ABC of atrial fibrillation. Antithrombotic treatment for atrial fibrillation.

Antithrombotic prophylaxis with long term warfarin or aspirin reduces thromboembolic risk in atrial fibrillation. Identification, risk assessment, and regular review of all patients with atrial fibrillation should be routine in general and hospital practice. Risk stratification is easily performed on clinical grounds--echocardiography may refine it.     

Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

Atrial fibrillation (AF) remains one of the leading causes of morbidity and mortality in the world which are related to palpitations, fainting, congestive heart failure or stroke. The mechanism for atrial fibrillation has been identified as electrical remodeling, structure remodeling and intracellular calcium handling remodeling. microRNAs (miRNAs) have recently emerged as one of the important factors in regulating gene expression. So far, thousands of miRNA genes have been found in diverse animals with the function of regulating cell death, cell proliferation, haematopoiesis and even participate in the processing of cardiovascular disease. In this review, we summarize the mechanism of AF and the association of microRNAs network with AF. We provide a potential perspective of miRNAs as the therapeutic target for AF.     

Atrial pacing for rhythm control of atrial fibrillation

After atrial fibrillation (AF) develops, the first step is to search for and treat underlying (heart) s. Thereafter, AF should be treated. This includes prevention of cardiovascular morbidity and mortality, especially vascular events, and reduction of symptoms.1 The latter may be obtained by two treatment strategies: rhythm-control and/or rate-control treatment. Recent randomised trials have shown that rate control is not inferior to rhythm control with regard to cardiovascular morbidity and mortality.2 In these studies, predominantly elderly patients with underlying heart s (especially hypertension) were included. Patients with (severely) symptomatic AF and advanced heart failure were excluded. Since then, rate-control treatment has been adopted more frequently, even as first-choice therapy, especially in the elderly.     

Atrial extracellular matrix remodelling in patients with atrial fibrillation

Atrial fibrillation (AF) is the most frequent clinical arrhythmia. Atrial fibrosis is an important factor in initiating and maintaining AF. However, the collagen turnover and its regulation in AF has not been completely elucidated. We tested the hypothesis that the extracellular matrix changes are more severe in patients with permanent AF in comparison with those in patients in sinus rhythm (SR). Intraoperative biopsies from the right atrial appendages (RAA) and free walls (RFW) from 24 patients with AF undergoing a mini-Maze procedure and 24 patients in SR were investigated with qualitative and quantitative immunofluorescent and Western blot analyses. As compared with SR, all patients with AF exhibited dysregulations in collagen type I and type III synthesis/degradation. Tissue inhibitors of metalloproteinases (TIMP2) was significantly enhanced only in RAA-AF. As compared with SR, collagen VI, matrix metalloproteinases MMP2, MMP9 and TIMP1 were significantly increased while TIMP3 and TIMP4 remained unchanged in all AF groups. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a newly discovered MMPs inhibitor, was elevated in RFW as compared to RAA-AF (P<0.05) and RFW-SR (P<0.05). The level of transforming growth factor (TGF)-beta1 was higher in AF than SR. Smad2 and phosphorylated Smad2 showed an elevation in RFW-AF as compared to RFW-SR, RAA-AF, and RAA-SR groups (P<0.05). CONCLUSIONS: Atrial fibrosis in AF is characterized by severe alterations in collagen I and III synthesis/degradation associated with disturbed MMP/TIMP systems and increased levels of RECK. TGF-beta1 contributes to atrial fibrosis via TGF-beta1-Smad pathway by phosphorylating Smad2. These processes culminate in accumulations of fibrillar and non-fibrillar collagens leading to excessive atrial fibrosis and maintainance of AF.     

Implementing evidence based medicine in general practice: audit and qualitative study of antithrombotic treatment for atrial fibrillation

ObjectiveTo determine the extent to which implementation of an evidence based treatment, antithrombotic treatment in atrial fibrillation, is possible in general practice.DesignAudit and qualitative study of patients with atrial fibrillation and an educational intervention for patients judged eligible for antithrombotic treatment.SettingSouth east England.Subjects56 patients with a history of atrial fibrillation.InterventionsAssessment and interview to ascertain patients'' views on antithrombotic treatment.ResultsOut of 13 239 patients, 132 had a history of atrial fibrillation of which 100 were at risk of thromboembolism. After the study, 52 patients were taking warfarin. Of the remaining 48 patients (of whom 41 were taking aspirin), eight were too ill to participate, 16 were unable to consent, four refused the interview, and 20 declined warfarin. Patients declining warfarin were inclined to seek a higher level of benefit than those taking it, as measured by the minimal clinically important difference. Qualitative data obtained during the interviews suggested that patients'' health beliefs were important factors in determining their choice of treatment.ConclusionPatients’ unwillingness to take warfarin seemed to be a major factor in limiting the number who would eventually take it.

Key messages

• After a structured intervention only half of a group of apparently eligible patients ended up taking warfarin for their atrial fibrillation
• Implementation of warfarin treatment for patients with atrial fibrillation was constrained by patients who were either too ill to take the drug or were unable to give consent
• These constraints are compounded by the unwillingness of patients to reduce their risk by taking a proved drug
• The number needed to treat, a key statistic in evidence based medicine, probably often overestimates the value of treatment in routine general practice and may not be sufficient to persuade patients of the benefit of treatment