Author + information
- Received April 16, 2015
- Revision received December 17, 2015
- Accepted December 27, 2015
- Published online June 1, 2016.
- Jong Sung Park, MDa,b,
- HyeJin Hwang, MD, PhDa,
- Boyoung Joung, MD, PhDa,
- Moon-Hyoung Lee, MD, PhDa and
- Sung Soon Kim, MD, PhDa,c,∗ ()
- aDivision of Cardiology, Cardiovascular Center, Yonsei University Health System, Seoul, Republic of Korea
- bDivision of Cardiology, Cardiovascular Center, Dong-A University Medical Center, Busan, Republic of Korea
- cDivision of Cardiology, Korean Armed Forces Capital Hospital, Gyeonggi-do, Republic of Korea
- ↵∗Reprint requests and correspondence:
Dr. Sung Soon Kim, Division of Cardiology, Severance Cardiovascular Center, Yonsei University Health System, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Republic of Korea.
Objectives This study examined the clinical and electrocardiographic characteristics and electrophysiologic determinants of sustained slow pathway conduction (SSPC) during sinus rhythm.
Background SSPC during sinus rhythm in presence of dual atrioventricular (AV) nodal pathways has not been thoroughly studied.
Methods We studied 30 consecutive patients (19 men), whose median age was 31 years (interquartile range: 22 to 48 years); their electrocardiograms revealed 2 different PR intervals during nearly identical sinus rates. We measured the short and long PR intervals and their differences and examined the electrophysiologic determinants of SSPC during slow pathway (SP) ablation in 12 patients.
Results Among the 30 patients, 21 (70%) complained of major symptoms. The short and long PR intervals measured 202 ± 42 ms and 472 ± 110 ms, respectively, and their mean difference measured 270 ± 101 ms. During electrophysiologic studies, dual AV nodal and SSPC were observed in all patients. A markedly prolonged refractory period (593 ± 116 ms) and retrograde conduction block over the fast pathway (FP) were observed over a range of sinus cycle lengths (CLs). Ablation of the SP in 11 patients promoted FP conduction and shortened its effective refractory period from 593 ± 116 ms to 288 ± 90 ms. Over a median follow-up of 2 years (interquartile range: 1 to 3 years), all patients remained asymptomatic and without recurrences of SSPC or AV block.
Conclusions Two distinct PR intervals during sinus rhythm indicated the presence of dual AV nodal pathways. SSPC was promoted by a markedly impaired bidirectional conduction over the FP at critical sinus CL. SP ablation safely and effectively eliminated SSPC in symptomatic patients.
- atrioventricular node
- catheter ablation
- dual atrioventricular nodal pathway
- fast atrioventricular nodal pathway
- slow atrioventricular nodal pathway
Intermittent sustained slow pathway conduction (SSPC) during sinus rhythm on the surface electrocardiogram is rare (1). It has been typically observed during rapid atrial pacing in patients presenting with inducible atrioventricular (AV) nodal re-entrant tachycardia (2–4), although the first intracardiac documentation of SSPC during sinus rhythm was recorded in a patient who presented with a paroxysmal non–re-entrant supraventricular tachycardia (5). The present study describes the clinical manifestations and electrocardiographic observations recorded in 30 patients who presented with SSPC during sinus rhythm. We also studied the electrophysiologic determinants of SSPC during sinus rhythm and the effects of slow pathway (SP) ablation on fast pathway (FP) conduction in 12 symptomatic patients who underwent selective radiofrequency catheter ablation of the SP.
Between 1998 and 2014, we studied 30 consecutive patients (19 men) whose median age was 31 years (interquartile range: 22 to 48 years) and who presented with short and long PR intervals during nearly identical sinus rates, in the absence of structural heart disease and cardioactive medication that influenced AV nodal conduction. All patients underwent detailed cardiac investigations, including history, physical examination, transthoracic echocardiography, 24-h ambulatory electrocardiogram, exercise treadmill testing, and, if needed, isoproterenol infusion test.
Our institutional review board reviewed and approved the protocol of this study, which was conducted in accordance with institutional policies, national legal requirements, and the revised Declaration of Helsinki.
Electrocardiographic observations and measurements
Stable, short and long PR intervals during sinus rhythm were initially documented by 12-lead electrocardiograms in 13 patients and by 24-h ambulatory electrocardiograms in 17 patients. The measurements included the short and long PR intervals, their difference (Δ), and their corresponding sinus rates after the long PR interval had remained stable for ≥30 s. The appearance and disappearance of the long PR interval on the 24-h ambulatory electrocardiogram were analyzed in 28 patients.
Electrophysiologic studies and catheter ablation
Electrophysiologic studies and radiofrequency catheter ablation of the SP were performed in 12 patients (40%) who complained of prominent symptoms and requested a curative procedure. The indications to proceed with ablation of the SP were firmly ascertained by an unequivocal correlation between the symptoms reported by the patients and the periodic and sudden prolongation of the PR interval, which was confirmed by 24-h ambulatory electrocardiographic monitoring or by remote telemonitoring.
The electrophysiologic studies were performed in the post-absorptive and nonsedated state after a signed informed consent was obtained from each patient. Quadripolar, 4-F electrode catheters (St. Jude Medical, St. Paul, Minnesota) were introduced percutaneously from the left femoral vein and positioned in the high right atrium, the His bundle region, and at the right ventricular apex. A 6-F decapolar electrode catheter (St. Jude Medical) was advanced from the left subclavian vein into the coronary sinus. Surface electrocardiographic leads I, aVF, and V1, and all intracardiac electrograms were continuously recorded and stored on a computer-based digital amplifier/recorder (PrukaCardioLab IT System, GE Healthcare, Milwaukee, Wisconsin). Bipolar electrograms were recorded at a bandpass between 30 and 500 Hz. Stimuli, which were 2 ms in duration, were delivered at twice the end-diastolic threshold by a programmable digital stimulator (Bloom DTU 215, Fisher Medical Technologies, Denver, Colorado). Anterograde and retrograde AV nodal conduction was ascertained by incremental pacing and by the extrastimulation technique. The conduction properties and refractory periods, as defined previously (6), were measured, and AV nodal re-entrant supraventricular tachycardia was diagnosed by standard criteria (7).
For the ablation procedures, a 7-F, large-tip, 4-mm long, deflectable, quadripolar electrode catheter, with 2-mm interelectrode distance (Bard Electrophysiology, Lowell, Massachusetts) was introduced percutaneously from the right femoral vein and advanced to the right atrium. Radiofrequency energy was delivered as a continuous, modulated, sinusoidal waveform at 500 kHz in unipolar mode, between the distal tip of the ablation catheter and a large, posterior skin patch electrode, using a radiofrequency energy generator (Stockert EP Shuttle, Stockert, Freiburg, Germany). The energy was delivered in steps to ablate the SP from the right posterior and inferior aspect of the interatrial septum (8). Radiofrequency energy was delivered at least twice at 50 W, for 50 s, with the temperature limited to 50°C during SSPC, if possible. An ablation attempt was classified as successful when SSPC or anterograde dual AV node conduction was eliminated.
The 12 patients who underwent SP ablation were followed in our ambulatory department at 1 month after discharge and every 6 months thereafter. They were interviewed, and 12-lead and 24-h ambulatory electrocardiograms were recorded at each visit and analyzed by an investigator.
The values are expressed as mean ± SD, median (interquartile range), or count (percentage). The short and long PR intervals, and the electrophysiologic measurements made before and after SP ablation were analyzed using SPSS version 18.0 for Windows (IBM, Armonk, New York).
Among the 30 patients, 21 (70%) were symptomatic, of whom 14 (47%) presented initially with mild to moderate chest fluttering, chest pressure, or both, and 7 reported similar symptoms during detailed interrogation. These symptoms were closely correlated with intermittent SSPC during ambulatory electrocardiographic monitoring, whereas 9 patients were free from symptoms related to SSPC. All patients denied experiencing episodes of paroxysmal palpitation consistent with AV nodal re-entrant tachycardia. An abnormal electrocardiogram was the cause of referral of 16 (53%) patients. Associated cardiovascular disorders included vasovagal syncope in 5 patients, paroxysmal atrial fibrillation in 2 patients, and hypertension in 2 patients (Table 1).
Episodes of SP conduction occurred frequently throughout the day, particularly during sleep, and lasted a few seconds, or was sustained and stable for up to 30 min. The mean, stable, short and long PR intervals measured 202 ± 42 ms and 472 ± 110 ms, respectively. The mean (Δ) between short and long PR intervals was 270 ± 101 ms and was ≥200 ms in 26 of the 30 patients, although the sinus rates corresponding to each PR interval (69 ± 10 beats/min vs. 74 ± 15 beats/min) were similar. PR intervals >400 ms produced the P-on-T phenomenon in 24 patients (80%), and P-on-R was observed in 4 patients with >600-ms PR intervals (Figure 1).
Appearance and disappearance of SSPC during ambulatory electrocardiographic monitoring
The spontaneous onset during sinus rhythm and disappearance of SSPC in the absence of premature atrial and ventricular complexes or sinoatrial block were observed in 28 patients. In 2 patients, no episode of SSPC was observed during ambulatory electrocardiography or telemetry monitoring. Most of the patients underwent exercise testing without induction of the long PR interval during exercise. Isoproterenol was used in patients unable to exercise or who underwent the head-up tilt table test. In 1 patient, SSPC developed 5 min after the discontinuation of isoproterenol infusion during the head-up tilt table test.
A long PR interval developed abruptly in all patients (Figure 1A), preceded by a sudden, albeit minimal, lengthening of the sinus cycle length (CL), whereas the termination of SSPC coincided with a minimal, although sudden, shortening of the sinus CL (Figure 1B). The long PR interval occasionally ended with a blocked P-wave as the sinus CL lengthened further. The blocked P-wave was followed by a few sinus cycles with a short, fixed PR interval associated with a minimally shortened sinus cycle or atypical Wenckebach period, followed by SSPC with a minimal increase in the sinus CL (Figure 1C). This termination was often observed during sinus bradycardia, during sleep or early in the morning. A similar mode of termination could be reproduced by carotid sinus massage during SSPC (Figure 1D).
The electrophysiologic characteristics of dual AV nodal pathways before and after SP ablation are summarized in Table 2. Anterograde dual AV node conduction and SSPC were elicited by programmed electrical stimulation in all 12 patients. However, AV nodal re-entrant tachycardia, whether typical or atypical, was never induced, including during isoproterenol infusion. Frequent, isolated AV nodal echoes were observed during SSPC in Patient #5 only (Table 2). Intermittent, spontaneous SSPC was easily induced during sinus rhythm in 3 patients and by atrial pacing in 9 patients. The modes of induction were spontaneous deceleration of the sinus rate, atrial premature events, single atrial extrastimulation, and right atrial pacing. Programmed ventricular stimulation did not initiate SSPC, but it did terminate SSPC. The AH interval of the FP ranged between 80 and 190 ms, and that of the SP ranged between 380 and 480 ms. FP conduction was depressed with marked prolongation of the anterograde AV block CL, ranging from 480 to 1,000 ms (mean: 735 ± 148 ms) and a sinus CL ranging between 650 and 980 ms. The effective refractory period (ERP) of the FP was also markedly prolonged, from 400 to 710 ms (mean: 593 ± 116 ms). The conduction properties of the SP were also markedly depressed, although the AV block CL (mean: 622 ± 114 ms) and ERP (mean: 425 ± 160 ms) were shorter than those of the FP. Ventricular pacing revealed ventriculoatrial (VA) dissociation in 10 patients, and in 2 patients (Patients #5 and #10 in Table 2), it revealed prolonged VA block CLs of 460 and 750 ms, respectively. Patient #10 had a prolonged VA conduction time via a retrograde SP, which was eliminated by radiofrequency catheter ablation.
Post-ablation electrophysiologic studies
We used a standard posterior approach for the SP ablations, most of which were ablated at P2 and M1 sites. After successful ablation of the SP, anterograde dual AV nodal conduction was eliminated in 11 patients. Dual AV nodal conduction persisted in a single patient (Patient #2 in Table 2). However, after the ablation procedure, SSPC was no longer inducible with programmed electrical stimulation in any patient. In the 11 patients who underwent successful SP ablation (Figure 2A), the AV block CL of the FP was markedly shortened from 735 ± 148 ms to 438 ± 81 ms. The ERP of the FP was also significantly shortened (Figure 2B), except in 1 patient (Patient #2 in Table 2) in whom dual AV nodal conduction persisted, without shortening of the ERP of the FP. In 4 patients in whom SSPC was maintained by right atrial pacing, the AH interval over the SP shortened gradually while radiofrequency energy was being delivered to the SP area (Figure 3). In 6 patients who presented with first-degree AV block, the mean PR interval decreased from 257 ± 42 ms before ablation to 233 ± 48 ms after ablation of the SP (Table 2). No AV block was observed from injury to the FP. In-hospital telemetry and 24-h ambulatory electrocardiograms revealed no further SSPC, and no Wenckebach periodicity or transient complete AV block in any patient.
Over a median follow-up of 2 years (interquartile range: 1 to 3 years), no recurrence of SSPC was observed on 24-h ambulatory electrocardiography, and all patients remained free from symptoms attributable to an arrhythmia. A single patient developed asymptomatic, type I second-degree AV block. In patients whose pre-ablation recordings revealed the presence of first, or transient type I second- or third-degree AV block, repeat serial 24-h ambulatory electrocardiograms confirmed the elimination of the previously observed AV block.
Intermittent SSPC during sinus rhythm is a rare electrocardiographic manifestation of dual AV nodal physiology (9). Previous reports have described various electrocardiographic observations of SP conduction associated with minor variations in sinus CL and atrial and ventricular premature complexes (1,10). Detailed analyses of the beginning and end of SSPC suggest that an unusually prolonged refractoriness of the FP, repetitive concealed conduction between the SP and the FP, and autonomic influences on the AV node during sinus rhythm are involved in the periodic variations of the PR interval (10).
Determinants of SSPC
We identified several electrophysiologic factors that contributed to the development of SSPC during sinus rhythm. The anterograde and retrograde conductive properties of the FP were markedly abnormal, with very long AV block CL and ERP, and with VA dissociation. The anterograde conduction properties of the SP were also very fragile, although the anterograde AV block CL and ERP were shorter than those of the FP. Because these conduction abnormalities persisted over a range of sinus CLs, SSPC was easily initiated and maintained by the block in the FP and a shift of conduction to the SP, which was associated with sudden, although minimal, lengthening of the preceding sinus CL. This was probably due to transiently increased parasympathetic nervous activity (Figure 1A). Sustained SP conduction also disappeared without a blocked P wave when a decrease in vagal sympathetic activity or an increase in sympathetic activity promoted conduction over the FP and accelerated the sinus rate (Figure 1B). This coupled change in the PR interval and sinus CL seemed to be due to a differential sensitivity to vagal activity of a depressed FP, compared with the SP, at a time when the sinus CL was critically near the block CL of the FP. Another mode of termination of SSPC by a blocked P wave can be explained by a surge in vagal activity, which influences SP conduction and causes simultaneous conduction block over both pathways (Figure 1C). This type of termination was usually observed while patients were asleep or early in the morning (when vagal tone is increased); this was a mode of termination we could reproduce by carotid sinus massage during SSPC (Figure 1D). Therefore, the autonomic nervous system plays a critical role in the appearance and disappearance of SSPC besides the unique electrophysiologic characteristics of dual AV nodal physiology in susceptible patients.
Effects of SP ablation on the conduction properties of the FP
The abnormal conduction properties of the FP present before the ablation procedure might have raised concerns with respect to the risk of worsening AV conduction by ablation of the SP (11,12). In this study, catheter ablation of the SP improved the conduction properties of the FP. In patients with typical AV nodal re-entrant tachycardia, previous investigators observed that successful ablation of the SP shortens the refractoriness of the FP (12–14). They suggested that this might be caused by a loss of electrotonic interaction between the 2 pathways after the SP ablation.
Clinical implications of SSPC
Reports of intermittent episodes of SSPC have been rare since the first report by Schamroth and Perlman in 1973 (9), probably because of unfamiliarity with SSPC and its complex electrocardiographic interpretation, rather than its low prevalence. Mild to moderate symptoms were reported by two-thirds of our patients. The P-on-R (or on T) phenomenon due to SSPC causes AV dyssynchrony, a sudden increase in atrial pressure, and a vagally mediated reflex similar to the pacemaker syndrome (15). Sustained SP conduction during sinus rhythm is not simply of academic interest, and its electrocardiographic expression may not be as rare as suspected. As observed in our patients, SP conduction often simulates an accelerated junctional rhythm, with long PR intervals and P waves superimposed on the peak of the T-wave, typical or atypical Wenckebach block, and transient AV dissociation due to the emergence of a junctional escape rhythm during sinus bradycardia with a long PR interval. These manifestations of SP conduction often complicate the interpretation of electrocardiograms, which can be facilitated by an understanding of the background mechanism(s) of SSPC.
With regard to therapy, we wish to emphasize that SSPC is not a classic indication for ablation of the SP. In this study, the 12 patients who underwent SP ablation were highly symptomatic, with intermittent chest fluttering or discomfort that had been closely correlated with the periodic occurrence of SSPC. Electrophysiologic studies and ablation procedures should both be reserved for highly selected patients, whose symptoms: 1) have been closely correlated with lengthening of the PR interval by 24-h electrocardiographic or long-term remote monitoring; and 2) are poorly tolerated.
The prevalence of SSPC was not clarified by our study. Because its expression is unusual and its interpretation is challenging, it could easily be overlooked in clinical practice. Abnormal electrocardiograms without diagnosis of SSPC were the source of referrals for 50% of our patients. A greater awareness of this rhythm disturbance might increase the detection of SSPC. A second limitation was an insufficient electroanatomic understanding of SSPC. In particular, the progressive shortening of the AH interval during radiofrequency energy delivery to the SP, while maintaining SSPC with right atrial pacing (Figure 3), is not well understood. It might be explained by a progressive attenuation of the anisotropic conduction properties of the SP by the anatomic modifications of the posterior Koch triangle (16). A fundamental understanding of dual AV nodal conduction pathways should be correlated with anatomy and pathology by various experimental techniques (17,18). Nevertheless, this study is contributory, because it is the first to: 1) illustrate the unique electrophysiologic characteristics of the FP and SP in patients presenting with SSPC that develops during sinus rhythm; and 2) treat symptomatic patients with this disorder.
SSPC during sinus rhythm was characterized by 2 distinct PR intervals on 12-lead and 24-h ambulatory electrocardiograms. Its main determinants were: 1) markedly abnormal, bidirectional conduction properties of the FP; and 2) the influence of the parasympathetic system on the AV node. Catheter ablation of the SP normalized the anterograde conduction properties of the FP. Ablation of the SP safely and effectively eliminated SSPC in symptomatic patients.
COMPETENCY IN MEDICAL KNOWLEDGE: Understanding the background electrophysiology of SSPC during sinus rhythm may facilitate the interpretation of electrocardiograms complicated by atypical slow pathway conduction.
TRANSLATIONAL OUTLOOK: Further studies are needed to understand the electroanatomical mechanism of SSPC.
The authors thank Rodolphe Ruffy, MD, for reviewing our manuscript.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- cycle length
- effective refractory period
- fast pathway
- slow pathway
- sustained slow pathway conduction
- Received April 16, 2015.
- Revision received December 17, 2015.
- Accepted December 27, 2015.
- American College of Cardiology Foundation
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