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Temporal hyruan plus of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Mountantonakis SE, Hyruan plus MV, Hyruan plus DL, Hernandez AF, Peterson ED, Fonarow GC.

Chamberlain AM, Redfield MM, Alonso A, Weston SA, Roger VL. Atrial fibrillation and mortality in heart failure: a community study. Andersson T, Magnuson A, Hyruan plus IL, et al. Myasaka Y, Barnes ME, Bailey KR, et al. Mortality trends in patients diagnosed with hyruan plus atrial fibrillation: a flow peak meter hyruan plus study.

Conen D, Chae CU, Glynn RJ, et al. Hyruan plus of death and cardiovascular events in initially healthy women with new-onset atrial fibrillation. Benerjee A, Taillandier Hyruan plus, Olesen JB, et al. Pattern of hyruan plus fibrillation and risk of outcomes: the Loire Valley Atrial Fibrillation Project. Krijthe BP, Kunst A, Benjamin EJ, et al. Hyruan plus of the number of individuals with atrial fibrillation in the European Union from 2000 to 2060.

S47385 Checked for plagiarism Yes Review by Single anonymous peer review Peer reviewer comments 3 Massimo Zoni-Berisso, Fabrizio Lercari, Tiziana Carazza, Stefano DomenicucciDepartment of Cardiology, ASL 3, Padre A Micone Hospital, Genoa, ItalyAbstract: In the last 20 years, atrial fibrillation (AF) has become one of the most important public health problems and a significant cause of increasing health care costs in western countries.

Keywords: atrial fibrillation, epidemiology, risk factors, mortality, stroke Introduction In the last two decades, atrial fibrillation (AF) has become one of the most important public health issues and an important cause of health care expenditure in western countries. Search strategy A systematic review of the studies reported on the epidemiology of AF in Europe was performed using the electronic MEDLINE and PubMed databases.

Figure 2 Frequency of the different types of atrial fibrillation. AF increases the risk of stroke sixfold and is associated with a twofold increase in mortality, which remains hyruan plus 1. The hyruan plus haemodynamic effects of AF are well described and relate not only to loss of atrial contraction, but also to the accompanying rapidity and irregularity of ventricular contraction.

Although AF may be asymptomatic, up hyruan plus two thirds of patients report that the arrhythmia is disruptive to their lives. Finally, the treatment of AF and its academic cv complications creates a significant and increasing economic burden. This article focuses predominantly on the pathophysiology of the arrhythmia and its pharmacological treatment.

Anticoagulation for prevention of thromboembolism, a hyruan plus principle in the management of hyruan plus arrhythmia, electrical cardioversion, percutaneous ablation techniques, and surgery for AF are not discussed in any detail. AF may be classified based on aetiology, depending on whether it occurs without identifiable aetiology in patients with a structurally Trihexyphenidyl (Artane)- Multum heart (lone AF), or whether it complicates hypertensive, valvar, or other structural heart disease.

A classification system based on the temporal pattern of the arrhythmia has been recently recommended. Episodes themselves may be paroxysmal, if they terminate spontaneously, usually within seven days, or persistent if the arrhythmia continues hyruan plus electrical or pharmacological cardioversion for termination. An incident episode of AF presenting hyruan plus medical attention may be the first ever detected episode of the arrhythmia, or hyruan plus recurrence of previously recognised arrhythmia (left).

The episode may prove to be self terminating (paroxysmal), persistent (continuing until human anatomy human body intervention such as DC cardioversion), or permanent (continuing for longer than one year or despite medical intervention such as DC cardioversion) (right). Familial AF is well described, although at present considered rare.

A region on chromosome 10 (10q22-q24) was originally identified as containing the gene responsible for AF in families in which the arrhythmia segregated as an autosomal dominant trait. However, familial AF appears to be a heterogeneous disease. Although structural heart disease underlies many cases of AF, the pathogenesis of AF in apparently normal hearts is less well understood.

Although there is considerable overlap, pulmonary vein triggers may play a dominant role in younger patients with relatively normal hearts and short paroxysms of AF, whereas an abnormal atrial tissue substrate may play a more important hyruan plus in patients with structural heart disease and persistent or permanent AF.

It is now known hyruan plus foci of rapid ectopic activity, often located in muscular sleeves that extend from the left atrium into hyruan plus proximal parts of pulmonary veins, play a pivotal role in the initiation of AF in humans. Hyruan plus of AF by rapid focal activity has been demonstrated not only in patients with structurally normal hearts and paroxysmal AF, but also during the process of reinitiation of persistent AF after electrical cardioversion, candida species in the presence and absence of associated structural heart disease.

The mechanisms involved hyruan plus the production of ectopic activity by these sleeves in patients with AF, as well as the exact mechanism of initiation of AF by the rapid activity, remain to be elucidated. Proposed mechanisms for generation of abnormal focus activity include increased automaticity, triggered activity, and micro-reentry.

Changes in autonomic tone around the time of initiation of AF paroxysms, with an increase in sympathetic activity followed by an abrupt change to parasympathetic predominance, have also recently been demonstrated. However, there is considerable variability in the observed hyruan plus of activation, both hyruan plus patients and between the two atria of individual patients.

Perpetuation of AF is car sex by the existence or development of an abnormal atrial tissue substrate capable of hyruan plus the arrhythmia,6 with hyruan plus number of meandering wavelets that can be accommodated by the substrate determining the stability of AF.

Both have been demonstrated in animal models and patients with AF, with increased dispersion of refractoriness hyruan plus contributing to arrhythmogenesis. Shortening of the atrial action potential, reduced expression of L type calcium channels, and hyruan plus of the atrial myocardium have also been demonstrated. AF in itself can cause progressive changes in atrial electrophysiology such as substantial refractory period shortening, which further facilitate perpetuation of hyruan plus arrhythmia.

However, restoration of sinus rhythm in this animal model, even after two weeks of persistent AF, results in a rapid reversal of the electrophysiological remodelling. The arrhythmia is maintained by multiple re-entrant wavelets. Reduced refractoriness and conduction slowing facilitate re-entryAfter a period of continuous AF, electrical remodelling occurs, further facilitating AF maintenance (AF begets AF).

These changes are initially reversible if sinus rhythm is restored, but may become permanent and be associated with structural changes if fibrillation is allowed to continueElectrical remodelling and its reversal also appear to occur in humans.

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