Para-Hisian Pacing During Sinus Rhythm: Establishing Threshold Values to Distinguish Nodal From Septal Pathway Conduction.

OBJECTIVES: This study sought to identify minimum threshold values below which conduction over the atrioventricular (AV) node would be unexpected. BACKGROUND: Para-Hisian pacing is used to evaluate for the presence of a septal accessory pathway (AP); however, threshold values to differentiate nodal from AP conduction are unknown. METHODS: The authors performed high- and low-output para-Hisian pacing during sinus rhythm to capture the His and para-Hisian ventricular myocardium (H+V) and para-Hisian ventricular myocardium (V) alone, respectively. The change in stimulation (stim)-to-atrial electrogram interval after loss of His bundle capture in patients with (AP+) and without (AP-) a septal AP was evaluated. Stim-to-proximal coronary sinus (PCS) and stim-to-high right atrium (HRA) intervals were measured and within-patient differences (△) for V and H+V capture were calculated. RESULTS: A total of 23 AP+ and 45 AP- patients were evaluated. The difference in stimulus to earliest atrial signal in the high right atrial catheter seen with the loss of His bundle capture (△-stim-HRA) (21 ms; interquartile range [IQR]: 3 to 43 ms vs. 64 ms; IQR: 56 to 73 ms; p < 0.001) and difference in stimulus to earliest atrial signal in the proximal coronary sinus catheter seen with the loss of His Bundle capture (△-stim-PCS) (11 ms; IQR: 0 to 30 ms vs. 61 ms; IQR: 52 to 72 ms; p < 0.001) were shorter in AP+ patients. The shortest △-stim-PCS and △-stim-HRA in AP- patients were 37 ms and 32 ms, respectively, whereas the longest corresponding intervals in AP+ patients were 51 ms and 75 ms, respectively. CONCLUSIONS: A △-stim-PCS <37 ms or △-stim-HRA <32 ms confirmed the presence of a septal AP, whereas a value >51 ms for △-stim-PCS or >75 ms for △-stim-HRA excluded it. Alternatively, the minimum △-stim-PCS with loss of His capture compatible with AV nodal conduction in isolation was 37 ms, and a △-stim-PCS >51 ms effectively ruled out the presence of a septal AP.

Bundle Branch Re-Entrant Ventricular Tachycardia: Novel Genetic Mechanisms in a Life-Threatening Arrhythmia.

OBJECTIVES: This study sought to investigate for an underlying genetic etiology in cases of apparent idiopathic bundle branch re-entrant ventricular tachycardia (BBRVT). BACKGROUND: BBRVT is a life-threatening arrhythmia occurring secondary to macro-re-entry within the His-Purkinje system. Although classically associated with dilated cardiomyopathy, BBRVT may also occur in the setting of isolated, unexplained conduction system disease. METHODS: Cases of BBRVT with normal biventricular size and function were recruited from 6 North American centers. Enrollment required a clinically documented wide complex tachycardia and BBRVT proven during invasive electrophysiology study. Study participants were screened for mutations within genes associated with cardiac conduction system disease. Pathogenicity of identified mutations was evaluated using in silico phylogenetic and physicochemical analyses and in vitro biophysical studies. RESULTS: Among 6 cases of idiopathic BBRVT, each presented with hemodynamic compromise and 2 suffered cardiac arrests requiring resuscitation. Putative culprit mutations were identified in 3 of 6 cases, including 2 in SCN5A (Ala1905Gly [novel] and c.4719C>T [splice site mutation]) and 1 in LMNA (Leu327Val [novel]). Biophysical analysis of mutant Ala1905Gly Nav1.5 channels in tsA201 cells revealed significantly reduced peak current density and positive shifts in the voltage-dependence of activation, consistent with a loss-of-function. The SCN5A c.4719C>T splice site mutation has previously been reported as disease-causing in 3 cases of Brugada syndrome, whereas the novel LMNA Leu327Val mutation was associated with a classic laminopathy phenotype. Following catheter ablation, BBRVT was noninducible in all cases and none experienced a clinical recurrence during follow-up. CONCLUSIONS: Our investigation into apparent idiopathic BBRVT has identified the first genetic culprits for this life-threatening arrhythmia, providing further insight into its underlying pathophysiology and emphasizing a potential role for genetic testing in this condition. Our findings also highlight BBRVT as a novel genetic etiology of unexplained sudden cardiac death that can be cured with catheter ablation.

Electrophysiology testing and catheter ablation are helpful when evaluating asymptomatic patients with Wolff-Parkinson-White pattern: the con perspective.

The association between asymptomatic Wolff-Parkinson-White (WPW) syndrome and sudden cardiac death (SCD) has been well documented. The inherent properties of the accessory pathway determine the risk of SCD in WPW, and catheter ablation essentially eliminates this risk. An approach to WPW syndrome is needed that incorporates the patient's individualized considerations into the decision making. Patients must understand that there is a trade-off of a small immediate risk of an invasive approach for elimination of a small lifetime risk of the natural history of asymptomatic WPW. Clinicians can minimize the invasive risk by only performing ablation for patients with at-risk pathways.

Differential sequential septal pacing: a simple maneuver to differentiate nodal versus extranodal ventriculoatrial conduction.

BACKGROUND: Distinguishing retrograde nodal conduction from extranodal conduction using an accessory pathway (AP) can sometimes be challenging. OBJECTIVE: To distinguish nodal from extranodal ventriculoatrial (VA) conduction regardless of AP location by proposing a simple method. This method is based on the principle that moving the pacing site progressively from the basal region toward the entrance of the His-Purkinje system should shorten VA time for nodal but not for AP conduction. METHODS: Sixty-seven patients with supraventricular tachycardia were prospectively recruited. Quadripolar catheters were placed at the right ventricular (RV) apex, right atrium, and His and coronary sinus. The RV septum was sequentially paced at 4 sites: (1) basal, (2) high midventricle, (3) low midventricle, and (4) apex at a cycle length 100 ms shorter than the resting cycle length. The stimulus-to-atrial (SA) interval was measured by using the proximal coronary sinus atrial electrogram. RESULTS: Group 1 (n = 33) had nodal VA conduction; all patients had typical atrioventricular nodal reentrant tachycardia. Group 2 (n = 34) had extranodal VA conduction via an AP: 19 left-sided, 6 right-sided, and 9 posteroseptal. In group 1, the SA interval decreased significantly as pacing site moved closer toward the apex (site 1: 166 ± 35 ms, site 2: 153 ± 32 ms, site 3: 149 ± 32 ms, site 4: 154 ± 33 ms, P < .001, respectively, at sites 2-4 compared with site 1). In contrast, in group 2, the SA interval increased significantly toward the apex (site 1: 149 ± 45 ms, site 2: 158 ± 43 ms, site 3: 161 ± 43 ms, and site 4: 163 ± 40 ms, P < .001, respectively, at sites 2-4 compared with site 1). The SA interval at the high midventricular site (site 2) - SA interval at the base (site 1) ≤ 0 ms for nodal and > 0 ms for extranodal conduction had optimal sensitivity and specificity (nodal: selectivity = 97.0% and specificity = 85.3%; extranodal: selectivity = 85.3% and specificity = 97.0%). CONCLUSIONS: Differential sequential pacing of the RV septum reliably distinguishes retrograde atrioventricular nodal conduction from AP conduction.

Ventricular fibrillation induced by spontaneous hypothermia in a patient with early repolarization syndrome.

INTRODUCTION: The early repolarization (ER) pattern on ECG was originally described in the context of hypothermia. CASE SUMMARY: We present the case of a 34-year-old male with cardiac arrest in the context of spontaneous hypothalamic mediated thermal dysregulation after intracranial hemorrhage. Ventricular fibrillation with a marked ER pattern recurred with therapeutic hypothermia. Spontaneous hypothermia due to hypothalamic dysregulation was observed to enhance the amplitude of the ER pattern and was contemporaneous with recurrent ventricular fibrillation during follow-up. CONCLUSIONS: Hypothermia is an important trigger of VF in the setting of early repolarization syndrome, and warrants assessment as an environmental trigger of spontaneous events.

Voltage-guided ablation technique for cavotricuspid isthmus-dependent atrial flutter: refining the continuous line.

Ablation of the cavotricuspid isthmus has become first-line therapy for "isthmus-dependent" atrial flutter. The goal of ablation is to produce bidirectional cavotricuspid isthmus block. Traditionally, this has been obtained by creation of a complete ablation line across the isthmus from the ventricular end to the inferior vena cava. This article describes an alternative method used in our laboratory. There is substantial evidence that conduction across the isthmus occurs preferentially over discrete separate bundles of tissue. Consequently, voltage-guided ablation targeting only these bundles with large amplitude atrial electrograms results in a highly efficient alternate method for the interruption of conduction across the cavotricuspid isthmus. Understanding the bundle structure of conduction over the isthmus facilitates more flexible approaches to its ablation and targeting maximum voltages in our hands has resulted in reduction of ablation time and fewer recurrences.

Tachycardia induction with ventricular extrastimuli differentiates atypical atrioventricular nodal reentrant tachycardia from orthodromic reciprocating tachycardia.

BACKGROUND: Differentiating atypical atrioventricular nodal reentrant tachycardia (AVNRT) from septal orthodromic reentrant tachycardia (ORT(Septal)) is challenging in nonsustained tachycardia. When sustained, the postpacing interval minus tachycardia cycle length following entrainment (PPI(Entrainment) - TCL) and stimulation to atrial interval minus ventriculoatrial interval (Stim-A(Entrainment) - VA) are utilized. OBJECTIVE: We hypothesized that the first tachycardia cycle after tachycardia induction with right ventricular apical extrastimulation would yield comparable information to entrainment, precluding the need for sustained tachycardia. METHODS: Twenty-four patients with AVNRT (age 47 ± 18 years), 19 with ORT(Septal) (age 42 ± 17 years), and 15 with ORT over a left lateral accessory pathway (ORT(Left)) (age 41 ± 16 years) were included. The ventricular extrastimulus to atrial depolarization at tachycardia initiation (Stim-A(Initiation)) and tachycardia VA interval were measured to establish the Stim-A(Initiation) minus VA interval (Stim-A(Initiation) - VA). The ventricular extrastimulus to the subsequent right ventricular apical depolarization (postpacing interval at initiation, PPI(Initiation)) was utilized to obtain the PPI(Initiation) minus TCL (PPI(Initiation) - TCL). The AH interval associated with the PPI(Initiation) minus the AH in tachycardia was utilized to establish a corrected PPI(Initiation) minus TCL (cPPI(Initiation) - TCL). RESULTS: The intervals after tachycardia initiation were longer for AVNRT than for ORT: mean PPI(Initiation) - TCL (193 ± 44 vs 91 ± 73; P <.001), cPPI(Initiation) - TCL (174 ± 44 ms vs 88 ± 50 ms; P <.001), and Stim-A(Initiation) - VA (161 ± 45 ms vs 69 ± 53 ms; P <.001). The correlation coefficient for Stim-A(Initiation) minus VA against Stim-A(Entrainment) minus VA was 0.79 and for cPPI(Initiation) minus TCL against PPI(Entrainment) minus TCL was 0.71. cPPI(Initiation) minus TCL <115 ms or Stim-A(Initiation) - VA <85 ms was observed only in ORT. The converse was observed in AVNRT but also in ORT(Septal) over decremental accessory pathways and ORT(Left). CONCLUSION: Stim-A(Initiation) - VA < 85 ms or cPPI(Initiation) - TCL < 115 ms excludes AVNRT.

Determination of inadvertent atrial capture during para-Hisian pacing.

BACKGROUND: Inadvertent capture of the atrium will lead to spurious results during para-Hisian pacing. We sought to establish whether the stimulation-to-atrial electrogram interval at the proximal coronary sinus (stim-PCS) or high right atrium (stim-HRA) could signal inadvertent atrial capture. METHODS AND RESULTS: Para-Hisian pacing with and without intentional atrial capture was performed in 31 patients. Stim-HRA and stim-PCS intervals were measured with atrial capture, His plus para-Hisian ventricular (H+V) capture, and para-Hisian ventricular (V) capture alone. The mean stim-HRA interval was significantly shorter with atrial capture (66 ± 18 ms) than with H+V (121 ± 27 ms, P < 0.001) or V capture alone (174 ± 38 ms, P < 0.001). The mean stim-PCS interval was significantly shorter with atrial capture (51 ± 16 ms) than with H+V (92 ± 22 ms, P<0.001) or V capture alone (146 ± 33 ms, P < 0.001). A stim-PCS < 60 ms (stim-HRA < 70 ms) was observed only with atrial capture. A stim-PCS >90 ms (stim-HRA >100 ms) was observed only in the absence of atrial capture. A stim-HRA of < 85 ms was highly specific and stim-PCS of < 85 ms highly sensitive at identifying atrial capture. Stim-HRA intervals of 75 to 97 ms and stim-PCS intervals of 65 to 88 ms were observed with either atrial, His, or para-Hisian ventricular capture without atrial capture. In this overlap zone, all patients demonstrated a stim-PCS or stim-HRA interval prolongation of at least 20 ms when the catheter was advanced to avoid deliberate atrial pacing. The QRS morphology was of limited value in distinguishing atrial capture due to concurrent ventricular or H+V capture, as observed in 20 of 31 (65%) patients. CONCLUSIONS: Stim-PCS and stim-HRA intervals can be used to monitor for inadvertent atrial capture during para-Hisian pacing. A stim-PCS < 60 ms (or stim-HRA < 70 ms) and stim-PCS > 90 ms (or stim-HRA > 100 ms) were observed only with and without atrial capture, respectively, but there was significant overlap between these values. Deliberate atrial capture and loss of capture reliably identifies atrial capture regardless of intervals.

Entrainment for distinguishing atypical atrioventricular node reentrant tachycardia from atrioventricular reentrant tachycardia over septal accessory pathways with long-RP [corrected] tachycardia.

BACKGROUND: The response to right ventricular (RV) entrainment is useful to distinguish atypical AV node reentrant tachycardia from AV reentrant tachycardia using a septal accessory pathway. Whether entrainment can differentiate between AV node reentrant tachycardia and AV reentrant tachycardia in patients with long-RP tachycardia has not been systematically validated. METHODS AND RESULTS: Twenty-four patients with concealed septal accessory pathways who had an electrophysiology study between January 1, 2000, and January 1, 2010, were included (age, 38 ± 17 years; men, 17). Entrainment was performed from the RV apex pacing at cycle length 20 to 40 ms shorter than tachycardia cycle length (TCL). The mean TCL was 390 ± 80 ms, the mean AH interval during tachycardia was 151 ± 57 ms, and the mean ventriculoatrial (VA) time was 182 ± 103 ms. Twelve patients had typical accessory pathways (VA/TCL <40%), and 12 had slowly conducting accessory pathways (VA/TCL ≥ 40%). In all patients with typical accessory pathways, the postpacing interval minus the TCL (PPI-TCL) was <115 ms and the difference in the VA interval during pacing and tachycardia (StimA-VA) was <85 ms. On the other hand, in 6 of the 12 patients in the slowly conducting group, the PPI-TCL was >115 ms, and the StimA-VA was > 85 ms. CONCLUSIONS: Slowly conducting accessory pathways frequently yield RV entrainment criteria traditionally attributable to AV node reentry. Distinguishing AV node reentry from AV reentry in patients with long-RP tachycardia requires other criteria.

Complete antral encirclement is not required for pulmonary vein isolation.

BACKGROUND: Complete circumferential antral ablation may not be necessary for successful pulmonary vein (PV) isolation in patients with paroxysmal atrial fibrillation (AF). OBJECTIVE: We examined the feasibility of a noncircumferential approach limited to segments of the antra required for PV-atrial conduction. METHODS: During ablation for paroxysmal AF, each PV antrum was divided into six segments, and ablation was sequentially targeted to antral segments with the earliest activity until bidirectional isolation was achieved. Ablation at the ostium was avoided. Patients requiring complete circumferential ablation (circumferential group) were compared with those undergoing incomplete antral ablation (noncircumferential group) with respect to freedom from symptomatic atrial arrhythmia, procedure, and ablation times. RESULTS: Ninety-nine patients underwent ablation with successful isolation of PVs (n = 37 circumferential; n = 62 noncircumferential). There were no significant differences in age, gender, AF duration, or LA size. Procedure time (202 ± 45 vs. 185 ± 47 minutes; P = .06) and ablation time (51 ± 15 vs. 41 ± 14 minutes; P = .004) were shorter in the noncircumferential group. During follow-up (12 ± 6 months), freedom from symptomatic recurrence was 73% in both groups (P = .97), with organized atrial tachycardia being more common in the circumferential group (P = .06). In 22 patients undergoing repeat study, PV reconnection was demonstrated in 82% and 81% of PVs in each group. Reconnection in the noncircumferential group occurred in previously ablated segments in 10 (77%) of 13 cases. CONCLUSIONS: Noncircumferential antral ablation achieves similar success rates with shorter procedure and ablation times than circumferential ablation. Greater attention should be focused on producing permanent lesions rather than on completing antral encirclement after isolation is achieved.

Reduction of complex ventricular ectopy and improvement in exercise capacity with flecainide therapy in Andersen-Tawil syndrome.

Andersen-Tawil syndrome (ATS) is a rare inherited autosomal disorder characterized by the clinical triad of ventricular arrhythmias, hypokalaemic periodic paralyses, and skeletal developmental abnormalities, resulting in dysmorphic features. Although ATS patients have a high incidence of ventricular arrhythmias, the occurrence of sudden cardiac death is rare. In this report, we describe the successful use of flecainide in an ATS patient with a considerable ventricular arrhythmia burden who had not demonstrated any response to conventional beta-blocker therapy used in conjunction with potassium (K(+)) supplementation.

Characterization of electrograms associated with termination of chronic atrial fibrillation by catheter ablation.

OBJECTIVES: This study sought to determine the characteristics of atrial electrograms predictive of slowing or termination of atrial fibrillation (AF) during ablation of chronic AF. BACKGROUND: There is growing recognition of a role for electrogram-based ablation. METHODS: Forty consecutive patients (34 male, 59 +/- 10 years) undergoing ablation for chronic AF persisting for a median of 12 months (range 1 to 84 months) were included. After pulmonary vein isolation and roof line ablation, electrogram-based ablation was performed in the left atrium and coronary sinus. Targeted electrograms were acquired in a 4-s window and characterized by: 1) percentage of continuous electrical activity; 2) bipolar voltage; 3) dominant frequency; 4) fractionation index; 5) mean absolute value of derivatives of electrograms; 6) local cycle length; and 7) presence of a temporal gradient of activation. Electrogram characteristics at favorable ablation regions, defined as those associated with slowing (a >or=6-ms increase in AF cycle length) or termination of AF were compared with those at unfavorable regions. RESULTS: The AF was terminated by electrogram-based ablation in 29 patients (73%) after targeting a total of 171 regions. Ablation at 37 (22%) of these regions was followed by AF slowing, and at 29 (17%) by AF termination. The percentage of continuous electrical activity and the presence of a temporal gradient of activation were independent predictors of favorable ablation regions (p = 0.016 and p = 0.038, respectively). Other electrogram characteristics at favorable ablation regions were not significantly different from those at unfavorable ablation regions. CONCLUSIONS: Catheter ablation at sites displaying a greater percentage of continuous activity or a temporal activation gradient is associated with slowing or termination of chronic AF.

Effect of defibrillation testing on management during implantable cardioverter-defibrillator implantation.

BACKGROUND: Verification of defibrillation efficacy by defibrillation threshold (DFT) testing during implantable cardioverter-defibrillator implantation is the current standard. Generally, defibrillation of ventricular fibrillation at 10 J below the maximum output of a device is felt to establish an adequate safety margin. Nonetheless, DFT testing adds to cost and carries some potential for morbidity, whereas its impact on outcomes in the modern era of defibrillator technology is unclear. We aimed to determine the frequency that DFT testing resulted in a change at device implant and to identify clinical and echocardiographic predictors of the need for DFT testing. METHODS: We reviewed all implantable cardioverter-defibrillators that were implanted at the London Health Sciences Centre (Ontario, Canada) from June 1999 to August 2003 and used multivariate analysis to determine variables associated with DFT test failures and elevated DFT values. When a defibrillation failure was not observed, a lowest energy to defibrillate (LED) was recorded. RESULTS: Among 168 implants, DFT testing was successful with a minimum 10-J safety margin in 152 (90%), whereas the remaining 16 required changes at device implant. In a multivariate analysis, use of amiodarone was independently associated with DFT failure (odds ratio, 4.6; 95% confidence interval, 1.2-17.0). Significantly higher mean DFT/LED values were observed among patients on amiodarone (1.36 J; P = .0041). Those with nonischemic cardiomyopathy had a higher mean DFT/LED compared with those with ischemic cardiomyopathy (1.44 J; P = .028). CONCLUSIONS: Use of amiodarone is associated with a 4-fold increase in risk of DFT failure and subsequent need for changes at implant to achieve a safe threshold. Defibrillation threshold testing appears to be most useful for patients taking amiodarone.

Utility and cost effectiveness of temporary pacing using active fixation leads and an externally placed reusable permanent pacemaker.

Active-fixation leads and externally placed permanent pacemakers for temporary pacing may be beneficial because they allow for greater patient mobility and comfort and increased reliability of lead placement. The relative cost of this form of pacing may be prohibitive unless markedly prolonged pacing is required. Twenty patients (63 +/- 15 years of age, 15 men) underwent external "temporary permanent" pacing. Pacing duration and associated complications were recorded. Cost models were then constructed using data from the London Health Sciences Center business unit to compare the cost of traditional temporary pacing and this technique using a Medtronic KSR903 pacemaker and 5,076 leads. Direct costs were calculated based on the 2005 Ontario Health Insurance Plan fee schedule, combined with calculation of labor and materials. Pacing was undertaken for a median of 2 days (range 2 to 83). There were no complications during implantation or pacing or after system removal. Sensing was lost in only 1 instance, which was reprogrammed uneventfully. Cost comparison showed that, although active-fixation lead placement was initially more costly ($798.71 vs $471.91), the added reliability of the permanent system allowed ward telemetry instead of cardiac care unit monitoring. This resulted in cost equivalence after only 18 hours and conferred a cost savings of $456 per 24-hour period thereafter. As a result, a savings of $585.20 is projected for a modeled patient after 48 hours of temporary pacing. In conclusion, temporary pacing using this technique is a reliable and comfortable alternative to traditional temporary pacing and appears to be a cost-effective temporary pacing option after 18 hours.