Cardiac Society of Australia and New Zealand (CSANZ) Position Statement on the Follow-Up of Cardiovascular Implantable Electronic Devices 2022.

Recognising the need for a national approach for the recommended best practice for the follow-up of implanted cardiac rhythm devices to ensure patient safety, this document has been produced by the Cardiac Society of Australia and New Zealand (CSANZ). It draws on accepted practice standards and guidelines of international electrophysiology bodies. It lays out methodology, frequency, and content of follow-up, including remote monitoring; personnel, including physician, allied health, nursing and industry; paediatric and adult congenital heart patients; and special considerations including magnetic resonance imaging scanning, perioperative management, and hazard alerts.

Epidemiology and clinical characteristics of atrial fibrillation in patients with inherited heart diseases.

BACKGROUND: The prevalence and clinical course of atrial fibrillation (AF) in hypertrophic cardiomyopathy (HCM) is well described, though less so for other inherited cardiomyopathies (familial dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, left ventricular noncompaction); and inherited arrhythmia syndromes (long QT syndrome, Brugada syndrome or catecholaminergic polymorphic ventricular tachycardia [CPVT]). We examined the frequency, clinical characteristics and AF-related management and outcomes amongst this patient population. METHODS: We retrospectively studied consecutive probands with inherited cardiomyopathy (n = 962) and inherited arrhythmia syndromes (n = 195) evaluated between 2002 and 2018. RESULTS: AF was observed in 5% to 31% of patients, with the highest frequency in HCM. Age of AF onset was 45.8 ± 21.9 years in the inherited arrhythmia syndromes compared with 53.3 ± 15.3 years in the inherited cardiomyopathies, with four CPVT patients developing AF at a median age of 20 years. Overall, 11% of patients with AF had a transient ischemic attack or stroke of which a total of 80% were anticoagulated; with 48% of events occurring at a CHA2 DS2 -VASc < 2. Amongst sarcomere-positive HCM, AF was independently associated with age (odds ratio [OR], 1.05; 95% confidence interval [CI], 1.02-1.08; P = .0014), left atrial area (OR, 1.11; 95% CI, 1.05-1.17; P = .0005) and MYH7 variants (OR, 2.55; 95% CI, 1.16-5.61; P = .020). CONCLUSION: Up to one-third of inherited heart disease patients will develop AF. While common general population risk factors are key in patients with HCM, the genotype is independently associated with AF. Amongst inherited arrhythmia syndromes, AF is less common, though often occurs below the age of 50 years.

Recurrent immunosuppressive-responsive myocarditis in a patient with desmoplakin cardiomyopathy: a case report.

Background: Desmoplakin (DSP) cardiomyopathy is a rare genetic condition characterized by repeated inflammatory myocardial injury and is associated with ventricular arrhythmia and sudden cardiac death. Diagnosis is challenging and requires a combination of genetic testing and advanced imaging techniques. Case summary: We present the case of a 38-year-old woman with recurrent episodes of subclinical myocarditis. Investigation using cardiac magnetic resonance imaging (cMRI) and genetic testing revealed a diagnosis of DSP cardiomyopathy. Her disease was initially responsive to corticosteroid therapy but quickly relapsed when treatment was tapered. Management of her condition required significant immunosuppression and the subsequent insertion of an implantable cardiac defibrillator due to her risk of sudden cardiac death. Discussion: Cardiac MRI and genetic testing are key diagnostic techniques in the assessment of patients with recurrent myocarditis and cardiomyopathy. The management of cardiomyopathies with an inflammatory component is not completely understood; however, there is likely a key role for immune suppression therapies. Furthermore, there are several cardiomyopathy genetic variants including DSP which require careful risk stratification due to an increased risk of sudden cardiac death.

Left septal atrial tachycardias: electrocardiographic and electrophysiologic characterization of a paraseptal focus.

OBJECTIVE: The objective was to characterize the electrocardiographic and electrophysiological features of focal atrial tachycardia (FAT) originating from the left septum (LS). BACKGROUND: FAT is recognized to occur at predefined anatomic locations rather than randomly throughout the atria. We describe the ECG and EP features of ATs originating from the LS as an important site for apparent perinodal tachycardias. METHODS: Nine patients presenting with LS FAT from a consecutive series of 384 underwent EP/RFA for symptomatic FAT. RESULTS: The mean age was 56 ± 12 years; 7 female with symptoms for 36 ± 28 months. P wave morphology (PWM) was negative/positive in lead V1 and across the precordial leads and negative or negative/positive in inferior leads in all patients. Tachycardia was incessant in 6 out of 9 patients with a mean tachycardia cycle length 421 ± 56 milliseconds. His A was ahead of P wave in all patients (mean -15 ± 5 milliseconds) and earlier than CS proximal (mean 4 ± 9 milliseconds). Successful acute focal ablation achieved at a mean of 31 ± 12 milliseconds ahead of P wave with no recurrences at a mean follow-up of 30 ± 28 months. CONCLUSION: Although the left septum is an uncommon site for focal AT an awareness of this location for harboring foci is particularly important when mapping apparently right-sided septal tachycardias.

Longitudinal assessment of structural phenotype in Brugada syndrome using cardiac magnetic resonance imaging.

Background: Despite historically being considered a channelopathy, subtle structural changes have been reported in Brugada syndrome (BrS) on histopathology and cardiac magnetic resonance (CMR) imaging. It is not known if these structural changes progress over time. Objective: The study sought to assess if structural changes in BrS evolve over time with serial CMR assessment and to investigate the utility of parametric mapping techniques to identify diffuse fibrosis in BrS. Methods: Patients with a diagnosis of BrS based on international guidelines and normal CMR at least 3 years prior to the study period were invited to undergo repeat CMR. CMR images were analyzed de novo and compared at baseline and follow-up. Results: Eighteen patients with BrS (72% men; mean age at follow-up 47.4 ± 8.9 years) underwent serial CMR with an average of 5.0 ± 1.7 years between scans. No patients had late gadolinium enhancement (LGE) on baseline CMR, but 4 (22%) developed LGE on follow-up, typically localized to the right ventricular (RV) side of the basal septum. RV end-systolic volume increased over time (P = .04) and was associated with a trend toward reduction in RV ejection fraction (P = .07). Four patients showed a reduction in RV ejection fraction >10%. There was no evidence of diffuse myocardial fibrosis observed on parametric mapping. Conclusions: Structural changes may evolve over time with development of focal fibrosis, evidenced by LGE on CMR in a significant proportion of patients with BrS. These findings have implications for our understanding of the pathological substrate in BrS and the longitudinal evaluation of patients with BrS.

Right atrial remodeling is more advanced in patients with atrial flutter than with atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) and atrial flutter (AFL) are related arrhythmias with common triggers, yet in individual patients either AF or AFL often predominates. We performed detailed electrophysiologic (EP) and electroanatomic (EA) studies of the right atrium (RA) in patients with AF and AFL to determine substrate differences that may explain the preferential expression of AF/AFL in individual patients. METHODS: Patients with AF (n = 13) were compared to patients with persistent AFL (n = 10). Detailed studies were performed, and 3-dimensional electroanatomic mapping studies were created and the RA was divided into 4 segments for regional analysis. Global, septal, lateral, anterior, and posterior segments were compared for analysis of: bipolar voltage; proportion of low-voltage areas and areas of electrical silence; conduction times; and proportion of abnormal signals (fractionated signals and double potentials). RESULTS: Compared to patients with AF, patients with AFL had (1) lower bipolar voltage and an increase in the proportion of low-voltage areas; (2) an increase in the proportion of complex signals; and (3) prolongation of activation times. CONCLUSIONS: Patients with AFL showed more advanced remodeling than patients with AF with slowed conduction, lower voltage areas with regions of electrical silence, and a greater proportion of complex signals, particularly in the posterior RA. These changes facilitate the stabilization of AFL and may explain why some patients are more likely to develop AFL as a sustained clinical arrhythmia.

Electroanatomic remodeling of the left atrium in paroxysmal and persistent atrial fibrillation patients without structural heart disease.

INTRODUCTION: The nature of the atrial substrate thought to contribute toward maintaining atrial fibrillation (AF) outside the pulmonary veins remains poorly defined. Therefore, our objective was to determine whether patients with paroxysmal and persistent AF have an abnormal electroanatomic substrate within the left atrium (LA). METHODS AND RESULTS: Thirty-one patients with AF (17 paroxysmal AF and 14 persistent AF) were compared with 15 age-matched controls with left-sided supraventricular tachycardia (SVT). High-density 3-dimensional electroanatomic maps were created and the LA was divided into 8 segments for regional analysis. Bipolar voltage, conduction, and effective refractory periods (ERPs) of the posterior LA, left atrial appendage (LAA), and distal coronary sinus (CSd) and percentage complex signals were assessed. In the majority of LA regions, compared with controls, AF patients had: (1) lower mean voltage and a higher percentage low voltage; (2) slower conduction; and (3) more prevalent complex signals. Many of these changes were more marked in the persistent than the paroxysmal AF group. CONCLUSIONS: Patients with AF have lower regional voltage, increased proportion of low voltage, slowed conduction, and increased proportion of complex signals compared to controls. Many of these changes are more pronounced in persistent AF patients, suggesting there may be a progressive nature to the changes. Differences occurred in the absence of structural heart disease. These substrate abnormalities provide further insight into the progressive nature of atrial remodeling and the mechanisms involved in maintenance of AF.

Atrial electrical and structural remodeling associated with longstanding pulmonary hypertension and right ventricular hypertrophy in humans.

INTRODUCTION: Pulmonary hypertension (PH) is common to a range of cardiopulmonary conditions and is associated with atrial arrhythmias. However, little is known of the isolated atrial effects of PH and right atrial dilatation (RA) in humans. To avoid the confounding effects of PH-associated disease states, we performed detailed electrophysiological (EP) and electroanatomic (EA) mapping of the RA in patients with idiopathic PH. METHODS AND RESULTS: Eight PH patients (mean pulmonary arterial [PA] pressure 39.0 ± 15.8 mmHg) and 16 age-matched controls (mean PA pressure 11.5 ± 4.1 mmHg, P < 0.0001) were studied. Corrected sinus node recovery times (cSNRT), atrial effective refractory periods (ERPs), conduction delay at the crista terminalis (CT), and inducibility of atrial fibrillation (AF) were evaluated. EA mapping (pacing cycle length 600 and 300 milliseconds) was performed to determine RA global and regional voltage, conduction velocities, atrial activation times, fractionated electrograms and double potentials. Patients with PH demonstrated a prolongation in cSNRT without significant change in atrial ERP and an increase in AF inducibility. PH was associated with lower tissue voltage (1.8 ± 0.4 mV in PH vs 2.2 ± 0.4 mV in controls, P = 0.02), increased low voltage areas (13.7 ± 8.2% in PH vs 6.2 ± 3.7% in controls, P < 0.01) and the presence of electrically silent areas. Conduction velocities were slower (global 67.3 ± 5.6 cm/s vs 92.8 ± 4.0 cm/s, P < 0.001) and fractionated electrograms and double potentials were more prevalent (14.7 ± 4.4% vs 6.3 ± 4.1, P < 0.01) in PH compared with controls, respectively. CONCLUSION: Idiopathic PH is associated with RA remodeling characterized by: generalized conduction slowing with marked regional abnormalities; reduced tissue voltage; and regions of electrical silence. These changes provide important insights into the isolated effects of PH fundamental to a range of clinical conditions associated with AF.

Electroanatomic remodelling of the pulmonary veins associated with age.

AIMS: Increasing age is a significant risk factor for developing atrial fibrillation (AF). Pulmonary vein (PV) triggers are critical in the mechanism of AF, but little is known of the substrate changes that occur within the PVs with ageing. Therefore, we sought to identify whether ageing is associated with electroanatomic changes within the pulmonary veins. METHODS AND RESULTS: Twenty-five patients undergoing ablation for left-sided supraventricular tachycardia had high-density 3D electroanatomic maps of all four PVs created. Patients were divided into two groups: group 1 aged <50 years and group 2 aged >50 years. Mean-voltage (MV), % low-voltage (LV < 0.5 mV), conduction, signal complexity, and PV muscle sleeve length and diameter were assessed. Age was 33 ± 8 vs. 66 ± 8 years for groups 1 and 2, respectively (P < 0.001). Group 2 demonstrated: (i) lower MV within the PVs (1.66 ± 1.1 vs. 1.88 ± 1.1 mV, P < 0.001); (ii) increased % LV (5.0 vs. 1.1%, P < 0.001), and increased voltage heterogeneity within the PVs (65 ± 14 vs. 55 ± 8%, P < 0.05); (iii) regional and global conduction slowing in the PVs; and (iv) increased % complex signals within the PVs (1.4 vs. 0.4%, P = 0.009). There was no difference in PV sleeve length or diameter. CONCLUSION: Increasing age is associated with PV electroanatomic changes characterized by a significant reduction in PV voltage, conduction slowing, and increasing signal complexity. These observations provide new insights into the potential mechanisms behind the increased prevalence of AF with advancing age.

Atrial fibrillation management during septal myectomy for hypertrophic cardiomyopathy: A systematic review.

INTRODUCTION: Atrial fibrillation is common in patients with hypertrophic cardiomyopathy, and significantly impacts mortality and morbidity. In patients with atrial fibrillation undergoing septal myectomy, concomitant surgery for atrial fibrillation may improve outcomes. METHODS: A systematic review was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. All studies reporting the outcomes of combined septal myectomy and atrial fibrillation surgery were included. RESULTS: A total of 10 observational studies were identified, including 644 patients. Most patients had paroxysmal atrial fibrillation. The proportion with prior unsuccessful ablation ranged from 0 to 19%, and preoperative left atrial diameter ranged from 44 ± 17 to 52 ± 8 mm. Cox-Maze IV (n = 311) was the most common technique used, followed by pulmonary vein isolation (n = 222) and Cox-Maze III (n = 98). Patients with persistent or longstanding atrial fibrillation more frequently received Cox-Maze III/IV. Ranges of early postoperative outcomes included: mortality 0 to 7%, recurrence of atrial tachyarrhythmias 4.4 to 48%, cerebrovascular events 0 to 1.5%, and pacemaker insertion 3 to 21%. Long-term data was limited. Freedom from atrial tachyarrhythmias at 1 year ranged from 74% to 96%, and at 5 years from 52% to 100%. Preoperative predictors of late atrial tachyarrhythmia recurrence included left atrial diameter >45 mm, persistent or longstanding preoperative atrial fibrillation and longer atrial fibrillation duration. CONCLUSION: In patients with atrial fibrillation undergoing septal myectomy, the addition of ablation surgery adds low overall risk to the procedure, and likely reduces the risk of recurrent atrial fibrillation in the long term. Future randomised studies comparing septal myectomy with or without concomitant AF ablation are needed.

The role of genetic testing in diagnosis and care of inherited cardiac conditions in a specialised multidisciplinary clinic.

BACKGROUND: The diagnostic yield of genetic testing for inherited cardiac diseases is up to 40% and is primarily indicated for screening of at-risk relatives. Here, we evaluate the role of genomics in diagnosis and management among consecutive individuals attending a specialised clinic and identify those with the highest likelihood of having a monogenic disease. METHODS: A retrospective audit of 1697 consecutive, unrelated probands referred to a specialised, multidisciplinary clinic between 2002 and 2020 was performed. A concordant clinical and genetic diagnosis was considered solved. Cases were classified as likely monogenic based on a score comprising a positive family history, young age at onset, and severe phenotype, whereas low-scoring cases were considered to have a likely complex aetiology. The impact of a genetic diagnosis was evaluated. RESULTS: A total of 888 probands fulfilled the inclusion criteria, and genetic testing identified likely pathogenic or pathogenic (LP/P) variants in 330 individuals (37%) and suspicious variants of uncertain significance (VUS) in 73 (8%). Research-focused efforts identified 46 (5%) variants, missed by conventional genetic testing. Where a variant was identified, this changed or clarified the final diagnosis in a clinically useful way for 51 (13%). The yield of suspicious VUS across ancestry groups ranged from 15 to 20%, compared to only 10% among Europeans. Even when the clinical diagnosis was uncertain, those with the most monogenic disease features had the greatest diagnostic yield from genetic testing. CONCLUSIONS: Research-focused efforts can increase the diagnostic yield by up to 5%. Where a variant is identified, this will have clinical utility beyond family screening in 13%. We demonstrate the value of genomics in reaching an overall diagnosis and highlight inequities based on ancestry. Acknowledging our incomplete understanding of disease phenotypes, we propose a framework for prioritising likely monogenic cases to solve their underlying cause of disease.

Atrial electrical and structural changes associated with longstanding hypertension in humans: implications for the substrate for atrial fibrillation.

UNLABELLED: INTRODUCTION: Hypertension (HT) is the most common modifiable risk factor for atrial fibrillation (AF), yet little is known of the atrial effects of chronic HT in humans. We aimed to characterize the electrophysiologic (EP) and electroanatomic (EA) remodeling of the right atrium (RA) in patients with chronically treated systemic HT and left ventricular hypertrophy (LVH) without a history of AF. METHODS AND RESULTS: Twenty patients with (systolic BP 145 ± 10 mmHg) and without (BP 119 ± 11 mmHg, P < 0.01) systemic HT underwent detailed conventional EP and EA voltage and activation mapping. We measured RA refractoriness at the coronary sinus and high septum at cycle lengths (CLs) 600 and 450 ms, and RA conduction velocities, activation times, and voltages at a global and regional level at CLs 600 ms and 300 ms. HT was associated with slowing of global (73 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) and regional conduction velocity particularly in the posterior RA (70 ± 17 cm/s vs 96 ± 12 cm/s in controls, P < 0.01) at the crista terminalis (fractionation and double potentials in HT 72%± 4 vs 43%± 23 in controls, P = 0.04). Mean RA voltage was similar between the 2 groups, however HT was associated with an increase in areas of low voltage (<0.5 mV; HT 13% vs controls 9%, P = 0.04). Sustained AF was induced in 30% HT patients and no controls. CONCLUSION: Chronically treated systemic HT with LVH is accompanied by atrial remodeling characterized by: (i) global conduction slowing, (ii) regional conduction delay particularly at the crista terminalis, and (iii) increased AF inducibility. These changes may in part be responsible for the increased propensity to AF associated with systemic HT.

Low risk of major complications associated with pulmonary vein antral isolation for atrial fibrillation: results of 500 consecutive ablation procedures in patients with low prevalence of structural heart disease from a single center.

OBJECTIVES: To report the major complication rate associated with pulmonary vein antral isolation (PVAI) in a consecutive series of 500 patients from a single center. BACKGROUND: Catheter ablation for atrial fibrillation (AF) is an established procedure for refractory AF. However, the risk of major complications has been reported to range from 3.9% to 4.5% and continues to represent a cause for concern. We hypothesized that these studies may have overestimated the rate of major complications associated with PVAI in patients with a low prevalence of structural heart disease (SHD). METHODS: Data were prospectively collected from 500 consecutive AF ablation procedures on 424 patients (mean age 55 ± 11 years, 79% men, paroxysmal AF-80% and persistent AF-20%, CHADS2 scores of 0, 1, 2, 3 present in 64%, 28%, 7%, 1%, respectively), performed between July 2006 and September 2009. All procedures were performed under general anesthesia with intraoperative transesophageal echo. PVAI was performed using a nonfluoroscopic mapping system with an endpoint of PV isolation. Adjunctive left atrial ablation was performed in 21% of patients only. Major complications were defined from a compilation of those reported in 5 prior studies reporting complications. RESULTS: In 500 procedures, there were no instances of death, stroke/TIA, cardiac tamponade, atrioesophageal fistula, or PV stenosis. Major complications occurred in 4 procedures (0.8%): esophageal hematoma (TEE probe)--2; pharyngeal trauma--1; and retroperitoneal hematoma-1. CONCLUSIONS: AF ablation can be performed safely in young patients without structural heart disease with a low risk (<1%) of major complications when using a strategy of PVAI.

Electroanatomic properties of the pulmonary veins: slowed conduction, low voltage and altered refractoriness in AF patients.

INTRODUCTION: Rapid PV activity is critical in initiating and maintaining AF. The underlying substrate responsible for this remains uncertain. We sought to identify if patients with paroxysmal (PAF) and persistent atrial fibrillation (PeAF) have an abnormal substrate within the pulmonary veins (PVs). METHODS AND RESULTS: Thirty-nine patients with AF (21 PAF, 18 PeAF) were compared with 15 age-matched controls with left-sided accessory pathways (AVRT). High-density 3D electroanatomic maps of the PVs were created. PV voltage, conduction, PV muscle sleeve length, effective refractory periods (ERPs) of the PVs, posterior left atrium (PLA), left atrial appendage (LAA) and distal coronary sinus (CSd), and signal complexity were assessed. Compared with controls, the PVs of AF patients had (1) lower mean-voltage and a higher % low-voltage; (2) shorter PV muscle sleeves; (3) slower conduction; (4) shorter ERP; and (5) more prevalent complex signals. Compared with the PAF group, the PeAF group had (1) higher % low voltage; (2) slower conduction; and (3) more complex signals. In PAF patients, the PLA and LAA ERPs were longer than controls and the PV ERP was shorter than controls; in PeAF patients PLA and LAA ERPs were reduced, but to a lesser extent than in the PVs. AF induction occurred during PV ERP testing in both AF groups, but not controls. CONCLUSIONS: PAF and PeAF patients demonstrate electrical and electroanatomic remodeling of the PVs compared to control patients without prior AF. Some of these changes were more marked in PeAF.

The relationship between complex fractionated electrograms and atrial low-voltage zones during atrial fibrillation and paced rhythm.

AIMS: Mapping of atrial fibrillation (AF) involves identification of low-voltage regions associated with complex fractionated electrograms (CFE) which theoretically represent abnormal substrate and targets for ablation. Whether low-voltage CFE areas also identify abnormal substrate during paced rhythm is unknown. METHODS AND RESULTS: Twelve patients with persistent AF undergoing ablation of AF had high-density three-dimensional electroanatomic maps created during AF and paced rhythm (24 maps) and the mean voltage during AF and paced rhythm was compared for eight segments of the left atrium (LA). The following were correlated during AF and paced rhythm: regional mean voltage; %low voltage (defined as <0.5 mV); and extent of CFE. In addition, the relationship between the extent of CFE in AF: (i) %low voltage and (ii) conduction during paced rhythm were determined. Mean voltage was lower during AF than paced rhythm for all regions and globally (0.7 ± 0.2 mV vs. 2.1 ± 0.6 mV, P < 0.001). The regional and overall %low voltage of the LA was greater during AF than paced rhythm (53 ± 19% vs. 9 ± 2%, P < 0.001). There was no correlation between mean voltage or %low voltage during AF and paced rhythm. Complex fractionated electrograms were prevalent throughout all regions during AF, but did not correlate with %low voltage, fractionation, or slowed conduction during paced rhythm. CONCLUSION: Areas of CFE and low voltage recorded during AF frequently demonstrate normal atrial myocardial characteristics (normal conduction, electrograms, and voltage) during sinus rhythm. Therefore, AF CFE sites do not necessarily identify regions of an abnormal atrial substrate. However, this does not exclude the possibility that CFE might identify a focal driver or source occurring in a region of normal atrial myocardium.

Long-term outcome following ablation of atrial flutter occurring late after atrial septal defect repair.

AIMS: In patients with surgical atrial septal defect (ASD) repair, late atrial flutters (AFLs), including cavotricuspid isthmus (CTI)-dependent and non-CTI-dependent scar-related flutter (AFL), are common. Radiofrequency ablation (RFA) of these arrhythmias has a high acute success rate. We aimed to characterize the long-term freedom from atrial arrhythmias in this population. METHODS: Twenty consecutive patients undergoing RFA for AFL late after ASD repair were included. Electrophysiological assessment included multipolar activation, entrainment, and electroanatomic mapping. Clinical, electrocardiograph, and Holter monitoring follow-up was conducted every 6 months. RESULTS: Mean age was 53 ± 13 years. Time from surgical repair to RFA was 29 ± 15 years. All patients had CTI-dependent AFL (20/20). There were 1.6 ± 0.7 arrhythmias per patient; other arrhythmias included non-CTI-dependent AFL (14), focal atrial tachycardia (two), and atrioventricular nodal reentry tachycardia (two) . Acute success was obtained in 100%. Five patients with recurrent AFL (three CTI dependent, two non-CTI dependent) at 13 ± 8 months had successful repeat RFA. At 3.2 ± 1.6 years follow-up since the last procedure, 90% of patients with successful RFA for AFL remained free of their clinical arrhythmia. However, 30% of the original 20 patients had documented atrial fibrillation (AF) 2.1 ± 1.6 years after the last procedure; five (25%) required AF intervention. One stroke (5%) occurred in the context of late AF. CONCLUSION: RFA of AFL occurring late after surgical ASD repair has a low long-term risk of recurrence, although 25% of patients required two procedures. However, there is a high late incidence of AF (30%), with an additional 25% of patients requiring intervention for AF.

Stroke risk and antithrombotic strategies in atrial fibrillation.

BACKGROUND AND PURPOSE: Although the stroke rate associated with atrial fibrillation has declined over the last 10 years, the emerging atrial fibrillation epidemic threatens to increase the incidence of cardioembolic stroke. Summary of Review-Oral anticoagulants are superior antithrombotic agents but are underused due to fear of bleeding and uncertainty about which patients will benefit. Individualized decisions on antithrombotic therapy require balancing the competing risks of thromboembolism and bleeding. The CHADS2 (Congestive heart failure, Hypertension, Age > 75 years, and Diabetes mellitus, and 2 points for prior Stroke/transient ischemic attack) score and other schemes provide an estimate of thromboembolic risk; however, the external validity of these estimates in the context of well-controlled risk factors, or a hypercoagulable state, is uncertain. Moreover, it is very difficult to estimate bleeding risk. Recent studies highlight the need for meticulous international normalized ratio control to achieve optimal outcomes hampered by the high bleeding risk during oral anticoagulant inception and other limitations of warfarin. Dabigatran is at least as efficacious as warfarin in preventing stroke and systemic embolism for patients in whom the risk of thromboembolism outweighs bleeding risk. In addition, the results of ongoing trials evaluating alternative anticoagulants such as oral anti-Xa agents are awaited. In this review, we discuss emerging therapies including available and completed trials of direct antithrombins and anti-Xa agents, including ximelagatran, idraparinaux, and dabigatran; and new device therapies including left atrial appendage occlusion devices. CONCLUSIONS: In light of these promising new therapies, it is likely that atrial fibrillation thromboembolism guidelines will need to be rewritten and frequently updated.

Vagal paroxysmal atrial fibrillation: prevalence and ablation outcome in patients without structural heart disease.

INTRODUCTION: The prevalence of vagal and adrenergic atrial fibrillation (AF) and the success rate of pulmonary vein isolation (PVI) are not well defined. We investigated the prevalence of vagal and adrenergic AF and the ablation success rate of antral pulmonary vein isolation (APVI) in patients with these triggers compared with patients with random AF. METHODS AND RESULTS: Two hundred and nine consecutive patients underwent APVI due to symptomatic drug refractory paroxysmal AF. Patients were diagnosed as vagal or adrenergic AF if >90% of AF episodes were related to vagal or adrenergic triggers; otherwise, a diagnosis of random AF was made. Clinical, electrocardiogram (ECG), and Holter follow-up was every 3 months in the first year and every 6 months afterward and for symptoms. Of 209 patients, 57 (27%) had vagal AF, 14 (7%) adrenergic AF, and 138 (66%) random AF. Vagal triggers were sleep (96.4%), postprandial (96.4%), late post-exercise (51%), cold stimulus (20%), coughing (7%), and swallowing (2%). At APVI, 94.3% of patients had isolation of all veins. Twenty-five (12%) patients had a second APVI. At a follow-up of 21 +/- 15 months, the percentage of patients free of AF was 75% in the vagal group, 86% in the adrenergic group, and 82% for random AF (P = 0.51). CONCLUSION: In patients with PAF and no structural heart disease referred for APVI, vagal AF is present in approximately one quarter. APVI is equally effective in patients with vagal AF as in adrenergic and random AF.

Long-term outcome following successful catheter ablation of atrial tachycardia originating from the pulmonary veins: absence of late atrial fibrillation.

OBJECTIVES: This study aimed to characterize the long-term outcome and incidence of atrial fibrillation (AF) in patients following catheter ablation of focal atrial tachycardia (AT) from the pulmonary veins (PV). BACKGROUND: Although both AT and AF may originate from ectopic foci within PVs, it is unknown whether PV AT patients subsequently develop AF. METHODS: Twenty-eight patients with 29 PV ATs (14%) from a consecutive series of 194 patients who underwent RFA for focal AT were included. Patients with concomitant AF prior to the index procedure were excluded. RESULTS: The minimum follow-up duration was 4 years; mean age 38 +/- 18 years with symptoms for 6.5 +/- 10 years, having tried 1.5 +/- 0.9 antiarrhythmic drugs. The distribution of foci was: left superior 12 (41%), right superior 10 (34%), left inferior 5 (17%), and right inferior 2 (7%). The focus was ostial in 93% and 2-4 cm distally within the vein in 7%. Mean tachycardia cycle length was 364 +/- 90 ms. Focal ablation was performed in 25 of 28 patients. There were 6 recurrences with 5 from the original site. Twenty-six patients were available for long-term clinical follow-up. At a mean of 7.2 +/- 2.1 years, 25 of 26 (96%) were free from recurrence off antiarrhythmic drugs. No patients developed AF. CONCLUSIONS: Focal ablation for tachycardia originating from the PVs is associated with long-term freedom from both AT and AF. Therefore, although PV AT and PV AF share a common anatomic distribution, PV AT is a distinct clinical entity successfully treated with focal RFA and not associated with AF in the long term.

Linear ablation of right atrial free wall flutter: demonstration of bidirectional conduction block as an endpoint associated with long-term success.

INTRODUCTION: Ablation for atypical atrial flutter (AFL) is often performed during tachycardia, with termination or noninducibility of AFL as the endpoint. Termination alone is, however, an inadequate endpoint for typical AFL ablation, where incomplete isthmus block leads to high recurrence rates. We assessed conduction block across a low lateral right atrial (RA) ablation line (LRA) from free wall scar to the inferior vena cava (IVC) or tricuspid annulus in 11 consecutive patients with atypical RA free wall flutter. METHOD AND RESULTS: LRA block was assessed following termination of AFL, by pacing from the ablation catheter in the low lateral RA posterior to the ablation line and recording the sequence and timing of activation anterior to the line with a duodecapole catheter, and vice versa for bidirectional block. LRA block resulted in a high to low activation pattern on the halo and a mean conduction time of 201 +/- 48 ms to distal halo. LRA conduction block was present in only 2 out of 6 patients after termination of AFL by ablation. Ablation was performed during sinus rhythm (SR) in 9 patients to achieve LRA conduction block. No recurrence of AFL was observed at long-term follow-up (22 +/- 12 months); 3 patients developed AF. CONCLUSION: Termination of right free wall flutter is often associated with persistent LRA conduction and additional radiofrequency ablation (RFA) in SR is usually required. Low RA pacing may be used to assess LRA conduction block and offers a robust endpoint for atypical RA free wall flutter ablation, which results in a high long-term cure rate.