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Invasive Measurements of Atrioventricular Conduction Parameters<br />
Prior to and Following Ventricular Septal Defect Closure with t
Nearly two decades have elapsed since the early percutaneous closure of ventricular septal defects (VSD),1,2 and controversies surrounding such techniques persist.3 The early types of devices developed for VSD closure were associated with low success rates and high morbidity; this was attributed in part to the design of the devices and the fact that they were not specifically designed for paramembranous VSD (pm- VSD) anatomy.1,4,5 The pilot devices helped to elucidate the expected efficacy of the procedure, as well as the related complications, such as device embolization, hemolysis, aortic regurgitation and atrioventricular (AV) valve regurgitation. In addition, conduction disturbances and AV block represented a significant concern due to the anatomical proximity of the conduction system. Nowadays, with the pm-VSD Amplatzer device the procedure has a high success rate (90.7–100%) and a reported incidence of complications between 9.1 and 29%.6–9 However, complete AV block remains a preoccupying concern, with a reported incidence between 0 and 6%.6–11 The alternative, surgical closure of pm-VSD is not free of AV conduction complications. The literature documented very well this complication in association with simple defects in the last four decades, as well as the advanced technical improvements to the surgical approach in order to reduce the incidence of complete AV block from 4% to ~0%.12–15
Due to concerns about AV block with pm-VSD device closure, we studied the AV conduction before and after device deployment. This report describes AV conduction parameters and the changes observed both invasively and on surface ambulatory electrocardiography before and after percutaneous closure of pm-VSD using the Amplatzer device.
Material and Methods
Patients population. Between January 2004 and May 2005, 67 patients had a percutaneous pm-VSD closure using the Amplatzer device in the two participating institutions. Among those, electrophysiology study (EPS) was performed on 19 patients (11 girls, 8 boys) based on the availability of the institutional electrophysiologist. Mean age was 8.9 ± 4.5 years (range 2.8–17.1 years), mean weight was 37.9 ± 23.7 kg (14.8–76.9 kg) (Table 1).
Procedure. All patients underwent right and left cardiac catheterization and angiography under general anesthesia along with transesophageal echocardiography guidance. The technique for pm-VSD closure by Amplatz device has been previously reported.6,16
Two femoral venous access sheaths were used for the electrophysiological study (EPS) performed during the procedure prior to and following closure of the pm-VSD. A baseline EPS was carried out using standard techniques with thecatheters initially positioned in the high right atrium and at the right AV junction for His bundle recording. After completion of decremental atrial pacing and right atrial refractory period determination, the high right atrium catheter was positioned to the right ventricular apex for ventriculo-atrial conduction analysis. Basic intervals were measured: PA, AH, HV (or AV intervals when His potential could not be recorded), PR interval and QRS duration. AV conduction was assessed along with the cycle length at which Wenckebach periodicity occurred and effective refractory period of the AV node. The presence or absence of VA conduction was noted and the cycle length at which Wenckebach periodicity of the retrograde conduction system occurred was reported. The same stimulation protocol was performed at the beginning of the catheterization (prior to any catheter manipulation) and after device release. An increase in electrophysiology parameters of more than 15% from baseline was chosen as the cutoff for assessment of outcome. The 15% cutoff was chosen as three-fold the mean RR variability (5%) after versus before device implantation calculated in this series.
Holter monitoring and a Bruce exercise test prior to pm- VSD closure and at 3-month follow up were obtained.
Definition. In this study the term “septal anchorage” was used when the Amplatzer device was centered on the ventricular septal defect and “aneurysmal anchorage” when the device was maintained in position tilted into the aneurysm, therefore reducing hypothetical stretching of the septal defect and surrounding conduction tissue. The size of pmVSD represents the septal defect size measured either by angiography or by transesophageal echocardiography (Table 2). It does not represent the shunt diameter at the orifice of the septal aneurysm.
Statistical analysis. Results are expressed as mean ± standard deviation (range). We used the Student’s t-test for continuous data with normal distribution, and analysis of variance for non-normal distribution data. Paired t-test was used for parameter comparison before and after intervention. We used χ2 or Fisher’s exact tests for nonparametric data. A p-value < 0.05 was considered statistically significant.
Results
Device closure of the pm-VSD was successful for all 19 patients. Procedural data are summarized in Tables 1 and 2, and EPS data are in Table 3.
Invasive EP parameters. No significant change for PR, QRS, PA, or AH measurements was observed. During recordings after device deployment artifacts were observed due to proximity between the electrode catheter and the device. Gentle manipulation of the electrode catheter was mandatory to prevent dislodgment of the device. Therefore, His bundle recordings were measurable in 5/19 patients after device deployment showing significant change in HV interval (p = 0.017). When AV interval was used as a surrogate no significant change was observed. EPS parameters with an increased measurement of 15% or more were observed in 18/19 patients (95%). These findings were recorded for one to two EPS parameters in 9/18 (50%) patients, and for 3 or more in the other 9/18 (50%) patients.
Surface ECG parameters. Conduction anomalies were encountered in 6/18 (31%) patients, transient in 2 and persistent in 4 during the follow-up period of 1.9 ± 0.8 years. While none of the studied patients developed complete AV block, neither immediately nor at last follow-up, persistent 1st degree AV block occurred in 2 patients. The first case was documented in a 15-year-old 3 months after the procedure (Patient 3). His PR interval increased progressively from 153 to 190 then 200 msec. EPS changes were mainly a 17% increase of cycle length at which anterograde Wenckeback periodicity occurred, with no significant change for PR, QRS, PA, or AH measurements. The second case occurred in a 12-year-old (Patient 6) with a PR increase from 184 msec before the device to 208 msec documented at one month follow up. In this case no AV block was recorded at discharge (PR 172 msec), but several EPS parameters increased compared to baseline (PA 59%, HV 35%, AV 10%, PR 14%, anterograde Wenckebach cycle length 50%, AVNERP 16%). Curiously a 7.8-year-old girl (Patient 14) who presented with a first-degree AV block (PR 260 msec) before the procedure, showed regression to normal AV conduction (PR 164 msec) at 6-month follow up.
New onset complete right bundlebranch block (CRBBB) was observed in 2 patients. CRBBB was transient in 1 (Patient 11). Her EP parameters showed the following increments, PR 16.8%, QRS 10%, anterograde Wenckebach cycle length 37.5%, and AVNERP 70%. Upon hospital discharge there was no conduction abnormality. A CRBBB was noted 1 month later, regressing to incomplete block at 3 months and returning to normal QRS configuration at 8 months and again at 2.1-year follow up. In the second patient (Patient 7), a CRBBB was recorded immediately after procedure, which is persistent at 2.4-year follow up. The only significant EPS finding for this patient was a 21% increase of AV interval. Finally, a CRBBB was recorded in a 17-year-old girl prior to the procedure and remained unchanged during 1-year follow up. New onset incomplete right bundlebranch block (IRBBB) was observed in 2 cases. The first patient (Patient 19) had the following increments in EPS parameters, AH 37%, HV 50%, AV 42%, PR 26%, and QRS 12%. The second patient (Patient 13) showed the following increments QRS 44%, retrograde Wenckebach cycle length 38% and AVNERP 21%. Two other patients (Patients 1 and 2) had preexisting IRBB with no subsequent change.
Twenty-four hour Holter monitoring was obtained at 3 months in 12/19 (63.2%) patients with no arrhythmias or new conduction abnormalities observed at low or high heart rate. A treadmill exercise test was also performed 3 months after the procedure in 10/19 (52.6%) patients, with no arrhythmias or new conduction abnormalities at rest, exercise or recovery. Exercise capacity was normal in all, maximum heart rate 90% ± 7 (82–100%), duration 12 minutes ± 2 (9.6–15.3 minutes), and metabolic equivalents 13.8 ± 2.6 (10–17 METS).
Procedural correlation. With respect to procedural parameters and biometric parameters, the only detectable risk factor associated with the occurrence of new onset conduction disturbances on surface ECG was the large device size (p = 0.03). More precisely, there were no identifiable relationships with indexed device size (p > 0.5), age (p > 0.6), device anchoring at VSD margins or in the septal aneurysm (p = 0.3), procedure time (p = 0.7) or fluoroscopy time (p = 0.6).
With respect to EPS changes, there were no detectable relationships with procedure parameters or biometric parameters, such as device size (p = 0.5), indexed device size (p = 0.94), device anchoring at VSD margins or in the septal aneurysm (p = 0.48). There was no significant relationship between the incidence of conduction disturbance and size difference between the device and VSD measurements by angiography (-0.51 mm ± 3 mm ), or by trans-esophageal echocardiography (1.71 mm ± 2.25 mm; p = 0.2). In contrast, and among the changes in EPS parameters described above, anterograde Wenckebach periodicity had a predictive value of new conduction disturbance (p = 0.003).
Discussion
The identification of predictive risk factors of AV conduction abnormalities following percutaneous pm-VSD closure has become an important concern since the description of AV block following Amplatzer device closure.6–11,17 This manuscript is based on our hypothesis that catheter manipulation during the procedure as well as anatomical proximity between the device and the conduction system may lead to conduction system dysfunction. To our knowledge, this is the first report on invasive EPS related to percutaneous pm- VSD closure. We were indeed able to record a minimum of 15% change in many electrophysiologic parameters in almost all of our patients (95%). These invasive EP measurements correspond to 31% of patients demonstrating conduction disturbances detectable on ambulatory surface ECG, yet no complete AV block occurred in the study population.
There are several studies identifying AV block as a recurrent complication of pm-VSD device closure with an overall incidence of implantable pacemaker requirement between 0 to 3.4% (Table 4). The first multinational trial of pm-VSD closure using the Amplatzer device yielded 1 case of LBBB (4.3%), which resolved spontaneously at 3 weeks.6 Similarly, a U.S. trial reported 3 patients with conduction anomalies (8.6%), including complete AV block, LBBB and RBBB.18 Larger series (87–186 patients) report higher incidence of conduction abnormalities ranging between 9.1–13%.7,8,10 While the incidence of branch block varies between 0 and 10%, reported complete AV block ranges between 1.1–5.7% (Table 4). Another large Indian series of 137 subjects including 91 pm-VSD, closed mainly with Amplatzer device, report 3 cases of transient LBBB and 2 cases with complete AV block, both resolving spontaneously after 1 and 5 days.19 Complete AV block may be asymptomatic in some cases,10 which puts patients at risk of sudden death up to 25 years later according to surgical series,12–14 which is the reason for pacemaker implantation rather than observation.
Some investigators have suggested that the mechanism behind device-induced AV block is related to compression of the AV node with secondary local edema and inflammation, 22 mainly related to device oversizing.11 Therefore, corticosteroids and aspirin have been used empirically by many authors when AV block occurs shortly after device implantation.7,8,10,22 The hypothesis of larger devices being more likely to cause AV conduction disturbances is appealing, such as reported in ASD closure using the Amplatzer device.20,21 In the present limited series, analysis of demographic and technical data support this hypothesis. Indeed, the only identifiable risk factor for new onset AV conduction abnormality was related to large device size. In contrast, indexed device size or device-to-defect ratio were not significantly associated with AV conduction disturbances, most likely because of our adherence to a policy limiting the procedure to moderate or small VSDs as well as avoidance of oversizing in our series. Holzer et al report that children under 10 kg have a significantly higher incidence of overall complications, without specific reference to AV block.8 In a series of 30 patients with muscular VSD, Thanopoulos et al reported that small children requiring a large device are more likely to develop AV block.23
In the Canadian multicenter pilot study of 60 pm-VSD cases, including 32 cases from our sites, complete AV block occurred in 4 patients (6.7%).11 A permanent pacemaker implant was required in 3 (5%). Minor AV conduction disturbances were also encountered (3 CRBBB, 2 IRBBB, 1 LBBB), with an incidence of overall conduction abnormalities of 16.7%. Identifiable risk factors in the overall group were oversizing of the device, the absence of septal aneurysm, and paramembranous or high-muscular VSD. Because invasive EPS assessment was not part of the pan- Canadian protocol, the only available EPS data are reported in this manuscript.
Conclusion
In conclusion, this reported cohort, demonstrated that EPS is feasible without complications related to EPS catheter manipulation and the potential hazard to the freshly implanted device. However, missing His recording after implantation represents a technical limitation. Another limitation of this study may be attributable to the lack of a standardized anesthetic protocol, which was not evaluated in this report. Nevertheless, our results suggest that the closure of pm-VSD with an Amplatzer device promotes relative changes in the electrophysiologic parameters of the AV conduction system. These changes had suggestive but limited predictivity of new conduction abnormalities due to the small numbers. From this perspective, our experience should encourage investigators for a wider application of invasive EPS evaluation in order to further identify relationships between conduction disturbances and percutaneous closure of pm-VSD.
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