Cardiac vagus nerve denervation by pulmonary vein isolation was effective for swallowing-induced atrial tachycardia.

Swallowing-induced atrial tachycardia (SIAT) is a relatively rare arrhythmia. A 56-year-old woman was admitted to treat atrial tachycardia that occurs by not only eating and drinking but also yawning. Both the right and left upper pulmonary veins were suspected as the earliest activation site of the tachycardia and the abnormal activation of ectopies themselves were suppressed after pulmonary vein isolation (PVI). In a 24-hour Holter electrocardiogram, the HF component of the analysis of heart rate variability was suppressed both at 1 day and at 2 years after ablation. In this case, cardiac vagal nerve denervation by PVI was effective for SIAT.

Impacts of the body size on the left atrial wall thickness and atrial fibrillation recurrence after catheter ablation.

The increased body size correlates with the occurrence of atrial fibrillation (AF); however, the impact of the body size on the AF recurrence after ablation remains unclear. We enrolled 283 AF patients (179 paroxysmal, 51 persistent, and 53 long-standing persistent) who received ablation and assessed the correlation between the body surface area (BSA) and the AF recurrence. Furthermore, we measured the left atrial wall thickness using computed tomography. During the 12-month follow-up period, the AF freedom rates for patients with paroxysmal AF, persistent AF, and long-standing persistent AF were 83%, 76%, and 77%, respectively. The left atrial dimension, BSA, and body mass index (BMI) were higher in the AF-recurrent group compared with the AF-free group (left atrial dimension: 44.1 ± 7.5 mm vs. 41.7 ± 6.5 mm, P = 0.019; BSA: 1.81 ± 0.20 m2 vs. 1.72 ± 0.19 m2, P = 0.002; BMI 25.0 ± 3.2 kg/m2 vs. 24.0 ± 3.2 kg/m2, P = 0.035). The multivariate analysis revealed that only the BSA was an independent predictor of the AF recurrence after ablation (hazard ratio 6.843; 95% confidence interval 1.523-30.759, P = 0.012). The BSA significantly correlated with the left atrial wall thickness (R = 0.306, P < 0.001), and the left atrial wall thickness was higher in the AF-recurrent group compared with the AF-free group (2.00 ± 0.20 mm vs. 1.87 ± 0.17 mm, P < 0.001). The large body size correlates with the AF recurrence after ablation, which could be attributed to an increase in the left atrial wall thickness.

Improvement of Hemodynamic Parameters in Patients With Preserved Left Ventricular Systolic Function by Catheter Ablation of Atrial Fibrillation　- A Prospective Study Using Impedance Cardiography.

BACKGROUND: The effects of catheter ablation for atrial fibrillation (AF) on hemodynamic parameters in patients with preserved left ventricular (LV) systolic function are unclear. Methods and Results: We enrolled 178 patients with AF (paroxysmal, 108; persistent, 70) with preserved LV systolic function who underwent AF ablation. The stroke volume index (SVI) was repeatedly measured using impedance cardiography. Reduced SVI (SVI, <33 mL/m2) was observed in 55% of patients before ablation. In patients with paroxysmal AF, the SVI did not change immediately after ablation (from 35±6 mL/m2to 35±5 mL/m2; P=0.652); however, it increased 1 month after ablation and further increased 6 months after ablation (1 month, 37±6 mL/m2, P<0.001; 6 months, 38±6 mL/m2, P<0.001). In patients with persistent AF, the SVI increased immediately after ablation (from 30±5 mL/m2to 36±6 mL/m2; P<0.001) and further increased until 6 months after ablation (1 month, 37±6 mL, P<0.001; 6 months, 38±5 mL/m2, P<0.001). The baseline SVI was the strongest predictor of the cardiac function improvement with an area under the curve of 0.828. CONCLUSIONS: The restoration and maintenance of sinus rhythm using catheter ablation increased the SVI in patients with preserved LV systolic function.

Vasovagal syncope is associated with poor prognosis in patients with left ventricular dysfunction.

Vasovagal syncope (VVS) is known to have a benign prognosis and be associated with enhanced contraction and activation of the left ventricular (LV) mechanoreceptors. However, a little is known about VVS in patients with LV dysfunction. The present study aimed to investigate the prevalence and prognosis of VVS in patients with LV dysfunction. We enrolled 368 patients with unexplained syncope. In 7 of these patients, LV ejection fraction was lower than 40%. The results of a head-up tilt test (HUT) and the recurrence of syncope were compared between these 7 patients with LV dysfunction and the remaining patients. Positive HUT was obtained in the 6 patients (86%) with LV dysfunction; this rate tended to be higher as compared with normal cardiac function (192/361, 53%, P = 0.069). In patients with LV dysfunction, response in HUT was mostly vasodepressor type (62%); however, most of HUT responses were mixed type in patients with normal LV function (67%). Among patients with positive HUT, the recurrent rate of syncope after HUT was higher in those with LV dysfunction than in those with normal LV function (67 vs. 21%, P = 0.008). VVS in patients with LV dysfunction may be refractory to treatment and could be associated with poor prognosis.

Citrus fruits induced swallow syncope with atrioventricular block or sinus arrest.

Swallow syncope is a relatively rare syndrome and caused by various foods and drinks. A 76-year-old man was admitted with frequent syncope while eating. Holter electrocardiogram revealed frequent occurrence of atrioventricular block during meals. Both atrioventricular block and sinus arrest were induced by only eating citrus fruits, citrus jelly, and acidic foods but not by other drinks and foods. These arrhythmias were suppressed after administration of atropine. No further episodes of syncope recurred after the implantation of a DDD pacemaker. This case indicated that acidic stimulation of citrus induced a vasovagal reflex via esophageal nociceptors leading to syncope.

Latent pathogenicity of the G38S polymorphism of KCNE1 K+ channel modulator.

KCNE1 encodes a modulator of KCNQ1 and KCNH2 channels. Although KCNE1(G38S), a single-nucleotide polymorphism (SNP) causing a G38S substitution in KCNE1, is found frequently, whether and how this SNP causes long QT syndrome (LQTS) remains unclear. We evaluated rate-dependent repolarization dynamics using Holter electrocardiogram (ECG) to assess the pathogenicity of KCNE1(G38S). Forty-five patients exhibiting long QT intervals, as assessed by their baseline ECGs, and 16 control subjects were enrolled. KCNE1(G38S) carriers were identified using genome sequencing. LQTS patients were classified into LQT1 or LQT2 using genetic analysis or epinephrine test. QT-RR relations were determined using 24-h Holter ECG recordings. Among the 15 patients (33.3 %) with KCNE1(G38S), four patients without any mutations or amino acid changes in other major cardiac ion channels were categorized as KCNE1(G38S) carriers. In the QT-RR regression lines, the QT-RR slope was greater in the KCNE1(G38S) carriers and the LQT2 patients (0.215 ± 0.021 and 0.207 ± 0.032, respectively) than in the LQT1 patients (0.163 ± 0.014, P < 0.05) and the control subjects (0.135 ± 0.025, P < 0.001). The calculated QT intervals at an RR interval of 1200 ms were longer in the KCNE1(G38S) carriers and LQT1 and LQT2 patients than in the control subjects. Patients with KCNE1(G38S) had a rate-dependent repolarization abnormality similar to patients with LQT2 and, therefore, may have a potential risk to develop lethal arrhythmias.

Coefficient of Variation of P-Wave Duration Is a Novel Atrial Heterogeneity Index to Predict Recurrence of Atrial Fibrillation After Catheter Ablation.

INTRODUCTION: Atrial conduction heterogeneity is associated with progression of atrial fibrillation (AF). However, the relationship between P-wave parameters representing atrial conduction heterogeneity and AF recurrence after catheter ablation (ABL) is still unclear. METHODS AND RESULTS: Subjects of the study were 126 consecutive patients with AF (78 paroxysmal and 48 persistent) who had received ABL. Coefficient of variation of P-wave duration (CV-PWD) was determined with all 12 surface electrocardiographic leads as an index of atrial conduction heterogeneity. Rates of freedom from AF recurrence were 78% and 77% in patients with paroxysmal and persistent AF, respectively, over a 12-month follow-up. CV-PWD measured before ABL was smaller in AF-free patients compared with AF-recurrent patients (0.089 ± 0.019 vs. 0.129 ± 0.042, P < 0.001). CV-PWD significantly decreased after ABL in AF-free patients, but did not change in AF-recurrent patients. CV-PWD after ABL was also smaller in AF-free patients compared with AF-recurrent patients (0.087 ± 0.025 vs. 0.133 ± 0.035, P < 0.001). In receiver operating curve analysis, CV-PWD before and after ABL achieved area under the curve of 0.829 and 0.854, respectively, for the ability to predict AF recurrence. CV-PWD correlated positively with left atrial (LA) diameter and negatively with LA appendage flow velocity. CONCLUSION: CV-PWD is a useful index to predict AF recurrence after ABL for both patients with paroxysmal and persistent AF. ABL may suppress AF by decreasing atrial conduction heterogeneity.

Differentiation of Slow-Slow Form of AVNRT from AVRT through a Posteroseptal Accessory Pathway by Retrograde P-Wave Amplitude.

BACKGROUND: This study aimed to clarify whether retrograde P-wave amplitude during tachycardia can be used to differentiate slow-slow form of atrioventricular nodal reentrant tachycardia (S/S-AVNRT) from atrioventricular reentrant tachycardia through a posteroseptal accessory pathway (PS-AVRT). METHODS: Sixteen patients with S/S-AVNRT and 14 patients with PS-AVRT constituted the study group. Electrocardiographic and electrophysiological parameters were compared between both the groups. HA(CS-His), which indicates the location of the earliest atrial activation site during tachycardia, was calculated as the difference of the shortest HA interval in the His bundle region and the coronary sinus region. RESULTS: Negative deflection of the retrograde P wave during tachycardia was significantly greater in S/S-AVNRT than in PS-AVRT in the inferior leads (lead aVF, -0.22 ± 0.04 mV vs -0.10 ± 0.07 mV; P < 0.001). Among the electrocardiographic parameters, retrograde P-wave amplitude in lead aVF had the highest diagnostic accuracy (area under the curve 0.975, sensitivity 93%, and specificity 88% for a cutoff value of -0.16 mV). HA(CS-His) was negatively greater in S/S-AVNRT than in PS-AVRT (-24 ± 13 ms vs -3 ± 18 ms; P = 0.001), and was significantly correlated with the retrograde P-wave amplitude in lead aVF (P = 0.004). CONCLUSION: Deeper negative deflection of the retrograde P wave in the inferior lead can help differentiate S/S-AVNRT from PS-AVRT.

Effect of irbesartan on development of atrial fibrosis and atrial fibrillation in a canine atrial tachycardia model with left ventricular dysfunction, association with p53.

Effects of an angiotensin II receptor blocker, irbesartan (IRB), on the development of atrial fibrosis and atrial fibrillation (AF) were assessed in a canine model of atrial tachycardia remodeling (ATR) with left ventricular dysfunction, together with its possible association with involvement of p53. Atrial tachypacing (400 bpm for 4 weeks) was used to induce ATR in beagles treated with placebo (ATR-dogs, n = 6) or irbesartan (IRB-dogs, n = 5). Non-paced sham dogs served as control (Control-dogs, n = 4). ATR- and IRB-dogs developed tachycardia-induced left ventricular dysfunction. Atrial effective refractory period (AERP) shortened (83 ± 5 ms, p < 0.05), inter-atrial conduction time prolonged (72 ± 2 ms, p < 0.05), and AF duration increased (29 ± 5 s, p < 0.05 vs. baseline) after 4 weeks in ATR-dogs. ATR-dogs also had a larger area of atrial fibrous tissue (5.2 ± 0.5 %, p < 0.05 vs. Control). All these changes, except for AERP, were attenuated in IRB-dogs (92 ± 3 ms, 56 ± 3 ms, 9 ± 5 s, and 2.5 ± 0.7 %, respectively; p < 0.05 vs. ATR for each). In ATR-dogs, p53 expression in the left atrium decreased by 42 % compared with Control-dogs (p < 0.05); however, it was highly expressed in IRB-dogs (+89 % vs. ATR). Transforming growth factor (TGF)-ß1 expression was enhanced in ATR-dogs (p < 0.05 vs. Control) but reduced in IRB-dogs (p < 0.05 vs. ATR). Irbesartan suppresses atrial fibrosis and AF development in a canine ATR model with left ventricular dysfunction in association with p53.

Abnormal repolarization dynamics in a patient with KCNE1(G38S) who presented with torsades de pointes.

Risk of G38S, major KCNE1 polymorphism [KCNE1(G38S)], for long QT syndrome (LQTS) remains unclear. A 72-year-old woman was admitted with recurrent torsades de pointes (TdP). She had remarkable QT prolongation (corrected QT interval 568 ms) under conditions of hypokalemia and hypomagnesemia. After correction of this electrolytic imbalance, TdP was suppressed and metoprolol was started. The QT-RR slope in 24-hour Holter electrocardiogram was steep and this enhanced bradycardia-dependent QT prolongation was similar to that in LQTS. She carried KCNE1(G38S). Patients with KCNE1(G38S) could have similar potential risk of ventricular arrhythmia as with LQTS. Analysis of QT-RR relationship could also evaluate the latent arrhythmogenicity of KCNE1(G38S).

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

BACKGROUND: 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. METHODS: Beat-to-beat QT and RR intervals in CM5 lead were measured automatically in 13 patients with both AF and SR on the single 24-hour Holter electrocardiology recording. QT-RR relation was analyzed at six periods of time: 1 hour before AF onset (Pre(0-1h)), 0-1 hour and 4-5 hours after AF onset (AF(0-1h) and AF(4-5h)), and 0-1 hour, 2-3 hours, and 4-5 hours after the restoration of SR (SR(0-1h), SR(2-3h), and SR(4-5h)). RESULTS: QT-RR slope was gradually decreased after AF onset and gradually returned to the baseline level after restoration of SR. The slope became greater at SR(4-5h) than at AF(4-5h) and AF(0-1h). In patients receiving antiarrhythmic drugs (AADs; n = 5), QT-RR slope was greater at SR(4-5h) than in those not receiving AADs (n = 8). CONCLUSION: In patients with paroxysmal AF, bradycardia-dependent QT prolongation was attenuated during AF, and was corrected and gradually augmented along with continuation of SR, especially in patients receiving AADs. This could increase the risk of developing torsade de pointes.

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.

Glycine/Serine polymorphism at position 38 influences KCNE1 subunit's modulatory actions on rapid and slow delayed rectifier K+ currents.

BACKGROUND: KCNE1 encodes a modulator of KCNH2 and KCNQ1 delayed rectifier K(+) current channels. KCNE1 mutations might cause long QT syndrome (LQTS) by impairing KCNE1 subunit's modulatory actions on these channels. There are major and minor polymorphismic KCNE1 variants whose 38(th) amino acids are glycine and serine [KCNE1(38G) and KCNE1(38S) subunits], respectively. Despite its frequent occurrence, the influence of this polymorphism on the K(+) channels' function is unclear. METHODS AND RESULTS: Patch-clamp recordings were obtained from human embryonic kidney -293T cells. KCNH2 channel current density in KCNE1(38S)-transfected cells was smaller than that in KCNE1(38G)-transfected cells by 34%. The voltage-sensitivity of the KCNQ1 channel current in KCNE1(38S)-transfected cells was lowered compared to that in KCNE1(38G)-transfected cells, with a +13mV shift in the half-maximal activation voltage. KCNH2 channel current density or KCNQ1 channel voltage-sensitivity was not different between KCNE1(38G)-transfected cells and cells transfected with both KCNE1(38G) and KCNE1(38S). Moreover, the KCNH2 channel current in KCNE1(38S)-transfected cells was more susceptible to E4031, a QT prolonging drug and a condition with hypokalemia, than that in KCNE1(38G)-transfected cells. CONCLUSIONS: Homozygous inheritance of KCNE1(38S) might cause a mild reduction of the delayed rectifier K(+) currents and might thereby increase an arrhythmogenic potential particularly in the presence of QT prolonging factors. By contrast, heterozygous inheritance of KCNE1(38G) and KCNE1(38S) might not affect the K(+) currents significantly. (Circ J 2014; 78: 610-618).

Characterization of a novel mutant KCNQ1 channel subunit lacking a large part of the C-terminal domain.

A mutation of KCNQ1 gene encoding the alpha subunit of the channel mediating the slow delayed rectifier K(+) current in cardiomyocytes may cause severe arrhythmic disorders. We identified KCNQ1(Y461X), a novel mutant gene encoding KCNQ1 subunit whose C-terminal domain is truncated at tyrosine 461 from a man with a mild QT interval prolongation. We made whole-cell voltage-clamp recordings from HEK-293T cells transfected with either of wild-type KCNQ1 [KCNQ1(WT)], KCNQ1(Y461X), or their mixture plus KCNE1 auxiliary subunit gene. The KCNQ1(Y461X)-transfected cells showed no delayed rectifying current. The cells transfected with both KCNQ1(WT) and KCNQ1(Y461X) showed the delayed rectifying current that is thought to be mediated largely by homomeric channel consisting of KCNQ1(WT) subunit because its voltage-dependence of activation, activation rate, and deactivation rate were similar to the current in the KCNQ1(WT)-transfected cells. The immunoblots of HEK-293T cell-derived lysates showed that KCNQ1(Y461X) subunit cannot form channel tetramers by itself or with KCNQ1(WT) subunit. Moreover, immunocytochemical analysis in HEK-293T cells showed that the surface expression level of KCNQ1(Y461X) subunit was very low with or without KCNQ1(WT) subunit. These findings suggest that the massive loss of the C-terminal domain of KCNQ1 subunit impairs the assembly, trafficking, and function of the mutant subunit-containing channels, whereas the mutant subunit does not interfere with the functional expression of the homomeric wild-type channel. Therefore, the homozygous but not heterozygous inheritance of KCNQ1(Y461X) might cause major arrhythmic disorders. This study provides a new insight into the structure-function relation of KCNQ1 channel and treatments of cardiac channelopathies.

Xanthine oxidase inhibition prevents atrial fibrillation in a canine model of atrial pacing-induced left ventricular dysfunction.

AIMS: Oxidative stress could be a possible mechanism and a therapeutic target of atrial fibrillation (AF). Xanthine oxidase (XO) inhibition reduces oxidative stress, but the effects of XO inhibitor on AF have not been evaluated. Hence, we assessed the effects of XO inhibitor, allopurinol, on progression of atrial vulnerability in dogs associated with tachycardia-induced cardiomyopathy. METHODS AND RESULTS: The dogs were subjected to atrial tachypacing (ATP, 400 bpm) without atrioventricular block for 4 weeks. The dynamics of atrial-tachycardia remodeling were evaluated in allopurinol-treated dogs (ALO, n = 5), placebo-treated controls (CTL, n = 6), and sham-operated dogs (n = 6). In CTL dogs, 4 weeks of ATP significantly increased AF duration (DAF; from 0.2 ± 0.2 seconds to 173 ± 67 seconds, P < 0.05) and decreased atrial effective refractory period (ERP; from 152 ± 9 milliseconds to 80 ± 4 milliseconds at a cycle length of 350 milliseconds, P < 0.01). Allopurinol attenuated the ATP effects on ERP (118 ± 6 milliseconds, P < 0.01) or DAF (0.6 ± 0.3 seconds, P < 0.05). In CTL dogs, ATP-induced rapid ventricular responses decreased left ventricular ejection fraction (LVEF; from 58.6 ± 0.1 to 23.5 ± 2.4%, P < 0.01), and increased left atrial diameter (LAD; from 17 ± 1 mm to 24 ± 1 mm, P < 0.01). ATP increased atrial fibrosis when compared with sham-operated dogs (CTL 10.7 ± 0.8% vs Sham 1.1 ± 0.3%, P < 0.01). Allopurinol suppressed atrial fibrosis (2.3 ± 0.6%, P < 0.01 vs CTL) and eNOS reduction without affecting LVEF (20.6 ± 2.2%, ns) and LAD (23 ± 1 mm, ns). CONCLUSION: Allopurinol suppresses AF promotion by preventing both electrical and structural remodeling. These results suggest that XO may play an important role in enhancement of atrial vulnerability, and might be a novel target of AF therapy.

Anticoagulation control quality affects the D-dimer levels of atrial fibrillation patients.

BACKGROUND: Anticoagulation control quality affects the incidence of thromboembolic events in atrial fibrillation (AF) patients. However, the effects of anticoagulation control quality on the prothrombotic state of AF patients are unclear. METHODS AND RESULTS: Ninety-five AF patients who had been treated with warfarin were prospectively followed-up for 449 ± 92 days. We analyzed whether time in the therapeutic range (TTR) of the international normalized ratio (INR) of prothrombin time, percentage of INR values in the range (%INR), and coefficient of variation of INR values (CV-INR) were related to D-dimer levels. The mean values of TTR, %INR, and CV-INR were 62%, 59%, and 0.19, respectively, and their median values were 67%, 63%, and 0.19, respectively. TTR was significantly correlated with %INR (R(2) = 0.917, P<0.01), but not with CV-INR (R(2) = 0.050, P = 0.26). The mean and median D-dimer levels were 0.79 and 0.60 µg/ml, respectively. Low TTR, low %INR, and high CV-INR were found to contribute to high D-dimer levels (P = 0.02, 0.03, and 0.02, respectively). CONCLUSIONS: In AF patients treated with warfarin, not only the duration outside the target INR range, but also the fluctuation in INR level may influence the prothrombotic state.

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 I(f) current inhibitor ivabradine, effectively slowed the patient's 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.

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.

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.