Warfarin doses for anticoagulation therapy in elderly patients with chronic atrial fibrillation

OBJECTIVES:Atrial fibrillation is the most common sustained arrhythmia and is associated with poor outcomes, including stroke. The ability of anticoagulation therapy to reduce the risk of stroke has been well established; however, the prevalence of anticoagulation therapy use in the Public Health System is unknown. The aim of this study is to evaluate both the prevalence of anticoagulation therapy among patients with atrial fibrillation and the indications for the treatment.METHODS:In this cross-sectional study, we included consecutive patients who had atrial fibrillation documented by an electrocardiogram performed between September 2011 and March 2012 at a university hospital of the Public Health System. The variables analyzed included the risk of a thromboembolic event and/or bleeding, the use of antiplatelet or anticoagulation therapy, the location where the electrocardiogram report was initially reviewed and the specialty of the physician who initially reviewed it.RESULTS:We included 162 patients (mean age 68.9 years, 56% men). Hypertension (90.1%), heart failure (53.4%) and stroke (38.9%) were the most prevalent diseases found. Only 50.6% of the patients knew that they had atrial fibrillation. Regarding the use of therapy, only 37.6% of patients classified as high risk according to the CHADS2 scores and 35.5% according to the CHA2DS2VASc used oral anticoagulation. A presumptive diagnosis of heart failure and the fact that the electrocardiogram was evaluated by a cardiologist were the only independent predictors of the use of anticoagulants.CONCLUSIONS:Our study found a low prevalence of oral anticoagulation therapy among patients with atrial fibrillation and an indication for stroke prophylaxis for the use of this therapy, including among those with high CHADS2 and CHA2DS2VASc scores.

Section: Discussionmentioning

confidence: 99%

Prevalence of oral anticoagulation in atrial fibrillation

Bartholomay¹,

Polli²,

Borges³

et al. 2014

“…In the United States, the number of persons with AF is currently estimated at 2.3 million and is projected to reach 15.9 million by 2050 (3). This prevalent dysrhythmia is associated with decreased quality of life, reduced exercise tolerance, impaired cognition, tachycardiomyopathy, thromboembolism, congestive heart failure, and even death (1,4,5). Patients with AF have a 5-fold increased risk of ischemic stroke (6), and the mortality rate of patients with AF is approximately 2-fold greater than that of individuals with a normal sinus rhythm (7).…”

Section: Introductionmentioning

confidence: 99%

Prevalence and spectrum of Nkx2.5 mutations associated with idiopathic atrial fibrillation

Xie¹,

Chang²,

Xu³

et al. 2013

OBJECTIVE:The aim of this study was to evaluate the prevalence and spectrum of Nkx2.5 mutations associated with idiopathic atrial fibrillation (AF).METHODS:A cohort of 136 unrelated patients with idiopathic atrial fibrillation and 200 unrelated, ethnically matched healthy controls were enrolled. The coding exons and splice junctions of the Nkx2.5 gene were sequenced in 136 atrial fibrillation patients, and the available relatives of mutation carriers and 200 controls were subsequently genotyped for the identified mutations. The functional characteristics of the mutated Nkx2.5 gene were analyzed using a dual-luciferase reporter assay system.RESULTS:Two novel heterozygous Nkx2.5 mutations (p.N19D and p.F186S) were identified in 2 of the 136 unrelated atrial fibrillation cases, with a mutational prevalence of approximately 1.47%. These missense mutations co-segregated with atrial fibrillation in the families and were absent in the 400 control chromosomes. Notably, 2 mutation carriers also had congenital atrial septal defects and atrioventricular block. Multiple alignments of the Nkx2.5 protein sequences across various species revealed that the altered amino acids were completely conserved evolutionarily. Functional analysis demonstrated that the mutant Nkx2.5 proteins were associated with significantly reduced transcriptional activity compared to their wild-type counterpart.CONCLUSION:These findings associate the Nkx2.5 loss-of-function mutation with atrial fibrillation and atrioventricular block and provide novel insights into the molecular mechanism involved in the pathogenesis of atrial fibrillation. These results also have potential implications for early prophylaxis and allele-specific therapy of this common arrhythmia.

“…The lifetime risk of developing AF is approximately 25% in individuals aged 40 years or older (2). The chaotic heart rhythm is responsible for a variety of symptoms, including palpitations, dizziness, and shortness of breath, and it is associated with degraded quality of life, reduced exercise capacity, cognitive dysfunction, tachycardiomyopathy, thromboembolic strokes, congestive heart failure, and even death (1,3,4). The mortality rate of patients with AF is approximately two times that of subjects with a normal sinus rhythm (5).…”

Section: Introductionmentioning

confidence: 99%

Novel GATA5 loss-of-function mutations underlie familial atrial fibrillation

et al. 2012

OBJECTIVE:This study aimed to identify novel GATA5 mutations that underlie familial atrial fibrillation.METHODS:A total of 110 unrelated patients with familial atrial fibrillation and 200 unrelated, ethnically matched healthy controls were recruited. The entire coding region of the GATA5 gene was sequenced in 110 atrial fibrillation probands. The available relatives of the mutation carriers and 200 controls were subsequently genotyped for the identified mutations. The functional effect of the mutated GATA5 was characterized using a luciferase reporter assay system.RESULTS:Two novel heterozygous GATA5 mutations (p.Y138F and p.C210G) were identified in two of the 110 unrelated atrial fibrillation families. These missense mutations cosegregated with AF in the families and were absent in the 400 control chromosomes. A cross-species alignment of GATA5 protein sequence showed that the altered amino acids were completely conserved evolutionarily. A functional analysis revealed that the mutant GATA5 proteins were associated with significantly decreased transcriptional activation when compared with their wild-type counterpart.CONCLUSION:The findings expand the spectrum of GATA5 mutations linked to AF and provide novel insights into the molecular mechanism involved in the pathogenesis of atrial fibrillation, suggesting potential implications for the early prophylaxis and personalized treatment of this common arrhythmia.