A New Vision at the Interface of Atrial Fibrillation and Stroke.

Introduction: Current evidence questions the linear sequence traditionally described in atrial fibrillation, blood stasis, intracavitary thrombus, and embolization to the central nervous system. Currently, new perspectives have been described based on questions from the linearly traditional chronology of events; it is within this scope that the article has its objective. Evidences: The association of the two entities is biologically plausible and supported by different cohorts with a higher risk of developing atrial fibrillation, especially in the cardioembolic form. Concepts (temporal dissociation, biological gradient, etc.) determine the existence of other factors associated with cardioembolism, not exclusively by atrial fibrillation. The entire cascade of events associated with myopathy and atrial remodeling can generate damage to the myocyte and amplify the prothrombotic status. It is important to clarify that atrial myopathy can present itself as atrial fibrillation initially or not, but should always be considered thrombogenic in all the contexts of their clinical presentation. Considering atrial heart disease as a cause of embolic stroke, it could explain that one-third of strokes are considered cryptogenic. Conclusions: The traditional model exclusively associating the presence of atrial fibrillation in the genesis of thromboembolism is incomplete. The concept of atrial cardiopathy where cardioembolism occurs in a non-atrial fibrillation dependent manner fits better with current data. The future challenge is to effectively detect the various manifestations of atrial heart disease, generating direct implications for the identification of patients at risk of stroke and also for better management after a cardioembolic event.

Association of the left common ostium with clinical outcome after pulmonary vein isolation in atrial fibrillation.

INTRODUCTION: Electrical pulmonary vein isolation (PVI) is used for the invasive treatment of atrial fibrillation (AF). However, despite the procedure's technical evolution, the rate of AF recurrence due to electrical reconnection of the PVs is high. The aims of this study was to assess the influence of left common pulmonary venous ostium (LCO) on clinical outcomes following PVI. METHODS: Retrospective cohort of 254 patients who underwent the first procedure of PVI from the years 2013-2018 was assessed. Patients with persistent AF of long duration and extra-pulmonary focus associated with triggers for arrhythmia were excluded. Patients were stratified into two groups according to the presence of a LCO and received follow up for atrial tachyarrhythmia-free survival. The mean follow-up period was 28 ± 1.73 months. RESULTS: The majority were men (68.5%), with a mean age of 54 ± 12 years. With respect to the atrial anatomy, LCO occurred in 23.6% of cases after pulmonary venous angiotomography. The arrhythmia-free survival rate was 79.5% in the follow-up period. The Cox regression model was utilized and the adjusted hazard ratio for LCO was 0.36 (95% CI 0.15-0.87; p = 0.02) in terms of age, body mass index, left atrium diameter, bi-directional blocking of the cavotricuspid isthmus, persistent AF, left ventricular ejection fraction adjusted model. CONCLUSION: Anatomic abnormality with the presence of the LCO is present in a quarter of patients undergoing AF ablation, which is associated with a lower rate of arrhythmia recurrence in our population.

Polymorphism of the Beta-1 Gly389Arg receptor in patients with dual atrioventricular nodal physiology.

INTRODUCTION: Gly389Arg ß1 adrenergic receptor polymorphisms seem to exert an influence on the modulation of the adrenergic effect in several types of patients. This study aimed to determine the prevalence of Gly389Arg polymorphisms among patients with evidence of double nodal pathway and to correlate the electrophysiological properties with the different genotypes of the respective polymorphisms. METHODS: A cross-sectional, descriptive and analytical study was designed to assess 49 patients, with evidence of double nodal pathway, submitted to electrophysiological study. Genomic DNA was extracted from peripheral blood leukocytes and the genotypes of the Arg389Gly polymorphisms were identified in all individuals by PCR/RFLP (polymerase chain reaction/restriction fragment length polymorphism). RESULTS: The majority of patients were female and had supraventricular tachycardia (75.5%). The prevalence of Arg389Arg genotype was found in 32 patients (65.3%), Arg389Gly genotype in 16 patients (32.7%) and Gly389Gly genotype in 1 patient (2%). With respect to the induction of nodal reentrant tachycardia, it was possible to induce non-isoproterenol tachycardia in 32 patients (65.3%), of whom 24 had the Arg389Arg genotype and 8 the Arg389Gly and Gly389Gly genotype (p = 0.05). The resting heart rate of patients of the Arg389Arg genotype was 81 ± 18 bpm and the Arg389Gly and Gly389Gly genotype of 71 ± 9 bpm (p = 0.044). Body mass index (BMI) among patients with genotype Arg389Gly and Gly389Gly was 29.8 ± 7.1 and patients with the Arg389Arg genotype was 26.2 ± 4.6 (p = 0.034). CONCLUSION: The Arg389Arg genotype was more easily related to triggering arrhythmia, higher resting heart rate and lower BMI.