Yosuke Nakatani

Vagal activity modulates spontaneous augmentation of J-wave elevation in patients with idiopathic ventricular fibrillation

BACKGROUND Although J-wave elevation in the inferolateral leads could be related to idiopathic ventricular fibrillation (IVF), little is known about the pathophysiologic characteristics of J-wave elevation in patients with IVF. OBJECTIVE This study aimed to determine the relationship between augmentation of J-wave elevation and changes in RR interval or autonomic nervous activities in patients with IVF. METHODS Eight patients with IVF and 22 controls with J-wave elevation (≥0.1 mV) in lead V5 were studied. The J-wave amplitude was automatically measured in lead CM5 of a digital Holter electrocardiogram, and the J-RR relationship was determined. Based on the analysis of heart rate variability, the relationship between the J-wave amplitude and the natural logarithm of high-frequency (HF) components (J-ln HF relationship) or the ratio of low frequency (LF) components to HF components (J-LF/HF relationship) was also determined. RESULTS The J-RR slope (mm/s) was greater in patients with IVF than in controls (3.5 ± 0.7 vs 2.4 ± 0.8; P <.01), as was J-wave amplitude (mm) at an RR interval of 1.2 seconds (2.8 ± 0.9 vs 2.0 ± 0.6; P <.05). The J-wave amplitude was correlated positively with ln HF and negatively with LF/HF, and the slopes of both J-ln HF and J-LF/HF regression lines were greater in patients with IVF than in controls. During an entire 24-hour period, there was no difference between the 2 groups in either HF or LF/HF. Nine of the total 11 episodes (82%) of spontaneous ventricular fibrillation occurred between 18:00 and 6:00. CONCLUSIONS In patients with IVF as compared with control subjects, J-wave elevation was more strongly augmented during bradycardia and was associated with an increase in vagal activity. This could be related to the occurrence of ventricular fibrillation predominantly at night in patients with IVF.

Tranilast Prevents Atrial Remodeling and Development of Atrial Fibrillation in a Canine Model of Atrial Tachycardia and Left Ventricular Dysfunction

OBJECTIVES This study sought to assess the effects of tranilast on atrial remodeling in a canine atrial fibrillation (AF) model. BACKGROUND Tranilast inhibits transforming growth factor (TGF)-β1 and prevents fibrosis in many pathophysiological settings. However, the effects of tranilast on atrial remodeling remain unclear. METHODS Beagles were subjected to atrial tachypacing (400 beats/min) for 4 weeks while treated with placebo (control dogs, n = 8) or tranilast (tranilast dogs, n = 10). Sham dogs (n = 6) did not receive atrial tachypacing. Atrioventricular conduction was preserved. Ventricular dysfunction developed in the control and tranilast dogs due to rapid ventricular responses. RESULTS Atrial fibrillation duration (211 ± 57 s) increased, and AF cycle length and atrial effective refractory period shortened in controls, but these changes were suppressed in tranilast dogs (AF duration, 18 ± 10 s, p < 0.01 vs. control). The L-type calcium channel α1c (Cav1.2) micro ribonucleic acid expression decreased in control dogs (sham 1.38 ± 0.24 vs. control 0.65 ± 0.12, p < 0.01), but not in tranilast dogs (0.97 ± 0.14, p = not significant vs. sham). Prominent atrial fibrosis (fibrous tissue area, sham 0.8 ± 0.1 vs. control 9.3 ± 1.3%, p < 0.01) and increased expression of tissue inhibitor of metalloproteinase protein 1 were observed in control dogs but not in tranilast dogs (fibrous tissue area, 1.4 ± 0.2%, p < 0.01 vs. control). The TGF-β1 (sham 1.00 ± 0.07 vs. control 3.06 ± 0.87, p < 0.05) and Rac1 proteins were overexpressed in control dogs, but their overexpression was inhibited in tranilast dogs (TGF-β1, 1.28 ± 0.20, p < 0.05 vs. control). CONCLUSIONS Tranilast prevented atrial remodeling and suppressed AF development in a canine model. Its inhibition of TGF-β1 and Rac1 overexpression may contribute to its antiremodeling effects.

Location of epicardial adipose tissue affects the efficacy of a combined dominant frequency and complex fractionated atrial electrogram ablation of atrial fibrillation

BACKGROUND Epicardial adipose tissue (EAT) is located adjacent to high dominant frequency (DF) sites. OBJECTIVE This study aimed to clarify the relationship between the EAT location and efficacy of a combined high DF site and continuous complex fractionated activation electrogram (CFAE) site ablation. METHODS Fifty-five patients with nonparoxysmal atrial fibrillation (AF) (26 (47%) persistent and 29 (53%) long-standing persistent) underwent pulmonary vein isolation followed by high DF site and continuous CFAE site ablation. High DF sites (DF ≥8 Hz) and continuous CFAE sites (fractionated intervals ≤50 ms) were targeted. The patients were divided into an AF-free group and an AF-recurrent group. RESULTS The AF freedom rate on antiarrhythmic drugs in patients with persistent and long-standing persistent AF was 88.5% and 75.9% over a 12-month follow-up period, respectively. The total EAT, left atrial (LA)-EAT, and right atrial (RA)-EAT volumes did not indicate significant differences between the AF-free and AF-recurrent groups. In the LA, the overlap between high DF sites and EAT was larger in the AF-free group than in the AF-recurrent group (57.0% ± 33.3% vs 22.6% ± 23.3%; P < .01). However, this overlap did not differ between the AF-free and AF-recurrent groups in the RA (20.4% ± 28.2% vs 19.0% ± 24.4%; P = .91). The overlap between continuous CFAE sites and EAT did not differ between the 2 groups in both the LA and the RA. CONCLUSION High DF sites that overlap with EAT may be important sources of AF. However, the contribution of EAT to the AF substrate may differ between the LA and the RA.

Early repolarization in Wolff-Parkinson-White syndrome: prevalence and clinical significance.

AIMS Idiopathic ventricular fibrillation (IVF) with early repolarization (ER) has recently been reported; however, ER is a common finding in healthy subjects and is also found sporadically in patients with Wolff-Parkinson-White (WPW) syndrome. The present study was designed to evaluate the prevalence and clinical significance of ER in patients with WPW syndrome. METHODS AND RESULTS One hundred and eleven patients with WPW syndrome were studied retrospectively. Early repolarization was defined as QRS slurring or notching with J-point elevation ≥ 1 mm. The prevalence of ER was determined before and after successful catheter ablation. Before ablation, ER was found in 35 of 75 patients with a left free wall, 6 of 23 with a right free wall, and 7 of 13 with a septal accessory pathway (48 of 111, 43% as a whole). Early repolarization was always observed in leads with positive deflection of the initial part of the delta wave. After successful ablation of accessory pathways, ER was preserved in 28 (25%), disappeared in 20 (18%), and newly developed in 8 (7%) patients. In the remaining 55 (50%) patients, ER was not observed either before or after ablation. In patients with persistent ER, the amplitude and width of ER were significantly decreased 3-7 days after the ablation (1.7 ± 0.7 vs. 1.4 ± 0.6 mm, P < 0.005 and 42 ± 11 vs. 34 ± 9 ms, P < 0.001, respectively). CONCLUSION In patients with WPW syndrome, ER could be partly related to early depolarization through the accessory pathway. However, persistent ER and new ER appearing after the ablation were frequently found. Therefore, in these patients, mechanisms other than early depolarization may be involved in the genesis of ER.

Electrophysiological and anatomical differences of the slow pathway between the fast-slow form and slow-slow form of atrioventricular nodal reentrant tachycardia.

AIMS This study aimed to clarify whether electrophysiological and anatomical properties of the slow pathway (SP) could be different between the fast-slow form (F/S) and the slow-slow form (S/S) atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS Nine patients with F/S and 15 patients with S/S of atypical AVNRT were studied. The patients with S/S were divided into two groups; those with the anterograde SP being eliminated (S/S aSP-E) or preserved (S/S aSP-P) during catheter ablation. HA (CS-His) was determined as the difference of the shortest HA interval between the His bundle region and the coronary sinus (CS) region. The ratio of the amplitudes of atrial and ventricular potential (A/V ratio) of the successful ablation site of the SP was also evaluated. Effective refractory period of the retrograde SP was shorter and HA intervals during both tachycardia and ventricular pacing were longer in F/S than in S/S. HA (CS-His) did not differ between F/S and S/S (-4.3 ± 20.2 vs.-4.4 ± 18.4 ms, NS). The A/V ratio was significantly greater in the S/S aSP-P group compared with the both groups of F/S and S/S aSP-E (0.83 ± 0.29 vs. 0.38 ± 0.09 and 0.26 ± 0.15 ms, P < 0.01). CONCLUSION Properties of the retrograde SP differ between F/S and S/S of AVNRT. Fast-slow form may utilize the same pathway for the retrograde conduction as the anterograde SP in S/S.

Junctional rhythm associated with ventriculoatrial block during slow pathway ablation in atypical atrioventricular nodal re-entrant tachycardia

AIMS We assessed responses to slow pathway ablation with respect to the appearance of ventriculoatrial (VA) block during junctional rhythm in both typical and atypical types of atrioventricular nodal re-entrant tachycardia (AVNRT). METHODS AND RESULTS The 31 subjects included 16 patients with slow-fast type of typical AVNRT and 15 patients with atypical AVNRT (9 patients with fast-slow type and 6 patients with slow-slow type). During atypical AVNRT, the HA interval was prolonged (>70 ms) and the earliest atrial activation was located around the coronary sinus (CS) ostium. The difference in atrial activation times at the CS ostium and His-bundle area [A(CS-His)] during AVNRT was measured. Slow pathway ablation was performed using a classical electro-anatomical approach. In typical AVNRT, A(CS-His) was -21.3 +/- 3.4 ms, and the HA interval was 34 +/- 14 ms. During slow pathway ablation, all patients with typical AVNRT had junctional rhythm with retrograde atrial conduction. In contrast, in patients with atypical AVNRT, A(CS-His) was 12 +/- 19.3 ms and the HA interval was 189 +/- 77 ms. In 13 of the 15 patients with atypical AVNRT, slow pathway ablation induced junctional rhythm, which was not associated with retrograde atrial conduction. After ablation, AVNRT became non-inducible and antegrade atrioventricular (AV) conduction was preserved in all patients. CONCLUSION In patients with atypical AVNRT, junctional rhythm with VA block during slow pathway ablation is commonly observed and indicates the success of the ablation of retrograde slow pathway conduction, but has no relation to the risk of subsequent AV block. During junctional rhythm, occasional appearance of the sinus beats with intact antegrade AV conduction is essential for safety of ablation.

Narrow QRS ventricular tachycardia from the posterior mitral annulus without involvement of the His-Purkinje system in a patient with prior inferior myocardial infarction

A 54-year-old man with prior inferior myocardial infarction suffered from monomorphic ventricular tachycardia (VT) with narrow QRS complex of 120 ms. During VT, a fragmented prepotential preceding QRS onset by 30 ms at the right ventricular posterior septum and a late diastolic potential preceding QRS onset by 70 ms at the infarcted posterior mitral annulus were recorded. Radiofrequency energy delivered to the late diastolic potential at the posterior mitral annulus eliminated VT. During sinus rhythm, the late diastolic potential shifted to the end of QRS complex and no Purkinje potentials were observed. Synchronized excitation of both ventricles from the posterior infarcted mitral annulus in this patient may make the QRS width during VT narrow, without involvement of the His-Purkinje system.

Recurrent syncope in two patients with a sigmoid-shaped interventricular septum and no left ventricular hypertrophy.

Sigmoid‐shaped interventricular septum (SIS) is not uncommon in elderly patients and is considered a normal part of the aging process. However, several patients have been reported to have clinical symptoms due to the narrowing of the left ventricular outflow tract (LVOT). Two patients with SIS presented with recurrent episodes of syncope after drinking or taking sublingual nitroglycerin (NG). In both patients, a head‐up tilt test involving provocation with alcohol, NG, or isoproterenol induced the vasovagal reflex along with an increase in the pressure gradient between the apex and LVOT. The patients experienced no further episodes of syncope after initiating bisoprolol treatment. In patients with SIS, induction of the vasovagal reflex via an increase in left ventricular (LV) pressure due to LVOT obstruction concomitant with increased LV construction is a potentially important cause of syncope, which may be effectively prevented by beta‐blockers.

Time-Dependent Changes in QT Dynamics after Initiation and Termination of Paroxysmal Atrial Fibrillation.

Little is known about time‐dependent changes in QT dynamics after initiation of atrial fibrillation (AF) and after restoration of sinus rhythm (SR) in patients with paroxysmal AF.

Atrioventricular Node Ablation and Pacemaker Implantation for Recurrent Syncope in a Patient With Postural Tachycardia Syndrome (POTS)

Ablate and Pace for POTS. A 42‐year‐old woman with postural tachycardia syndrome (POTS) was admitted to our hospital with severe palpitations, light‐headedness, and syncope. Several drugs had been administered previously, but all had been discontinued due to intolerable adverse effects or limited efficacy. One of the drugs, the If current inhibitor ivabradine, effectively slowed the patients heart rate and relieved the symptoms, but was discontinued due to allergy. After unsuccessful sinus node ablation, atrioventricular node ablation and dual chamber pacemaker implantation was performed, which dramatically improved her symptoms and eliminated syncope. Atrioventricular node ablation could modify the cardiac autonomic balance and thereby suppressed the excessive orthostatic sympathetic activity. (J Cardiovasc Electrophysiol, Vol. pp. 1‐4)