basal left ventricular myocardium. [ABSTRACT FROM AUTHOR]

The article presents a case study of 43-year-old woman with a history of multiple episodes of paroxysmal supraventricular tachycardia and suffered an abrupt change in the atrio-his interval during Long RP Tachycardia. Topics discussed include differential diagnosis of long RP tachycardias; development of atrioventricular (AV) block during the ongoing tachycardia rules out the diagnosis of AV nodal reentrant tachycardia AVRT; and change in the antegrade AV nodal pathway.

Amiodarone is used commonly and effectively in the treatment of arrhythmia; however, it may cause thyrotoxicosis categorized into two types: iodine-induced hyperthyroidism (type 1 amiodarone-induced thyrotoxicosis (AIT)) and destructive thyroiditis (type 2 AIT). We experienced a case of type 2 AIT, in which high-dose steroid was administered intravenously, and we finally decided to perform total thyroidectomy, resulting in a complete cure of the AIT. Even though steroid had been administered to the patient (maximum 80 mg of prednisolone), the operation was performed safely and no acute adrenal crisis as steroid withdrawal syndrome was found after the operation. Few cases of type 2 AIT that underwent total thyroidectomy with high-dose steroid administration have been reported. The current case suggests that total thyroidectomy should be taken into consideration for patients with AIT who cannot be controlled by medical treatment and even in those under high-dose steroid administration. [ABSTRACT FROM AUTHOR]

The length of the slow pathway (SP-L) in atrioventricular (AV) nodal reentrant tachycardia (NRT) has never been measured clinically. We studied the relationship among (a) SP-L, i.e., the distance between the most proximal His bundle (H) recording and the most posterior site of radiofrequency (RF) delivery associated with a junctional rhythm, (b) the length of Koch's triangle (Koch-L), (c) the conduction time over the slow pathway (SP-T), measured by the AH interval during AVNRT at baseline, and (d) the distance between H and the site of successful ablation (SucABL-L) in 26 women and 20 men (mean age 64.6 ± 11.6 years), using a stepwise approach and an electroanatomic mapping system (EAMS). SP-L (15.0 ± 5.8 mm) was correlated with Koch-L (18.6 ± 5.6 mm; R = 0.1665, P < 0.005), SP-T (415 ± 100 ms; R = 0.3425, P = 0.036), and SucABL-L (11.6 ± 4.7 mm; R = 0.5243, P < 0.0001). The site of successful ablation was located within 10 mm of the posterior end of the SP in 38 patients (82.6 %). EAMS-guided RF ablation, using a stepwise approach, revealed individual variations in SP-L related to the size of Koch's triangle and AH interval during AVNRT. Since the site of successful ablation was also correlated with SP-L and was usually located near the posterior end of the SP, ablating anteriorly, away from the posterior end, is not a prerequisite for the success of ablation procedures. [ABSTRACT FROM AUTHOR]

After entrainment pacing, the postpacing interval of a diastolic potential may be misinterpreted if the distal tip of the ablation catheter captures a remote bystander pathway adjacent to the critical isthmus of a complex reentrant circuit in a structurally diseased heart. We discuss this possible pitfall of entrainment mapping of reentrant ventricular tachycardia, observed after a healed myocardial infarction. [ABSTRACT FROM AUTHOR]

Purpose: Late ventricular potentials (LPs) are considered to be useful for identifying patients with heart failure at risk of developing ventricular arrhythmias. I-metaiodobenzylguanidine (MIBG) scintigraphy, which is used to evaluate cardiac sympathetic activity, has demonstrated cardiac sympathetic denervation in patients with malignant ventricular tachyarrhythmias. This study was undertaken to clarify the relationship between LPs and I-MIBG scintigraphy findings in patients with dilated cardiomyopathy (DCM). Methods: A total of 56 patients with DCM were divided into an LP-positive group ( n = 24) and an LP-negative group ( n = 32). During the compensated period, the delayed heart/mediastinum count (H/M) ratio, delayed total defect score (TDS), and washout rate (WR) were determined from I-MIBG images and plasma brain natriuretic peptide (BNP) concentrations were measured. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular ejection fraction (LVEF) were simultaneously determined by echocardiography. Results: LVEDV, LVESV, LVEF and plasma BNP concentrations were similar in the two groups. However, TDS was significantly higher (35 ± 8 vs. 28 ± 6, p < 0.005), the H/M ratio was significantly lower (1.57 ± 0.23 vs. 1.78 ± 0.20, p < 0.005), and the WR was significantly higher (60 ± 14% vs. 46 ± 12%, p < 0.001) in the LP-positive than in the LP-negative group. The average follow-up time was 4.5 years, and there were nine sudden deaths among the 56 patients (16.1%). In logistic regression analysis, the incidences of sudden death events were similar in those LP-negative with WR <50%, LP-negative with WR ≥50% and LP-positive with WR <50% (0%, 10.0% and 14.3%, respectively), but was significantly higher (41.2%) in those LP-positive with WR ≥50% ( p < 0.01, p < 0.05, and p < 0.05, respectively). Conclusion: The present study demonstrated that the values of cardiac I-MIBG scintigraphic parameters were worse in LP-positive DCM patients than in LP-negative DCM patients. Furthermore, in LP-positive DCM patients with a high WR, the incidence of sudden death events was higher than that in other subgroups of DCM patients. [ABSTRACT FROM AUTHOR]

Abstract: A 65-year-old man with a history of refractory paroxysmal atrial fibrillation (AF) underwent catheter ablation for persistent AF lasting 2 months. AF was not terminated after complete isolation of the 4 pulmonary veins (PV). Instead, it was transformed to a sustained atrial tachyarrhythmia with beat-to-beat variability in the atrial cycle length. A 12-lead electrocardiogram during tachycardia showed negative flutter-like waves in the inferior leads. Entrainment pacing along the tricuspid annulus confirmed the diagnosis of irregular cavotricuspid isthmus (CTI)-dependent typical atrial flutter (AFL). Linear ablation of the CTI terminated AFL and restored sinus rhythm. [Copyright &y& Elsevier]

The article presents a case study of a 40 year old man with history of multiple episodes of paroxysmal tachycardia who was referred to a hospital for electrophysiologic studies and catheter ablation. A discussion of diagnostic testing which was conducted on the patient, and of medical treatment which he received, is presented.

Introduction: Fasciculoventricular (FV) accessory pathways are rare variants of preexcitation syndrome and published data on the ECG of FV pathways are limited. The purpose of this study was to analyze the electrocardiographic characteristics of FV pathways. Methods: We enrolled 5 patients (mean age, 26.8 ± 15.1 years; range 15–49 years, 2 male) with FV pathways which were diagnosed based on the standard electrophysiologic criteria. According to the standard criteria for the ECG classification of manifest Wolff-Parkinson-White (WPW) syndrome, the ECGs were classified as type A, B or C. The polarity of delta wave in each lead of each patient was divided into positive, flat or negative and was applied to the stepwise ECG algorithms of atrioventricular accessory pathway previously published by Fitzpatrick, Arruda and Iturralde. Results: Type A was found in one patient (Case No 4), type B in one patient (Case No 5) and type C in three patients (Case No 1, 2 and 3). Based on stepwise ECG algorithm, all cases corresponded to the polarity of the delta wave in patients with right anteroseptal, posteroseptal, right anterolateral or left anterolateral AP. In all three cases exhibiting type C, the polarity of delta wave in lead V2 was flat. Conclusions: ECGs of FV pathways may be misidentified as ECG of WPW syndrome, and may present with any preexcitation pattern of type A, B or C. [Copyright &y& Elsevier]

Focal pseudo-atrial fibrillation (AF) developed in a 30-year-old woman after radiofrequency (RF) ablation of focal atrial tachycardia (AT) originating from the coronary sinus ostium. Programmed atrial stimulation occasionally induced, accelerated or terminated AT, and a spiky prepotential preceded the earliest atrial electrogram at the AT focus. After the first RF application, repetitive bursts of accelerated tachycardia developed, mimicking AF on the surface ECG. An additional RF application where the spiky prepotential was observed, eliminated the focal pseudo-AF. [Copyright &y& Elsevier]

Background: The purpose of this study was to identify the His-bundle (HB) versus right bundle branch (RBB) during electrophysiologic studies, using the V3 phenomenon, and to compare the timing of HB versus RBB potentials of sinus cycles (His-ventricular [H-V] interval). Methods: The study enrolled 16 patients without structural heart disease, who underwent electrophysiologic studies during which the H-V interval was within normal limits and the V3 phenomenon was induced during recordings of the HB and the RBB potentials by a multi-electrode catheter. The recording site of the earliest HB potential just before the V3 phenomenon was defined as the branching portion of His bundle (HBBP), the site immediately proximal to the HBBP as the HB, and the site immediately distal to the HBBP as the RBB. Results: The HBBP was identified in all patients. In all cases but one patient, the H-V interval measured at the HB adjacent to the HBBP was ≥35 ms. However, in 12 patients, the H-V interval measured at the RBB adjacent to the HBBP was also ≥35 ms. Conclusions: The electrophysiologic identification of HB versus RBB by simultaneous recordings of HB and RBB potentials during induction of the V3 phenomenon was feasible. When the discrimination between HB and RBB was based on the measurement of the H-V interval, the proximal portion of the RBB was frequently misidentified as the HB. [ABSTRACT FROM AUTHOR]

Double Potentials in CS. Introduction:In some patients with left AV accessory pathway (AP), double potentials are recorded along the coronary sinus (CS) during retrograde AP conduction only. This electrophysiologic study was performed to clarify the origin and clinical significance of double potentials in 11 patients.Methods and Results:The direction of activation of the first, relatively blunt component (DP1) was lateral to septal in 5 patients with anterior or anterolateral AP, centrifugal in 2 patients with posterior or posterolateral AP, and septal to lateral in 4 patients with posteroseptal AP, suggesting the earliest activation of DP1 was near the AP. The direction of activation of the second, sharper potentials (DP2) were septal to lateral in all patients. The double potentials were fused in the paraseptal CS region. Pacing from the lateral CS musculature or lateral left atrium reproduced the double potentials. The effective refractory period of the double potentials was reached by ventricular extrastimulation, and the left atrial deflection preceded the double potentials, excluding a ventricular or AP origin.Conclusion:In patients with connections between the paraseptal CS musculature and left atrium but no connections more laterally, retrograde left AP conduction is associated with double potentials in the CS recordings. The double potentials represent activation of the left atrial insertion of the AP (DP1) and later activation of the CS musculature (DP2) via connections between the paraseptal CS musculature and left atrium, respectively. The activation pattern of DP1 depends on AP location, thus providing important information for AP localization during CS mapping.(J Cardiovasc Electrophysiol, Vol. 15, pp. 1-6, December 2004) [ABSTRACT FROM AUTHOR]

Systolic and Diastolic Potentials in LV Septum.. Introduction:The aim of this study was to examine the electrophysiologic characteristics of the normal left interventricular septum (LIVS).Methods and Results:We explored the LIVS in search of endocardial potentials following ventricular electrograms during sinus rhythm in 28 patients without structural heart disease. In all patients, low-frequency (mean amplitude: 0.81± 0.33 mV) systolic potentials (LA1) were detected in a basal-to-apical activation sequence (earliest to latest QRS-LA1 interval: 93.3± 10.8 ms to 127.1± 16.6 ms). Programmed stimulation demonstrated decremental conduction properties, and the effective refractory period of the tissue between the ventricular electrogram and LA1 at baseline (376.7± 48.8 ms) was significantly prolonged by disopyramide (421.3± 54.1 ms, P<0.05 vs baseline). In 21 patients (75%), diastolic potentials (LA2) morphologically similar to LA1 (mean amplitude: 0.52± 0.17 mV) were detected in an apical-to-basal activation sequence (earliest to latest QRS-LA2 interval: 368.9± 32.4 ms to 440.7± 45.8 ms). Para-Hisian pacing with capture of the His bundle showed shorter S-LA1 and S-LA2 intervals compared to the beats without His-bundle capture but with ventricular capture (156.3± 11.2 ms vs 183.2± 12.3 ms, and 385.7± 21.6 ms vs 397.4± 23.4 ms, respectively, P<0.0001). At the same rate, the LA1-LA2 interval was significantly shorter during right ventricular apical than atrial overdrive pacing (220.4± 23.1 ms vs 261.4± 30.7 ms, P<0.0001).Conclusion:Unique myocardial bundles with slow conduction properties and various electrical connections with the specialized conduction system may exist in the LIVS of normal human hearts.(J Cardiovasc Electrophysiol, Vol. 15, pp. 1-9, September 2004) [ABSTRACT FROM AUTHOR]

Discusses the case of a 48-year-old man who was admitted to hospital for evaluation of paroxysmal tachycardia. Electrocardiogram (ECG) during the spontaneous tachycardia; Diagnose of typical atrial flutter; Normal 12-lead ECG during sinns rhythm; Patient's suffering from no serious diseases; Normal left ventricular function; Electrocardiographic characteristics of the atrial complexes during the new tachycardia; Entrainment studies during typical atrial flutterlike tachycadia induced after linear isthmus ablation.

We report the case of a patient with bundle branch reentrant ventricular tachycardia having two distinct components of the QRS complex due to simultaneous dual transseptal conduction. The macroreentrant circuit consisted of anterograde conduction down the left bundle branch and retrograde conduction up the right bundle branch. Extensively injured myocardium in the interventricular septum isolated the two separate transseptal passages, which exhibited a "fast" and "slow" conduction property, respectively. The QRS configuration resulted from a wavefront propagating from the left bundle branch via `last" trausseptal conduction, followed by another more delayed wavefront propagating via "slow" transseptal conduction, which played an important role in determining this unique QRS morphology. [ABSTRACT FROM AUTHOR]

The article reflects on the mechanism of cardiac rhythm at the onset of Long RP Tachycardia in light of a case study of 52-year-old woman with a history of several episodes of paroxysmal supraventricular tachycardia. Topics discussed include the electrocardiogram showing dual atrioventricular and ventriculoatrial nodal conduction, differentiation between atrial tachycardia and atrioventricular nodal reentrant tachycardia and ablation in right atrium.