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Case report on atrial tachycardia after persistent AF ablation illustrating the importance of considering the previous lesion set in the interpretation of diagnostic entrainment maneuvers.

Case report on a pitfall in the assessment of mitral isthmus block related to partial left atrium/coronary sinus disconnection.

Background— This study aimed to determine 5-year efficacy of catheter ablation for persistent atrial fibrillation (AF) using AF termination as a procedural end point. Methods and Results— One hundred fifty patients (57±10 years) underwent persistent AF ablation using a stepwise ablation approach (pulmonary vein isolation, electrogram-guided, and linear ablation) with the desired procedural end point being AF termination. Repeat ablation was performed for recurrent AF or atrial tachycardia. AF was terminated by ablation in 120 patients (80%). Arrhythmia-free survival rates after a single procedure were 35.3%±3.9%, 28.0%±3.7%, and 16.8%±3.2% at 1, 2, and 5 years, respectively. Arrhythmia-free survival rates after the last procedure (mean 2.1±1.0 procedures) were 89.7%±2.5%, 79.8%±3.4%, and 62.9%±4.5%, at 1, 2, and 5 years, respectively. During a median follow-up of 58 (interquartile range, 43–73) months after the last ablation procedure, 97 of 150 (64.7%) patients remained in sinus rhythm without antiarrhythmic drugs. Another 14 (9.3%) patients maintained sinus rhythm after reinitiation of antiarrhythmic drugs, and an additional 15 (10.0%) patients regressed to paroxysmal recurrences only. Failure to terminate AF during the index procedure (hazard ratio 3.831; 95% confidence interval, 2.070–7.143; P P =0.03), continuous AF duration ≥18 months (hazard ratio 1.984; 95% confidence interval, 1.024–3.846; P P =0.04) predicted arrhythmia recurrence. Conclusions— In patients with persistent AF, an ablation strategy aiming at AF termination is associated with freedom from arrhythmia recurrence in the majority of patients over a 5-year follow-up period. Procedural AF nontermination and specific baseline factors predict long-term outcome after ablation.

Das Screening nach Vorhofflimmern erfolgt vorwiegend mittels Langzeit-EKG. Dabei ist die Sensitivitat der Screeningmethode proportional zur Dauer und Anzahl der EKG-Aufzeichnungen.

Background Atrial fibrillation (AF) is common and may have severe consequences. Continuous long-term electrocardiogram (ECG) is widely used for AF screening. Recently, commercial ECG analysis software was launched, which automatically detects AF in long-term ECGs. It has been claimed that such tools offer reliable AF screening and save time for ECG analysis. However, this has not been investigated in a real-life patient cohort. Objective To investigate the performance of automatic software-based screening for AF in long-term ECGs. Methods Two independent physicians manually screened 22,601 hours of continuous long-term ECGs from 150 patients for AF. Presence, number, and duration of AF episodes were registered. Subsequently, the recordings were screened for AF by an established ECG analysis software (Pathfinder SL), and its performance was validated against the thorough manual analysis (gold standard). Results Sensitivity and specificity for AF detection was 98.5% (95% confidence interval 91.72%–99.96%) and 80.21% (95% confidence interval 70.83%–87.64%), respectively. Software-based AF detection was inferior to manual analysis by physicians (P < .0001). Median AF duration was underestimated (19.4 hours vs 22.1 hours; P < .001) and median number of AF episodes was overestimated (32 episodes vs 2 episodes; P < .001) by the software. In comparison to extensive quantitative manual ECG analysis, software-based analysis saved time (2 minutes vs 19 minutes; P < .001). Conclusion Owing to its high sensitivity and ability to save time, software-based ECG analysis may be used as a screening tool for AF. An additional manual confirmatory analysis may be required to reduce the number of false-positive findings.

Eine 50-jahrige Patientin stellt sich wegen seit letzter Nacht persistierenden Palpitationen, retrosternalem Druckgefuhl und Schweissausbruch auf der Notfallstation vor.

International audience; MDCT/MRI Fusion for the Guidance of VT Ablation. Background: Delayed enhancement (DE) MRI can assess the fibrotic substrate of scar-related VT. MDCT has the advantage of inframillimetric spatial resolution and better 3D reconstructions. We sought to evaluate the feasibility and usefulness of integrating merged MDCT/MRI data in 3D-mapping systems for structure–function assessment and multimodal guidance of VT mapping and ablation.Methods: Nine patients, including 3 ischemic cardiomyopathy (ICM), 3 nonischemic cardiomyopathy (NICM), 2 myocarditis, and 1 redo procedure for idiopathic VT, underwent MRI and MDCT before VT ablation. Merged MRI/MDCT data were integrated in 3D-mapping systems and registered to high-density endocardial and epicardial maps. Low-voltage areas (

The risk of sudden death is increased in athletes with a male predominance. Regular physical activity increases vagal tone, and may protect against exercise-induced ventricular arrhythmias. We investigated training-related modulations of the autonomic nervous system in female and male endurance athletes. Runners of a 10-mile race were invited. Of 873 applicants, 68 female and 70 male athletes were randomly selected and stratified according to their average weekly training hours in a low (≤4 h) and high (>4 h) volume training group. Analysis of heart rate variability was performed over 24 h. Spectral components (high frequency [HF] and low frequency [LF] power in normalized units) were analyzed for hourly 5 min segments and averaged for day- and nighttime. One hundred and fourteen athletes (50 % female, mean age 42 ± 7 years) were included. No significant gender difference was observed for training volume and 10-mile race time. Over the 24-h period, female athletes exhibited a higher HF and lower LF power for each hourly time-point. Female gender and endurance training hours were independent predictors of a higher HF and lower LF power. In female athletes, higher training hours were associated with a higher HF and lower LF power during nighttime. In male athletes, the same was true during daytime. In conclusion, female and male athletes showed a different circadian pattern of the training-related increase in markers of vagal tone. For a comparable amount of training volume, female athletes maintained their higher markers of vagal tone, possibly indicating a superior protection against exercise-induced ventricular arrhythmias.

Introduction: We hypothesized that organization indices based on the analysis of atrial ECG harmonic components may help identify patients (pts) with persistent AF (pAF) unresponsive to pulmonary vein isolation (PVI) and left atrial (LA) ablation. Using adaptive harmonic frequency tracking schemes, we computed on the atrial ECG: 1) the variance of the phase difference (aPD) between the dominant frequency (DF) and the 1st harmonic (H1), and 2) the organization index (AOI) defined as the ratio of the power of the DF and H1 over the total power of the unprocessed atrial signal as measures of AF regularity. Methods: In 34 consecutive pts (61±7 y, pAF duration: 19±11 m), PVI and LA ablation were performed until AF termination. 40-sec ECG time series devoid of QRST were recorded at baseline (BL), after PVI (end_PVI) and at the end of LA ablation (end_ABL). APD and AOI were estimated on leads V1 and V6b (placed on the pts back). Results: pAF was terminated within the LA in 68% (23/34 LT - left terminated) of the pts, while 32% (11/34 NLT - not left terminated) did not. The figure shows that: 1) LT pts displayed higher AOI values at BL indicative of greater atrial ECG organization that increased significantly (p

A new era of atrial fibrillation (AF) treatment began in 1997–1998 with the discovery that triggers within the pulmonary veins initiate AF and reports that elimination of these triggers is successful in treating AF in its paroxysmal form.1–3 However, in patients with persistent AF, the success rate of exclusive pulmonary vein isolation is substantially lower.4,5 To improve the outcome of persistent AF ablation, different ablation strategies have been explored, but to date the optimal strategy has not been defined. Although some groups argue that limited ablation, including pulmonary vein isolation and, if present, ablation of nonpulmonary vein triggers, is sufficient for persistent AF ablation, other groups, including ours, favor more extensive, substrate-based ablation in addition to pulmonary vein isolation. In this review, we will discuss the rationale for a substrate-based ablation strategy to treat persistent AF and show why elimination of triggers is not sufficient in most patients with persistent AF. Response by Roten et al on p 1232 In a simple model, an electric impulse in AF can form because of abnormalities in impulse generation (triggers) or can result from abnormal impulse propagation (reentry). By a strict definition, a trigger is a focal source of new impulse generation. The mechanism by which a new impulse can form is either abnormal automaticity or triggered activity. Trigger-ablation protocols target these sources of new impulse generation. Abnormal impulse propagation, on the other hand, depends on altered substrate properties causing nonuniform or slowed conduction. This in turn causes multiple forms of wave reentry thought to be responsible for AF perpetuation: random reentry (multiple wavelets), macro- and microreentry, or functional reentry (rotors). Substrate-based ablation strategies aim to abate abnormal impulse propagation and interrupt any form of atrial reentry. Triggers of paroxysmal AF are mainly located in the pulmonary …

With the widespread use of implantable cardioverter-defibrillators, an increasing number of patients present with ventricular tachycardia (VT). Large multicentre studies have shown that ablation of VT successfully reduces recurrent VT and this procedure is being performed by an increasing number of centres. However, for a number of reasons, many patients experience VT recurrence after ablation. One important reason for VT recurrence is the presence of an epicardial substrate involved in the VT circuit which is not affected by endocardial ablation. Epicardial access and ablation is now frequently performed either after failed endocardial VT ablation or as first-line treatment in selected patients. This review will focus on the available evidence for identifying VT of epicardial origin, and discuss in which patients an epicardial approach would be benefitial.

Background Diagnosing supraventricular arrhythmias by conventional long-term ECG can be cumbersome because of poor p-waves. Esophageal long-term electrocardiography (eECG) has an excellent sensitivity for atrial signals and may overcome this limitation. However, the optimal lead insertion depth (OLID) is not known. Methods We registered eECGs at different lead insertion depths in 27 patients and analyzed 199,716 atrial complexes with respect to signal amplitude and slope. Correlation and regression analyses were used to find a criterion for OLID. Results Atrial signal amplitudes and slopes significantly depend on lead insertion depth. OLID correlates with body height (r Spearman =0.71) and can be estimated by OLID [cm]=0.25*body height[cm]−7cm. At this insertion depth, we recorded the largest esophageal atrial signal amplitudes (1.27±0.86mV), which were much larger compared to conventional surface lead II (0.19±0.10mV, p Conclusion The OLID depends on body height and can be calculated by a simple regression formula.

Background— Catheter ablation of ventricular tachycardia (VT) is effective and particularly useful in patients with frequent defibrillator interventions. Various substrate modification techniques have been described for unmappable or hemodynamically intolerable VT. Noninducibility is the most frequently used end point but is associated with significant limitations, so the optimal end point remains unclear. We hypothesized that elimination of local abnormal ventricular activities (LAVAs) during sinus rhythm or ventricular pacing would be a useful and effective end point for substrate-based VT ablation. As an adjunct to this strategy, we used a new high-density mapping catheter and frequently used epicardial mapping. Methods and Results— Seventy patients (age, 67±11 years; 7 female) with VT and structurally abnormal ventricle(s) were prospectively enrolled. Conventional mapping was performed in sinus rhythm in all, and a high-density Pentaray mapping catheter was used in the endocardium (n=35) and epicardially. LAVAs were recorded in 67 patients (95.7%; 95% confidence interval, 89.2–98.9). Catheter ablation was performed targeting LAVA with an irrigated-tip catheter placed endocardially via a transseptal or retrograde aortic approach or epicardially via the subxiphoid approach. LAVAs were successfully abolished or dissociated in 47 of 67 patients (70.1%; 95% confidence interval, 58.7–80.1). In multivariate analysis, LAVA elimination was independently associated with a reduction in recurrent VT or death (hazard ratio, 0.49; 95% confidence interval, 0.26–0.95; P =0.035) during long-term follow-up (median, 22 months). Conclusions— LAVAs can be identified in most patients with scar-related VT. Elimination of LAVAs is feasible and safe and is associated with superior survival free from recurrent VT.

Partial Coronary Sinus Disconnection During Atrial Tachycardia. Introduction: Persistent atrial fibrillation (AF) ablation may lead to partial disconnection of the coronary sinus (CS). As a result disparate activation sequences of the local CS versus contiguous left atrium (LA) may be observed during atrial tachycardia (AT). We aimed to evaluate the prevalence of this phenomenon and its impact on activation mapping. Methods: AT occurring after persistent AF ablation were investigated in 74 consecutive patients. Partial CS disconnection during AT was suspected when double potentials with disparate activation sequences were observed on the CS catheter. Endocardial mapping facing CS bipoles was performed to differentiate LA far field from local CS potentials. Results: A total of 149 ATs were observed. Disparate LA CS activations were apparent in 20 ATs after magnifying the recording scale (13). The most common pattern (90) was distal to proximal endocardial LA activation against proximal to distal CS activation the latter involving the whole CS or its distal part. Perimitral macroreentry was more common when disparate LA CS activations were observed (67 vs 29; P = 0.002). Partial CS disconnection also resulted in "pseudo" mitral isthmus (MI) block during LA appendage pacing in 20 of patients as local CS activation was proximal to distal despite distal to proximal activation of the contiguous LA. Conclusion: Careful analysis of CS recordings during AT following persistent AF ablation often reveals disparate patterns of activation. Recognizing when endocardial LA activation occurs in the opposite direction to the more obvious local CS signals is critical to avoid misleading interpretations during mapping of AT and evaluation of MI block. (J Cardiovasc Electrophysiol Vol. pp. 1 11).

Prolonged ECG monitoring is standard for atrial fibrillation (AF) screening. This study investigated whether 7-day event triggered (tECG) ECG recording is equivalent to 7-day continuous Holter (cECG) ECG recording for AF screening.Both a cECG (Lifecard CF) and a tECG (R.Test Evolution 3) were simultaneously worn for 7 days by patients with known or suspected paroxysmal AF.In 100 corresponding recordings, median effective duration of monitoring was 165 h (range 10-170 h) for cECG and 137 h (0-169 h) for tECG (p0.001). Median number and total duration of arrhythmias (AF, atrial flutter or atrial tachycardia) of ≥30 s duration recorded by cECG were 10 (1-428) and 1030 min (≤1-10,020), respectively. An arrhythmia was recorded in 42 cECGs (42%) versus 37 tECGs (37%, p=0.56). Triggered ECG failed to record an arrhythmia in cECG positive cases because of interrupted monitoring in four cases and because of recording failure in one case. Sensitivity, specificity, and positive and negative predictive values of tECG therefore were 88%, 100%, 100%, and 92%, respectively. Quantitative cECG analysis required a median of 20 min (3-205 min) and qualitative tECG analysis 4 min (1-20 min; p0.001). Skin irritation was a frequent side effect (42%) resulting in premature removal of devices in 16% of patients.Sensitivity of tECG for AF screening as compared to cECG is lower, mainly because of shorter effective monitoring duration. Qualitative tECG analysis is less time consuming than quantitative cECG analysis. Skin irritation is a frequent side effect and reason for premature device removal.

Background Recently, several cases of symptomatic and/or electrically detectable intracardiac inside-out abrasions in silicon-coated Riata® and Riata® ST leads have been described. However, the prevalence in asymptomatic patients with unremarkable implantable cardioverter defibrillator (ICD) interrogation is unknown. The aim of this study was to determine the prevalence of asymptomatic and electrically undetectable intracardiac inside-out abrasion in silicon-coated Riata® and Riata® ST leads. Methods All 52 patients with an active silicone-coated Riata® and Riata® ST lead followed up in our outpatient clinic were scheduled for a premature ICD interrogation and a biplane chest radiograph. When an intracardiac inside-out abrasion was suspected, this finding was confirmed by fluoroscopy. Results Mean time since implantation was 71±18months. An intracardiac inside-out abrasion was confirmed by fluoroscopy in 6 patients (11.5%). Mean time from lead implantation to detection of intracardiac inside-out abrasion was 79±14months. In all patients with an intracardiac inside-out abrasion, ICD interrogation showed normal and stable electrical parameters. Retrospectively, in 4 of these 6 patients, a coronary angiography performed 25±18months before diagnosis of intracardiac inside-out abrasion already showed the defect. Despite undetected intracardiac inside-out abrasion, 2 of these 4 patients experienced adequate antitachycardia pacing and ICD-shocks. ICD leads were replaced in all 6 patients. Conclusions The prevalence of asymptomatic intracardiac inside-out abrasion in silicon-coated Riata® and Riata® ST leads is higher than 10% when assessed by fluoroscopy, and most intracardiac inside-out abrasions are not detectable by ICD interrogation.

BACKGROUND: J waves are the hallmark of both inferolateral early repolarization (ER) and Brugada syndrome. While ajmaline a class 1a antiarrhythmic drug accentuates the J wave in Brugada syndrome its effect on ER is unreported. OBJECTIVE: To describe the effect of ajmaline on the electrocardiogram in ER. METHODS: We analyzed electrocardiograms before and after the administration of intravenous ajmaline (1 mg/kg) in 31 patients with ER 21 patients with Brugada type 1 electrocardiogram (Br) and 22 controls. ER was defined as J point elevation of =1 mm with QRS slurring or notching in =2 inferolateral leads (I aVL II III aVF V4 V6). RESULTS: Ajmaline decreased mean J wave amplitude in the ER group from 0.2 ± 0.15 mV at baseline to 0.08 ± 0.09 mV (P < .001). The QRS width prolonged significantly in all 3 groups but the prolongation was significantly less in the ER group (+21 ms) than in the Br group (+36 ms; P < .001) or controls (+28 ms; P = .010). Decrease in mean inferolateral R wave amplitude was similar in all the groups (ER group 0.14 mV; Br group 0.11 mV; controls 0.13 mV; P = ns) but mean inferolateral S wave amplitude increased significantly less in the ER group (ER group +0.14 mV; Br group +16 mV; controls +0.20 mV; P < .001). CONCLUSIONS: Ajmaline significantly decreases the J wave amplitude in ER and prolongs the QRS width significantly less than in patients with Br. This indicates a different pathogenesis for both disorders. The altered terminal QRS vector probably is responsible for the decrease in the J wave amplitude in ER although a specific effect of ajmaline on J waves cannot be excluded.

Endurance athletes have an increased risk of developing atrial fibrillation (AF) at 40 to 50 years of age. Signal-averaged P-wave analysis has been used for identifying patients at risk for AF. We evaluated the impact of lifetime training hours on signal-averaged P-wave duration and modifying factors. Nonelite men athletes scheduled to participate in the 2010 Grand Prix of Bern, a 10-mile race, were invited. Four hundred ninety-two marathon and nonmarathon runners applied for participation, 70 were randomly selected, and 60 entered the final analysis. Subjects were stratified according to their lifetime training hours (average endurance and strength training hours per week × 52 × training years) in low (1,500 hours), medium (1,500 to 4,500 hours), and high (4,500 hours) training groups. Mean age was 42 ± 7 years. From low to high training groups signal-averaged P-wave duration increased from 131 ± 6 to 142 ± 13 ms (p = 0.026), and left atrial volume increased from 24.8 ± 4.6 to 33.1 ± 6.2 ml/m(2) (p = 0.001). Parasympathetic tone expressed as root of the mean squared differences of successive normal-to-normal intervals increased from 34 ± 13 to 47 ± 16 ms (p = 0.002), and premature atrial contractions increased from 6.1 ± 7.4 to 10.8 ± 7.7 per 24 hours (p = 0.026). Left ventricular mass increased from 100.7 ± 9.0 to 117.1 ± 18.2 g/m(2) (p = 0.002). Left ventricular systolic and diastolic function and blood pressure at rest were normal in all athletes and showed no differences among training groups. Four athletes (6.7%) had a history of paroxysmal AF, as did 1 athlete in the medium training group and 3 athletes in the high training group (p = 0.252). In conclusion, in nonelite men athletes lifetime training hours are associated with prolongation of signal-averaged P-wave duration and an increase in left atrial volume. The altered left atrial substrate may facilitate occurrence of AF. Increased vagal tone and atrial ectopy may serve as modifying and triggering factors.

Atrial flutter in the donor part of orthotopic heart transplants has been reported and successfully treated by radiofrequency ablation of the cavotricuspid isthmus, but mapping and ablation of atypical flutter circuits may be challenging.(1) Entrainment mapping has been used in combination with activation mapping to define the mechanism of atypical atrial flutter. Here, we report a case where colour-coded three-dimensional (3D) entrainment mapping allowed us to accurately determine and visualize the 3D location of the reentrant circuit and to plan the ablation of a left atrial flutter without the need for activation mapping.

A 43-year-old man was referred because of symptomatic, repetitive, supraventricular, premature beats, and non-sustained tachycardia. Prior anti-arrhythmic drug trials with metoprolol, flecainide, sotalol, and amiodarone had failed to improve the symptoms. The 12-lead ECG is shown in Figure 1 . …

BACKGROUND: Peak oxygen uptake (peak Vo(2)) is an established integrative measurement of maximal exercise capacity in cardiovascular disease. After heart transplantation (HTx) peak Vo(2) remains reduced despite normal systolic left ventricular function, which highlights the relevance of diastolic function. In this study we aim to characterize the predictive significance of cardiac allograft diastolic function for peak Vo(2). METHODS: Peak Vo(2) was measured using a ramp protocol on a bicycle ergometer. Left ventricular (LV) diastolic function was assessed with tissue Doppler imaging sizing the velocity of the early (Ea) and late (Aa) apical movement of the mitral annulus, and conventional Doppler measuring early (E) and late (A) diastolic transmitral flow propagation. Correlation coefficients were calculated and linear regression models fitted. RESULTS: The post-transplant time interval of the 39 HTxs ranged from 0.4 to 20.1 years. The mean age of the recipients was 55 +/- 14 years and body mass index (BMI) was 25.4 +/- 3.9 kg/m(2). Mean LV ejection fraction was 62 +/- 4%, mean LV mass index 108 +/- 22 g/m(2) and mean peak Vo(2) 20.1 +/- 6.3 ml/kg/min. Peak Vo(2) was reduced in patients with more severe diastolic dysfunction (pseudonormal or restrictive transmitral inflow pattern), or when E/Ea was > or =10. Peak Vo(2) correlated with recipient age (r = -0.643, p < 0.001), peak heart rate (r = 0.616, p < 0.001) and BMI (r = -0.417, p = 0.008). Of all echocardiographic measurements, Ea (r = 0.561, p < 0.001) and Ea/Aa (r = 0.495, p = 0.002) correlated best. Multivariate analysis identified age, heart rate, BMI and Ea/Aa as independent predictors of peak Vo(2). CONCLUSIONS: Diastolic dysfunction is relevant for the limitation of maximal exercise capacity after HTx.

Pre-excitation with R waves greater in amplitude than S waves in V1 and a positive delta wave in inferior leads are consistent with antegrade conduction over a left antero-lateral accessory pathway. In the presence of an accessory pathway, the most likely mechanism of the narrow QRS tachycardia is an orthodromic atrio-ventricular (AV) re-entrant tachycardia. The timing of the discrete P-wave visible during tachycardia at the beginning of the T-wave, best seen in lead V1 …

OBJECTIVE: To report a case of severe myopathy associated with concomitant simvastatin and amiodarone therapy. CASE SUMMARY: A 63-year-old white man with underlying insulin-dependent diabetes, recent coronary artery bypass surgery, and postoperative hemiplegia was treated with aspirin, metoprolol, furosemide, nitroglycerin, and simvastatin. Due to recurrent atrial fibrillation, oral anticoagulation with phenprocoumon and antiarrhythmic treatment with amiodarone were initiated. Four weeks after starting simvastatin 40 mg/day and 2 weeks after initiating amiodarone 1 g/day for 10 days, then 200 mg/day, he developed diffuse muscle pain with generalized muscular weakness. Laboratory investigations revealed a significant increase of creatine kinase (CK) peaking at 40 392 U/L. Due to a suspected drug interaction of simvastatin with amiodarone, both drugs were stopped. CK normalized over the following 8 days, and the patient made an uneventful recovery. An objective causality assessment revealed that the myopathy was probably related to simvastatin. DISCUSSION: Myopathy is a rare but potentially severe adverse reaction associated with statins. Besides high statin doses, concomitant use of fibrates, defined comorbidities, and concurrent use of inhibitors of cytochrome P450 are important additional risk factors. This is especially relevant if statins predominantly metabolized by CYP3A4 are combined with inhibitors of this isoenzyme. Amiodarone is a potent inhibitor of several different CYP isoenzymes, including CYP3A4. CONCLUSIONS: Avoiding the concomitant use of drugs with the potential to inhibit CYP-dependent metabolism (eg, amiodarone) or elimination of statins may decrease the risk of statin-associated myopathy. Alternatively, if drug therapy with a potent CYP inhibitor is inevitable, choosing a statin without relevant CYP metabolism (eg, pravastatin) should be considered.

In a letter to the editor, Dr Jastrzebski challenges the diagnosis of junctional ectopic tachycardia (JET) proposed in our case report.1 According to him, non-reentrant supraventricular tachycardia due to double firing must be considered in this case. As mentioned in our commentary, we initially considered double firing as a possible mechanism for the tachycardia, and are well aware that double firing can present with varying atrial-His (AH) intervals. Nevertheless, most cases of …