Chang Sheng Ma

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: Definition, characterization, and clinical implication

The atria provide an important contribution to cardiac function [1], [2]. Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. Atrial myocardium is affected by many cardiac and non-cardiac conditions [3] and is, in some respects, more sensitive than ventricular [4]. The atria are activated, besides the three specialised intermodal tracts [5], [6], through working cardiomyocytes, so that any architectural or structural change in the atrial myocardium may cause significant electrophysiological disturbances. In addition, atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli [3] and are susceptible to a range of genetic influences [7]. Responses include atrial cardiomyocyte hypertrophy and contractile dysfunction, arrhythmogenic changes in cardiomyocyte ion-channel and transporter function, atrial fibroblast proliferation, hyperinnervation, and thrombogenic changes [2]. Thus, atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk [1], [8]. n nVentricular cardiomyopathies have been well classified; however, a definition and detailed analysis of ‘atrial cardiomyopathy’ is lacking from the literature. The purpose of the present consensus report, prepared by a working group with representation from the European Heart Rhythm Association (EHRA), the Heart Rhythm Society (HRS), the Asian Pacific Heart Rhythm Society (APHRS), and Sociedad Latino Americana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE), was to define atrial cardiomyopathy, to review the relevant literature, and to consider the impact of atrial cardiomyopathies on arrhythmia management and stroke. n n1.1. Definition of atrial cardiomyopathy nThe working group proposes the following working definition of atrial cardiomyopathy: ‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’ (Table 1). n n n nTable 1 n nDefinition of atrial cardiomyopathy. n n n nMany diseases (like hypertension, heart failure, diabetes, and myocarditis) or conditions (like ageing and endocrine abnormalities) are known to induce or contribute to an atrial cardiomyopathy. However, the induced changes are not necessarily disease-specific and pathological changes often share many similarities [9], [10]. The extent of pathological changes may vary over time and atrial location, causing substantial intraindividual and interindividual differences. In addition, while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. There is no presently accepted histopathological classification of atrial pathologies. Therefore, we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies (Table 1; Fig. 1). We use the acronym EHRAS (for EHRA/HRS/ APHRS/SOLAECE), defining four classes: (I) principal cardiomyocyte changes [11], [12], [13], [14], [15]; (II) principally fibrotic changes [10], [14], [16]; (III) combined cardiomyocyte-pathology/fibrosis [9], [11], [12]; (IV) primarily non-collagen infiltration (with or without cardiomyocyte changes) [17], [18], [19]. This simple classification may help to convey the primary underlying pathology in various clinical conditions. The EHRAS class may vary over time and may differ at atrial sites in certain patients. Thus, this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV (Table 2). The classification may be useful to describe pathological changes in biopsies and to correlate pathologies with results obtained from imaging technologies etc. In the future, this may help to define a tailored therapeutic approach in atrial fibrillation (AF) (Fig. 1, Fig. 2, Fig. 3). n n n nFig. 1 n nHistological and pathopysiological classification of atrial cardiomyopathies (EHRA/HRS/APHRS/SOLAECE): EHRAS classification. The EHRAS class may vary over time in the cause of the disease and may differ at various atrial sites. Of note, the nature of ... n n n n n nFig. 2 n n(A) EHRAS Class I (biopsy): there are severe changes affecting ‘primarily’ the cardiomyocytes in terms of cell hypertrophy and myocytolysis; fibrosis is much less evident than myocyte modifications. (B) EHRAS Class II (biopsy): cardiomyocyte ... n n n n n nFig. 3 n nEHRAS Class IV (autopsy heart): this image shows a myocardial interstitial with some fibrosis but prominent amyloid (AL type) deposition (left-hand side, congo red staining under regular light microscope; right-hand side, congo red staining under polarised ... n n n n n nTable 2 n nEHRAS classification of atrial cardiomyopathy. n n n n n n2. Anatomical considerations and atrial muscular architecture n2.1. Normal atrial structures n n n2.1.1. Gross morphology nEach atrium has a morphologically characteristic atrial body and appendage (Fig. 4). In the body, there is a venous component with the orifices of the systemic or pulmonary veins (PVs) and a vestibular component that surrounds the atrial outlet [20]. The interatrial septum (IAS) separates the atrial bodies. The venous component of the left atrium (LA) is located posterosuperiorly and receives the PVs at the four corners, forming a prominent atrial dome. The LA is situated more posteriorly and superiorly than the right atrium separated by the obliquity of the plane of the IAS [21]. n n n nFig. 4 n nSchematic representations and heart dissections to show the arrangement of the myocardial strands in the superficial parts of the walls. (A) The dissection viewed from the anterior aspect display the interatrial muscle Bachmann bundle and its bifurcating ... n n n nThe LA appendage (LAA) is smaller than the right atrium appendage (RAA). Narrower and with different shapes has a distinct opening to the atrial body and overlies the left circumflex coronary artery. Its endocardial aspect is lined by a complex network of muscular ridges and mem-branes [22], [23]. Different LAA morphologies have been described, and it appears that LAA morphology correlates with the risk of thrombogenesis [24]. n nBachmann׳s bundle is a broad epicardial muscular band running along the anterior wall of both atria (Fig. 4). The rightward arms extend superiorly towards the sinus node and inferiorly towards the right atrioventricular groove, while the leftward arms blend with deeper myofibres to pass around the neck of the LAA and reunite posteriorly to join the circumferential vestibule of the LA. The walls of LA are non-uniform in thickness (1–15xa0mm) and thicker than the right atrium [25].

Antithrombotic therapy use in patients with atrial fibrillation before the era of non-vitamin K antagonist oral anticoagulants: the Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF) Phase I cohort

Aims The introduction of non-VKA oral anticoagulants (NOACs), which differ from the earlier vitamin K antagonist (VKA) treatments, has changed the approach to stroke prevention in atrial fibrillation (AF). GLORIA-AF is a prospective, global registry programme describing the selection of antithrombotic treatment in newly diagnosed AF patients at risk of stroke. It comprises three phases: Phase I, before the introduction of NOACs; Phase II, during the time of the introduction of dabigatran, the first NOAC; and Phase III, once NOACs have been established in clinical practice. Methods and results In Phase I, 1063 patients were eligible from the 1100 enrolled (54.3% male; median age 70 years); patients were from China (67.1%), Europe (EU; 27.4%), and the Middle East (ME; 5.6%). The majority of patients using VKAs had high stroke risk (CHA2DS2-VASc ≥ 2; 86.5%); 13.5% had moderate risk (CHA2DS2-VASc = 1). Vitamin K antagonist use was higher for persistent/permanent AF (47.7%) than that for paroxysmal (23.9%). Most patients in China were treated with antiplatelet agents (53.7%) vs. 27.1% in EU and 28.8% in ME. In China, 25.9% of patients had no antithrombotic therapy, vs. 8.6% in EU and 8.5% in ME. Conclusion Phase I of GLORIA-AF shows that VKAs were mostly used in patients with persistent/permanent (vs. paroxysmal) AF and in those with high stroke risk. Furthermore, there were meaningful geographical differences in the use of VKA therapy in the era before the availability of NOACs, including a much lower use of VKAs in China, where most patients either received antiplatelet agents or no antithrombotic treatment.

EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication.

The atria provide an important contribution to cardiac function [1], [2]. Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. Atrial myocardium is affected by many cardiac and non-cardiac conditions [3] and is, in some respects, more sensitive than ventricular [4]. The atria are activated, besides the three specialised intermodal tracts [5], [6], through working cardiomyocytes, so that any architectural or structural change in the atrial myocardium may cause significant electrophysiological disturbances. In addition, atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli [3] and are susceptible to a range of genetic influences [7]. Responses include atrial cardiomyocyte hypertrophy and contractile dysfunction, arrhythmogenic changes in cardiomyocyte ion-channel and transporter function, atrial fibroblast proliferation, hyperinnervation, and thrombogenic changes [2]. Thus, atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk [1], [8]. n nVentricular cardiomyopathies have been well classified; however, a definition and detailed analysis of ‘atrial cardiomyopathy’ is lacking from the literature. The purpose of the present consensus report, prepared by a working group with representation from the European Heart Rhythm Association (EHRA), the Heart Rhythm Society (HRS), the Asian Pacific Heart Rhythm Society (APHRS), and Sociedad Latino Americana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE), was to define atrial cardiomyopathy, to review the relevant literature, and to consider the impact of atrial cardiomyopathies on arrhythmia management and stroke. n n1.1. Definition of atrial cardiomyopathy nThe working group proposes the following working definition of atrial cardiomyopathy: ‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’ (Table 1). n n n nTable 1 n nDefinition of atrial cardiomyopathy. n n n nMany diseases (like hypertension, heart failure, diabetes, and myocarditis) or conditions (like ageing and endocrine abnormalities) are known to induce or contribute to an atrial cardiomyopathy. However, the induced changes are not necessarily disease-specific and pathological changes often share many similarities [9], [10]. The extent of pathological changes may vary over time and atrial location, causing substantial intraindividual and interindividual differences. In addition, while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. There is no presently accepted histopathological classification of atrial pathologies. Therefore, we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies (Table 1; Fig. 1). We use the acronym EHRAS (for EHRA/HRS/ APHRS/SOLAECE), defining four classes: (I) principal cardiomyocyte changes [11], [12], [13], [14], [15]; (II) principally fibrotic changes [10], [14], [16]; (III) combined cardiomyocyte-pathology/fibrosis [9], [11], [12]; (IV) primarily non-collagen infiltration (with or without cardiomyocyte changes) [17], [18], [19]. This simple classification may help to convey the primary underlying pathology in various clinical conditions. The EHRAS class may vary over time and may differ at atrial sites in certain patients. Thus, this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV (Table 2). The classification may be useful to describe pathological changes in biopsies and to correlate pathologies with results obtained from imaging technologies etc. In the future, this may help to define a tailored therapeutic approach in atrial fibrillation (AF) (Fig. 1, Fig. 2, Fig. 3). n n n nFig. 1 n nHistological and pathopysiological classification of atrial cardiomyopathies (EHRA/HRS/APHRS/SOLAECE): EHRAS classification. The EHRAS class may vary over time in the cause of the disease and may differ at various atrial sites. Of note, the nature of ... n n n n n nFig. 2 n n(A) EHRAS Class I (biopsy): there are severe changes affecting ‘primarily’ the cardiomyocytes in terms of cell hypertrophy and myocytolysis; fibrosis is much less evident than myocyte modifications. (B) EHRAS Class II (biopsy): cardiomyocyte ... n n n n n nFig. 3 n nEHRAS Class IV (autopsy heart): this image shows a myocardial interstitial with some fibrosis but prominent amyloid (AL type) deposition (left-hand side, congo red staining under regular light microscope; right-hand side, congo red staining under polarised ... n n n n n nTable 2 n nEHRAS classification of atrial cardiomyopathy. n n n n n n2. Anatomical considerations and atrial muscular architecture n2.1. Normal atrial structures n n n2.1.1. Gross morphology nEach atrium has a morphologically characteristic atrial body and appendage (Fig. 4). In the body, there is a venous component with the orifices of the systemic or pulmonary veins (PVs) and a vestibular component that surrounds the atrial outlet [20]. The interatrial septum (IAS) separates the atrial bodies. The venous component of the left atrium (LA) is located posterosuperiorly and receives the PVs at the four corners, forming a prominent atrial dome. The LA is situated more posteriorly and superiorly than the right atrium separated by the obliquity of the plane of the IAS [21]. n n n nFig. 4 n nSchematic representations and heart dissections to show the arrangement of the myocardial strands in the superficial parts of the walls. (A) The dissection viewed from the anterior aspect display the interatrial muscle Bachmann bundle and its bifurcating ... n n n nThe LA appendage (LAA) is smaller than the right atrium appendage (RAA). Narrower and with different shapes has a distinct opening to the atrial body and overlies the left circumflex coronary artery. Its endocardial aspect is lined by a complex network of muscular ridges and mem-branes [22], [23]. Different LAA morphologies have been described, and it appears that LAA morphology correlates with the risk of thrombogenesis [24]. n nBachmann׳s bundle is a broad epicardial muscular band running along the anterior wall of both atria (Fig. 4). The rightward arms extend superiorly towards the sinus node and inferiorly towards the right atrioventricular groove, while the leftward arms blend with deeper myofibres to pass around the neck of the LAA and reunite posteriorly to join the circumferential vestibule of the LA. The walls of LA are non-uniform in thickness (1–15xa0mm) and thicker than the right atrium [25].

Regional Differences in Antithrombotic Treatment for Atrial Fibrillation: Insights from the GLORIA-AF Phase II Registry

Introduction u2003Although guideline-adherent antithrombotic therapy (ATT) for stroke prevention in atrial fibrillation (AF) is associated with lower mortality and thromboembolism, ATT uptake shows geographic variation worldwide. We aimed to assess thromboembolic risk and baseline ATT by geographic region and identify factors associated with prescription of ATT in a large, truly global registry of patients with recently diagnosed AF. Methods and Results u2003Our analysis comprises 15,092 patients newly diagnosed with non-valvular AF at risk for stroke, enrolled in Phase II of Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF). Global oral anticoagulation (OAC) use was 79.9%, being highest in Europe (90.1%), followed by Africa/Middle East (87.4%) and Latin America (85.3%), North America (78.3%) and Asia (55.2%). Among OAC users, vitamin K antagonists (VKAs) have been replaced by non-VKA OACs (NOACs) as the more prevalent OAC option in all regions, with highest use in North America (66.5%) and lowest in Asia (50.2%). In Asia, OAC was 80.4% in community hospitals but only 49.8% in university hospitals and 42.6% in specialist offices, and varied from 21.0% in China to 89.7% in Japan (NOACs at 5.8% in China and 83.3% in Japan). Globally, 76.5% of low-risk patients were prescribed ATT (46.1% OAC), whereas 17.7% high-risk patients were not anticoagulated (Europe 8.8%; North America 18.9%; Asia 42.4%). Conclusion u2003Substantial inter- and intra-regional differences in ATT for stroke prevention in AF are evident in this global registry. While guideline-adherent ATT can be further improved, NOACs are the main contributor to high OAC use worldwide.

Predictors of recurrence after a repeat ablation procedure for paroxysmal atrial fibrillation: role of left atrial enlargement

AIMSnThis study sought to explore the predictors of recurrence in patients with paroxysmal atrial fibrillation (AF) undergoing repeat catheter ablation, especially the impact of left atrial (LA) remodelling after the original procedure on the outcome of repeat procedure.nnnMETHODS AND RESULTSnNinety-five patients undergoing repeat ablation were enrolled in this study. Repeat procedure endpoints were pulmonary vein isolation, linear block when linear ablation is performed, and non-inducibility of atrial tachyarrhythmia by burst pacing. Patients with LA enlargement between the pre-original procedure and pre-repeat procedure were categorized as Group 1 (35 patients), while individuals with no change or decrease of LA diameter were categorized as Group 2 (60 patients). The mean duration from the original procedure to the repeat procedure was 12 months (1-40 months). After 29.6 ± 20.5 (3-73) months follow-up from the repeat procedure, 33 patients experienced recurrence (34.7%). The recurrence rate was significantly higher in Group 1 than in Group 2 (51.4 VS. 25.0%, P = 0.017). In univariate analysis, LA remodelling was the only predictor of recurrence. In multivariate analysis, after adjustment for age and LA diameter, Group 1 had a greater risk of recurrence after the repeat procedure (hazard ratio = 2.22, 95% confidence interval: 1.02-4.81, P = 0.043).nnnCONCLUSIONSnLeft atrial enlargement after undergoing the original catheter ablation of paroxysmal AF was an independent risk factor of recurrence after repeat ablation.

International Collaborative Partnership for the Study of Atrial Fibrillation (INTERAF): Rationale, Design, and Initial Descriptives

Atrial fibrillation (AF) is a global problem with a significant impact on health outcomes, affecting up to 1% to 2% of the global adult population, and is projected to increase in both developed and developing countries over the coming decades.[1][1] AF is associated with higher mortality and

Persistence With Dabigatran Therapy at 2 Years in Patients With Atrial Fibrillation

BACKGROUNDnGuidelines recommend long-term oral anticoagulation therapy for stroke prevention in patients with atrial fibrillation (AF). Treatment discontinuation rates in vitamin K antagonist (VKA)-treated patients are high but may be lower with non-VKA oral anticoagulant agents.nnnOBJECTIVESnThe goal of this study was to describe and explore predictors of dabigatran etexilate persistence in patients with newly diagnosed AF over 2 years of follow-up.nnnMETHODSnConsecutive patients newly diagnosed with AF andxa0≥1 stroke risk factor were followed up for 2 years. Dabigatran nonpersistence was defined as discontinuation of dabigatran for >30xa0days. A multivariable Cox regression model included region as well as patient clinical and sociodemographic characteristics to explore predictors of nonpersistence.nnnRESULTSnEligible patients (Nxa0=xa02,932) tookxa0≥1 dabigatran dose; their mean age was 70.3 ± 10.2 years, and 55.3% were male. The 2-year probability of dabigatran persistence was 69.2%. Approximately 7% switched to a factor Xa inhibitor and 6% to a VKA. Approximately one-third of dabigatran discontinuations were primarily due to serious or nonserious adverse events. Patients from North America had the highest discontinuation risk, and Latin America had the lowest. Minimally symptomatic or asymptomatic AF and permanent AF were associated with a lower risk for dabigatran nonpersistence. Previous proton pump inhibitor use was associated with a higher risk for dabigatran nonpersistence.nnnCONCLUSIONSnProbability of treatment persistence with dabigatran after 2 years was approximately 70%. Nearly one-half of the patients who stopped dabigatran switched to another oral anticoagulant agent. Patients from Northxa0America, and those with paroxysmal, persistent, or symptomatic AF, may be at a higher risk for discontinuingxa0dabigatran.

Two-year follow-up of patients treated with dabigatran for stroke prevention in atrial fibrillation: Global Registry on Long-Term Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF) registry

Background and purpose GLORIA‐AF is a large, global, prospective registry program of newly diagnosed atrial fibrillation (AF) patients with ≥1 stroke risk factors. We describe the effectiveness and safety of dabigatran etexilate over 2 years from routine clinical practice in nearly 3000 patients from GLORIA‐AF who are newly diagnosed with non‐valvular AF and at risk of stroke. Methods Consecutive enrollment into phase II of GLORIA‐AF was initiated following approval of dabigatran for stroke prevention in non‐valvular AF. Within this Phase II, 2937 dabigatran patients completed 2‐year follow‐up by May 2016 and were eligible for analysis. Patients who took at least 1 dose of dabigatran (n = 2932) were used to estimate incidence rates. Results Overall incidence rates per 100 person‐years of 0.63 (95% confidence interval [CI], 0.42‐0.92) for stroke, 1.12 (0.83‐1.49) for major bleeding, 0.47 (0.29‐0.72) for myocardial infarction, and 2.69 (2.22‐3.23) for all‐cause death were observed. For patients taking 150 mg dabigatran twice daily (BID), corresponding rates (95% CI) were 0.56 (0.30‐0.94), 1.00 (0.64‐1.47), 0.48 (0.25‐0.83), and 2.07 (1.55‐2.72), respectively. For patients taking 110 mg dabigatran BID, event rates (95% CI) were 0.67 (0.33‐1.20), 1.16 (0.70‐1.80), 0.43 (0.17‐0.88), and 3.16 (2.36‐4.15). Conclusions These global data confirm the sustained safety and effectiveness of dabigatran over 2 years of follow‐up, consistent with the results from clinical trials as well as contemporary real‐world studies. What is known • Non–vitamin K antagonist (VKA) anticoagulants (NOACs) are the preferred therapy for prevention of ischemic stroke based on phase 3 trials, but there is insufficient information on their efficacy and safety in daily practice, based on prospectively collected data. What is new • This study shows that in non‐valvular AF patient population, with up to 2 years of follow‐up, the use of dabigatran led to a low incidence of ischemic stroke, major bleeding, and myocardial infarction in routine clinical care, confirming the sustained safety and effectiveness of dabigatran in clinical practice over 2 years of follow‐up.

Reconstruction left atrium and isolation pulmonary veins of paroxysmal atrial fibrillation using single contact force catheter with zero x-ray exposure: A CONSORT Study

Background: Conventional ablation of paroxysmal atrial fibrillation (PAF) is associated with radiation risks for patients and laboratory staff. Three-dimensional (3D) mapping system capable of showing contact force (CF) and direction of catheter tip may compensate for nonfluoroscopic safety issues. Objective: The aim of this study was to investigate the feasibility of zero x-ray exposure during reconstruction left atrium (LA) and ablation. Methods: Single, CF catheter, and 3D mapping system were used to reconstruct LA and isolate pulmonary veins (PV) in all patients. The patients were randomly divided into 2 groups after LA angiography. In group 1, reconstruction LA and isolation PV was performed with the help of 3D system (without x-ray), whereas in group 2, x-ray and 3D system were utilized to reconstruct LA and ablate PV antrum. After ablation, Lasso catheter was used to confirm the PV isolation. All patients were followed up to 12 months. Results: A total of 342 PAF patients were continuously enrolled. The basic clinical characteristics between the 2 groups had no significant difference. Parameters related to the procedure, average procedure time, ablation procedure time, average contact force (CF) applied, the percentage of time within CF settings, and average power applied during radiofrequency application showed no significant difference between the 2 groups. In group 1, the average fluoroscopy time before LA reconstruction was similar to that in group 2 (2.8u200a±u200a0.4 vs. 2.4u200a±u200a0.6 minutes, Pu200a=u200a.75). The average fluoroscopy time during ablation was significantly lower than that in group 2 (0 vs. 7.6u200a±u200a1.3 minutes, Pu200a<u200a.001). The total x-ray exposure dose of the procedure in group 1 was significantly lower than that in group 2 (19.6u200a±u200a9.4 vs. 128.7u200a±u200a62.5 mGy, respectively, Pu200a<u200a.001). Kaplan-Meier analysis indicated that there were no statistical differences in the probability of freedom from atrial arrhythmia (AF/AFL/AT) recurrence at 12 months between group 1 and group 2 (Pu200a=u200a.152). The success rate after a single ablation procedure and without drugs (Class I/III AAD) at 12 months was not significantly different between the 2 groups (67.6%, 95% confidence interval [CI]: 62%–79.5% in group 1 and 68.9%, 95% CI: 63%–80.7% in group 2, Pu200a=u200a.207). Procedural-related adverse events showed no significant different incidence between group 1 and group 2. A multivariate logistic regression analysis of risk factors was performed to evaluate the effectiveness outcome, which demonstrated that the percentage of CF (within the investigator-selected work ranges) during therapy was significantly associated with positive outcomes (odds ratio: 3.68; 95% CI: 1.65–10.6, Pu200a=u200a.008), whereas the LA dimension was negatively associated with effectiveness outcomes (odds ratio: 0.72; 95% CI: 0.52–0.84, Pu200a=u200a.016). Conclusions: Reconstruction LA and isolation PV ablation using single CF-assisted catheter without x-ray exposure was both safe and effective. CF was positively associated with effective outcomes and LA dimensions negatively with effective ones.

Clinical InvestigationsTwo-year follow-up of patients treated with dabigatran for stroke prevention in atrial fibrillation: GLORIA-AF Registry☆

Background and purpose GLORIA‐AF is a large, global, prospective registry program of newly diagnosed atrial fibrillation (AF) patients with ≥1 stroke risk factors. We describe the effectiveness and safety of dabigatran etexilate over 2 years from routine clinical practice in nearly 3000 patients from GLORIA‐AF who are newly diagnosed with non‐valvular AF and at risk of stroke. Methods Consecutive enrollment into phase II of GLORIA‐AF was initiated following approval of dabigatran for stroke prevention in non‐valvular AF. Within this Phase II, 2937 dabigatran patients completed 2‐year follow‐up by May 2016 and were eligible for analysis. Patients who took at least 1 dose of dabigatran (n = 2932) were used to estimate incidence rates. Results Overall incidence rates per 100 person‐years of 0.63 (95% confidence interval [CI], 0.42‐0.92) for stroke, 1.12 (0.83‐1.49) for major bleeding, 0.47 (0.29‐0.72) for myocardial infarction, and 2.69 (2.22‐3.23) for all‐cause death were observed. For patients taking 150 mg dabigatran twice daily (BID), corresponding rates (95% CI) were 0.56 (0.30‐0.94), 1.00 (0.64‐1.47), 0.48 (0.25‐0.83), and 2.07 (1.55‐2.72), respectively. For patients taking 110 mg dabigatran BID, event rates (95% CI) were 0.67 (0.33‐1.20), 1.16 (0.70‐1.80), 0.43 (0.17‐0.88), and 3.16 (2.36‐4.15). Conclusions These global data confirm the sustained safety and effectiveness of dabigatran over 2 years of follow‐up, consistent with the results from clinical trials as well as contemporary real‐world studies. What is known • Non–vitamin K antagonist (VKA) anticoagulants (NOACs) are the preferred therapy for prevention of ischemic stroke based on phase 3 trials, but there is insufficient information on their efficacy and safety in daily practice, based on prospectively collected data. What is new • This study shows that in non‐valvular AF patient population, with up to 2 years of follow‐up, the use of dabigatran led to a low incidence of ischemic stroke, major bleeding, and myocardial infarction in routine clinical care, confirming the sustained safety and effectiveness of dabigatran in clinical practice over 2 years of follow‐up.