Noninvasive predictors of perioperative atrial arrhythmias in patients with tetralogy of Fallot undergoing pulmonary valve replacement.

BACKGROUND: Patients with tetralogy of Fallot (TOF) have increased risk of atrial arrhythmias. HYPOTHESIS: A measure of atrial dispersion, the P-wave vector magnitude (Pvm), can identify patients at risk for perioperative atrial flutter (AFL) or intra-atrial re-entrant tachycardia (IART) in a large TOF cohort. METHODS: We performed a blinded, retrospective analysis of 158 TOF patients undergoing pulmonary valve replacement between 1997 and 2015. History of AFL/IART was documented using electrocardiogram, Holter monitor, exercise stress test, implanted cardiac device, and electrophysiology study. P-R intervals, Pvm, QRS duration, and QRS vector magnitude were assessed from resting sinus-rhythm 12-lead electrocardiograms and identification of those with AFL/IART was determined. RESULTS: Fourteen patients (8.9%) were found to have AFL/IART. Pvm, QRS duration, and QRS vector magnitude significantly differentiated those with AFL/IART from those without on univariate analysis: 0.09 ± 0.04 vs 0.18 ± 0.07 mV, 161.3 ± 21.9 vs 137.7 ± 31.4 ms, and 1.2 (interquartile range, 1.0-1.2) vs 1.6 mV (1.0-2.3), respectively (P < 0.05 for each). The Pvm had the highest area under the ROC curve (0.88) and was the only significant predictor on multivariate analysis, with odds ratio of 0.02 (95% confidence interval: 0.01-0.53). P-R duration, MRI volumes, and right-heart hemodynamics did not significantly differentiate those with vs those without AFL/IART. CONCLUSIONS: In TOF patients undergoing pulmonary valve replacement, Pvm has significant value in predicting those with perioperative AFL/IART. These clinical features may help further evaluate TOF patients at risk for perioperative atrial arrhythmias. Prospective studies are warranted.

Improved Ventricular Function after TEE-guided Cardioversion of Atrial Arrhythmias in Patients after the Fontan Operation.

OBJECTIVE: Atrial tachyarrhythmias frequently develop after the Fontan operation. Patients with Fontan physiology rely on atrial contribution to cardiac output, and thus control of atrial arrhythmias is important. Outcomes after cardioversion in patients after Fontan have not been reported. We sought to determine if cardioversion results in improved echocardiographic parameters or clinical symptomatology; and, discern risk factors for arrhythmia recurrence. DESIGN: We retrospectively analyzed the Mayo Clinic echocardiographic database to capture patients after the Fontan operation who underwent transesophageal echocardiography-guided electrical cardioversion from 2000-2015. Clinical and echocardiographic data were collected and compared at baseline and follow-up. RESULTS: Eight hundred ninety patients with prior Fontan operation underwent echocardiographic evaluation; 341 (38%) developed atrial arrhythmias. Thirty-six patients [20 males, median age 29 (12-51)] underwent transesophageal echocardiography-guided cardioversion of atrial arrhythmias [atrial flutter/intraatrial reentrant tachycardia (75%); atrial fibrillation (25%)]. At follow-up, improvements were noted in ejection fraction by 10% (P < .0001); atrioventricular valve regurgitation grade (39%) (P = .002); New York Heart Association (NYHA) class (61%) (P < .001); and resolution of spontaneous echo contrast in the Fontan circuit (65%) (P < .01). No embolic events occurred following cardioversion. Eighteen patients (50%) developed recurrent atrial arrhythmias at 15 (3-36) months after cardioversion. Five-year freedom from arrhythmia recurrence was 61%. Significant univariate predictors of arrhythmia recurrence were atrial flutter/intraatrial reentrant tachycardia (HR = 4.3, P = .02); NYHA ≥ II (HR = 4.1, P = .03); systemic right ventricle (HR = 5.2; P = .02); and ejection fraction ≤ 40% (HR = 2.8; P = .04). On multivariate analysis, only systemic right ventricle (HR = 3.7; P = .02) remained an independent predictor of arrhythmia recurrence. CONCLUSION: After the Fontan operation, cardioversion of atrial arrhythmias improves ventricular function, atrioventricular valve regurgitation grade, and NYHA class. Arrhythmia recurrence was common and patients with atrial flutter/intraatrial reentrant tachycardia, systemic right ventricle, or reduced ventricular function may be at risk of arrhythmia recurrence. Further studies are required to identify additional risk factors and protective factors for arrhythmia recurrence.

Mechanism of reentry induction by a 9-V battery in rabbit ventricles.

Although the application of a 9-V battery to the epicardial surface is a simple method of ventricular fibrillation induction, the fundamental mechanisms underlying this process remain unstudied. We used a combined experimental and modelling approach to understand how the interaction of direct current (DC) from a battery may induce reentrant activity within rabbit ventricles and its dependence on battery application timing and duration. A rabbit ventricular computational model was used to simulate 9-V battery stimulation for different durations at varying onset times during sinus rhythm. Corresponding high-resolution optical mapping measurements were conducted on rabbit hearts with DC stimuli applied via a relay system. DC application to diastolic tissue induced anodal and cathodal make excitations in both simulations and experiments. Subsequently, similar static epicardial virtual electrode patterns were formed that interacted with sinus beats but did not induce reentry. Upon battery release during diastole, break excitations caused single ectopics, similar to application, before sinus rhythm resumed. Reentry induction was possible for short battery applications when break excitations were slowed and forced to take convoluted pathways upon interaction with refractory tissue from prior make excitations or sinus beats. Short-lived reentrant activity could be induced for battery release shortly after a sinus beat for longer battery applications. In conclusion, the application of a 9-V battery to the epicardial surface induces reentry through a complex interaction of break excitations after battery release with prior induced make excitations or sinus beats.

Reentrant ventricular tachycardia originating from the periaortic region in the absence of overt structural heart disease.

BACKGROUND: In the absence of overt structural heart disease, most left ventricular outflow tract ventricular tachycardias (VTs) have a focal origin and are benign. We hypothesized that multiple morphologies (MMs) of inducible left ventricular outflow tract VT may indicate a scar-related VT that can mimic idiopathic VT. METHODS AND RESULTS: Of 54 consecutive patients referred for ablation of sustained outflow tract VT without overt structural heart disease, 24 had left ventricular outflow tract VT, 10 had MM VT, and 14 had a single VT (SM). The MM group were older (70.3±4.3 versus 53.9±15.9 years; P=0.004), had more hypertension (100% versus 29%; P=0.0006), and had longer PR intervals and QRS durations compared with the SM group. In contrast to the SM group, the MM group VTs had features consistent with reentry, including induction by programmed stimulation without isoproterenol, entrainment in some, and abnormal electrograms in the periaortic area. Periaortic region voltages suggested scar in the MM group, but not in the SM group. MRI in 2 MM patients was consistent with scar, but not in 10 SM patients. Longer radiofrequency applications were required in the MM group than in the SM group. At a median follow-up of 9.7 (3.0-32.0) months, recurrences tended to be more frequent in the MM group than in the SM group (70% versus 22%; P=0.07). CONCLUSIONS: VTs from small regions of periaortic scar can mimic idiopathic VT but are suggested by multiple VT morphologies and are more difficult to ablate. Whether these patients are at greater risk, as feared for other scar-related VTs, warrants further study.

Follow-up of a modified Fontan randomized trial for intraatrial reentrant tachycardia prophylaxis.

OBJECTIVE: Atrial arrhythmias represent significant morbidity and risk for mortality in Fontan patients. In a randomized trial involving patients undergoing a lateral tunnel Fontan between 1999 and 2001, Collins et al. investigated the safety and efficacy of a surgical atrial incision aimed at decreasing the incidence of intraatrial reentrant tachycardia (IART). The purpose of this study was to report the late follow-up of the aforementioned trial. DESIGN: All surviving patients previously enrolled in the randomized trial were eligible for this follow-up study. Patients' legal guardians were contacted for informed consent and data were obtained form a retrospective chart review. RESULTS: Of the 39 eligible patients, 29 were recruited: 15 in the intervention and 14 in the control groups. The median follow was 9.0 (1.2) years for the intervention group and 9.3 (1.1) years for the control group (P= .86). At most recent follow-up, there was no statistically significant difference in the demographic, echocardiographic, and electrophysiological data between the two groups. There was no late incidence of the primary outcome, IART. There were nine cases of late-onset sinus node dysfunction (SND): 5/15 in the intervention and 4/14 in the control groups (P= .99). There was only one late pacemaker implantation for early post-op SND. CONCLUSION: At late follow-up 9 years post-Fontan, IART had not occurred in either group. There was no evidence of late-onset complications related to the interventional atrial incision. Further follow-up is warranted for this cohort.

Focal initiation of sustained and nonsustained ventricular tachycardia in a canine model of ischemic cardiomyopathy.

INTRODUCTION: To define the role of focal and reentrant mechanisms underlying nonsustained (NSVT) and sustained ventricular tachycardia (SuVT) induced by programmed stimulation, 3-dimensional cardiac mapping was performed in 8 dogs with heart failure (HF) created by multiple intracoronary microsphere embolizations. METHODS AND RESULTS: Continuous recording from 232 intramural sites throughout the left and right ventricles and the interventricular septum was performed during programmed stimulation in the absence and presence of isoproterenol (Iso, 0.1 µg/kg/min). Sinus beats and the last extrastimuli preceding induced VT conducted with total activation times (TA) of 51 ± 10 and 111 ± 8 milliseconds, respectively, that did not change during Iso infusion (47 ± 4 and 109 ± 5 milliseconds, P = NS). NSVT was induced in 75% of HF dogs; SuVT was induced in 38%. In all cases, initiation and maintenance of SuVT and NSVT arose by a focal mechanism. Compared to NSVT, SuVT had a shorter coupling interval (CI; 150 ± 7 vs 186 ± 16, P < 0.05) and a predilection for certain critical subendocardial initiation sites (that were initiation sites for only 29% of NSVT beats). After 21-30 beats, acceleration of SuVT by a focal mechanism to a CI less than 120 milliseconds led to functional conduction delay (TA increasing from 111 ± 3 to 137 ± 3 milliseconds, P < 0.0001), intramural reentry, and transition to ventricular fibrillation. CONCLUSIONS: Thus, initiation of SuVT in a model of ischemic HF is due to a focal mechanism. However, subsequent acceleration of this focal mechanism can ultimately lead to functional conduction delay and development of intramural reentry.

Decremental accessory pathway conduction after ablation and antidromic atrioventricular reciprocating tachycardia 8 years after successful radiofrequency ablation.

INTRODUCTION: This is a rare case of antidromic reciprocating tachycardia developing 8 years after successful catheter ablation. RESULT: A 15-year-old girl had recurrence of palpitations 8 years after the ablation of manifest right posteroseptal accessory pathway. Atrial burst pacing revealed Wenckebach atrioventricular conduction with preexcitation. Wide QRS tachycardia with identical morphology to sinus rhythm associated with retrograde His potential recorded immediately after the V-wave was induced by isoproterenol infusion. Atrial premature stimulus applied at the identical timing of His potential advanced the subsequent ventricular beat and His potential. CONCLUSION: Catheter ablation may produce decremental accessory pathway conduction and rarely cause antidromic atrioventricular reciprocating tachycardia. This may be explained by a presence of "de novo" accessory pathway with decremental conduction properties that became manifest after the first ablation.

Wolff-Parkinson-White syndrome in the elderly: clinical and electrophysiological findings.

BACKGROUND: Screening for Wolff-Parkinson-White (WPW) syndrome is recommended in children and young adults. The aim of this study was to evaluate the clinical and electrophysiological characteristics of patent WPW syndrome in subjects > or =60 years of age. METHODS: Four-hundred and fifty-nine consecutive patients with WPW syndrome, aged 8-80 years, were recruited; 32 (7%) of these patients were > or =60 years of age. The clinical, electrophysiological and therapeutic data for these patients were evaluated. RESULTS: Sixteen men and 16 women, aged 60-81 years (67+/-4.5), were admitted for resuscitated sudden death (1), rapid atrial fibrillation (4), syncope (4), or junctional tachycardia (13); 10 patients were asymptomatic (10). Left lateral bundles of Kent were detected more frequently in patients over 60 years (56%) than in those<60 years of age (40.5%). Reciprocal tachycardia was induced in 58% of subjects<60 years of age and 53% of those > or =60 years old (difference not significant); atrial fibrillation was more frequent in subjects > or =60 years of age (37.5% vs. 19%) (p<0.05). The incidence of malignant forms of WPW syndrome was identical in older and younger subjects. Ablation of the accessory pathway was indicated 18 times; effective ablation of a left bundle of Kent required a second intervention more often in patients > or =60 years of age (22% vs. 5%) (p<0.05). CONCLUSION: WPW syndrome is not uncommon in subjects over 60 years of age (7%). Left lateral accessory pathways, that have similar conduction properties to those in much younger subjects, are common. Ablation of the bundle of Kent is often difficult but is indicated in symptomatic subjects or those with more serious forms of WPW syndrome.