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.

Risk stratification for cardiac mortality using electrocardiographic markers based on 24-hour Holter recordings: the JANIES-SHD study.

BACKGROUND: Recent guidelines have stated that left ventricular ejection fraction (LVEF) is the gold standard marker for identifying patients at risk for cardiac mortality. However, little information is present regarding electrocardiographic (ECG) markers. This study aimed to assess ECG markers for predicting mortality or serious arrhythmia in patients with structural heart disease (SHD). METHODS: In total, 1829 patients were enrolled into the Japanese Multicenter Observational Prospective Study (JANIES study). In this study, we analyzed data of 719 patients (569 men, age 64 ± 13 years) with SHD including mainly ischemic heart disease (65.8%). As ECG markers based on 24-hour Holter recordings, nonsustained ventricular tachycardia (NSVT), ventricular late potentials, and heart rate turbulence (HRT) were assessed. The primary endpoint was all-cause mortality, and the secondary endpoint was fatal arrhythmic events. RESULTS: During a mean follow-up of 21 ± 11 months, all-cause mortality was eventually observed in 39 patients (5.4%). Among those patients, 32 patients (82%) suffered from cardiac causes such as heart failure and arrhythmia. Multivariate Cox regression analysis showed that after adjustment for age and LVEF, documented NSVT [hazard ratio = 2.46, 95% confidence interval (CI): 1.16-5.18, p = 0.02] and abnormal HRT (hazard ratio = 2.40, 95% CI: 1.16-4.93, p = 0.02) were significantly associated with the primary endpoint. These two ECG markers also had significant predictive values with the secondary endpoint. The combined assessment of two ECG markers improved predictive accuracy. CONCLUSION: This study demonstrated that combined assessment of documented NSVT and abnormal HRT based on 24-hour Holter ECG recordings are recommended for predicting future serious events in this population.

Correlation between the left atrial low-voltage area and the cardiac function improvement after catheter ablation for paroxysmal atrial fibrillation.

BACKGROUND: The impact of the left atrial low-voltage area (LVA) on the cardiac function improvement following ablation for atrial fibrillation (AF) is unclear. METHODS: In 49 patients with paroxysmal AF who underwent ablation, the left ventricular stroke volume index (SVI) was repeatedly measured using an impedance cardiography until 6 months after ablation. We defined the cardiac function improvement as a 20% increase in the SVI. The LVA (the area with the voltage amplitude of <0.5 mV) was assessed before ablation. RESULTS: The reduced baseline SVI (<33 mL/m2) was observed in 18 (37%) patients. The SVI increased following ablation (from 36 ± 5 to 39 ± 6 mL/m2, P < .001). We observed the cardiac function improvement in 14 (29%) patients. The LVA was smaller in patients with the improved cardiac function than in those without (8.3% ± 5.2% vs 14.0% ± 8.5%, P = .026). The multivariate analysis revealed that only the LVA was independently associated with the cardiac function improvement (odds ratio, 0.878; 95% confidence interval: 0.778-0.991, P = .036). Furthermore, LVAs of the anterior (7.9% ± 7.6% vs 18.2% ± 15.5%, P = .022), septal (12.0 ± 7.3% vs 20.7% ± 13.8%, P = .031), and roof walls (6.9% ± 6.0% vs 16.9% ± 15.2%, P = .022) were smaller in patients with the improved cardiac function than in those without. CONCLUSIONS: The LVA was related to the cardiac function improvement following ablation in patients with paroxysmal AF.

Left atrial posterior wall isolation affects complex fractionated atrial electrograms in persistent atrial fibrillation.

BACKGROUND: The impact of left atrial posterior wall isolation (LAPWI) on the complex fractionated atrial electrogram (CFAE) is unknown. METHODS: CFAE mapping was performed before and after LAPWI in 46 patients with persistent atrial fibrillation (AF). RESULTS: LAPWI decreased both the variable (fractionated index ≤ 120 ms; from 60 ± 4 cm2 to 50 ± 4 cm2, P < 0.001) and continuous (fractionated index ≤ 50 ms; from 4.2 ± 1.0 cm2 to 3.5 ± 0.9 cm2, P = 0.036) CFAE areas. Especially, the CFAE areas on the bottom and roof walls of the left atrium and on the posterior and bottom walls of the right atrium significantly decreased after LAPWI. The distribution of variable CFAE areas was not different between the AF-recurrence (n = 9) and AF-free (n = 37) groups before LAPWI; however, it was larger in the anterior and septal walls of the right atrium in the AF-recurrence group than in the AF-free group after LAPWI (anterior wall, 8% ± 2% vs 5% ± 1%, P = 0.048; septal wall, 23% ± 4% vs 16% ± 1%, P = 0.043). The distribution of continuous CFAE areas on the bottom wall of the right atrium was larger in the AF-recurrence group than in the AF-free group both before LAPWI (30% ± 20% vs 4% ± 2%, P = 0.008) and after LAPWI (25% ± 25% vs 3% ± 1%, P = 0.027). CONCLUSIONS: LAPWI decreased the CFAE areas and affected their distribution, which contributed to AF recurrence.

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.

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.

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.

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.

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.

Paced QRS fragmentation is associated with spontaneous ventricular fibrillation in patients with Brugada syndrome.

BACKGROUND: Conduction abnormalities are involved in the pathogenesis of ventricular fibrillation (VF) in patients with Brugada syndrome (BrS). OBJECTIVE: We investigated whether right ventricular apical pacing (RVAP) could enhance the conduction abnormality and predict the susceptibility to VF in patients with BrS. METHODS: Twenty patients with BrS (n = 15) or early repolarization syndrome (ERS) (n = 5) having an implantable cardioverter-defibrillator and 11 patients with complete atrioventricular block having a pacemaker were studied. RESULTS: In BrS, 7 patients had a history of spontaneous VF [VF(+) group] and the remaining 8 did not [VF(-) group]. The number of spikes in fragmented QRS was counted during sinus rhythm and RVAP at rates of 80 and 110 beats/min, respectively. Patients with complete atrioventricular block had no spikes during RVAP. During sinus rhythm, no significant difference was observed in QRS spike numbers among VF(+), VF(-), and ERS groups. During RVAP at 110 beats/min, the sum of spike numbers in leads V1 and V2 increased and the duration of QRS fragmentation increased in the VF(+) group as compared with VF(-) and ERS groups [VF(+): 10.7 ± 3.7, 2.4 ± 3.2, and 2.4 ± 1.8 ms; P < .001; VF(-): 173 ± 32, 45 ± 44, and 49 ± 45 ms; P < .001]. According to the receiver operating characteristic analysis, the cutoff value of the sum of spike numbers in leads V1 and V2 to best discriminate between VF(+) and VF(-) groups was 4 in patients with BrS. CONCLUSION: RVAP manifested QRS fragmented spikes, which could be associated with spontaneous VF in patients with BrS.

Postmortem genetic analysis of sudden unexplained death syndrome under 50 years of age: A next-generation sequencing study.

BACKGROUND: Recent studies on the genetic analysis of victims of sudden unexplained death syndrome (SUDS) have shown diagnostic potential. Previously, such analyses mainly targeted the major channelopathy-associated genes. OBJECTIVE: The purpose of this study was to evaluate the utility of next-generation sequencing (NGS) in the postmortem diagnosis of SUDS. METHODS: Our data are derived from 25 cases of SUDS (21 men and 4 women; age 19-50 years). A total of 70 genes were examined by NGS, and the pathogenicity of any detected rare variants with minor allele frequencies of <0.5% was evaluated using a widely used database and eight in silico algorithms. RESULTS: Five known and 15 potentially pathogenic variants with a high in silico score were identified in 14 cases. In all, 6 channelopathy-related variants were identified in 5 cases, including 2 cases with history of arrhythmia; 11 cases had cardiomyopathy- or cardiac transcription factor-related variants. Three cases with desmosomal gene- or other cardiomyopathy-related variants showed possibly related pathologic changes. Three cases with RYR2 or TBX5 variants showed possible pathogenic fibrosis of the cardiac conduction system. Only 12 variants showed moderate or strong possible pathogenicity in SUDS cases compared with qualifying controls. CONCLUSION: Hereditary heart diseases other than channelopathy may also be a significant cause of SUDS, even if clinical and pathologic findings do not show advanced disease. A combination of gene analysis using NGS and some predictive methods for detecting variants and careful pathologic evaluation may provide a reliable diagnosis of hereditary heart disease for potential SUDS cases.

SCN5A(K817E), a novel Brugada syndrome-associated mutation that alters the activation gating of NaV1.5 channel.

BACKGROUND: Brugada syndrome (BrS) is an inherited lethal arrhythmic disorder characterized by syncope and sudden cardiac death from ventricular tachyarrhythmias. Here we identified a novel K817E mutation of SCN5A gene in a man with type 1 BrS electrocardiogram pattern using next-generation sequencing targeted for 73 cardiac disorder-related genes. SCN5A encodes the α-subunit of NaV1.5 voltage-gated Na(+) channel, and some of its mutations are linked to BrS. The proband had no mutation in any of the other arrhythmia-related genes sequenced. OBJECTIVE: We investigated whether the K817E mutation causes a functional change of NaV1.5 channel responsible for the BrS phenotype. METHODS: We compared the electrophysiological properties of the whole-cell currents mediated by wild-type and mutant channels heterologously expressed in human embryonic kidney 293 cells by using a voltage-clamp technique. RESULTS: The K817E mutation reduced the Na(+) current density by 39.0%-91.4% at membrane potentials from -55 to -5 mV. This reduction resulted from a ~24-mV positive shift in the voltage dependence of activation. The mutation also decelerated recovery from both fast and intermediate inactivation, whereas it had little effect on the cell surface expression, single-channel conductance, voltage-dependence of fast inactivation, entry into intermediate inactivation, use-dependent loss of channel availability, or closed-state inactivation. CONCLUSION: The K817E mutation of SCN5A gene leads to loss of function of NaV1.5 channel and may underlie the BrS phenotype of the proband.

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.

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).

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.

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.

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.