We did a comprehensive review of work published from January, 1966, to November, 2001, that was relevant to atrial fibrillation from PubMed/Medline, EMBASE, and Cochrane Library databases. A few articles that were published before 1966, but addressed major contributions to this subject were also included. We selected studies that contributed most to the knowledge of the epidemiology and pathogenesis of the disease. In the case of studies on treatment of atrial fibrillation, we selected large
SeminarAtrial fibrillation: strategies to control, combat, and cure
Section snippets
Epidemiology
Atrial fibrillation is the commonest sustained cardiac arrhythmia. Prevalence of this disorder increases with age, rising above 5% in people older than 65.6 The disorder is also becoming more prevalent with time, even after adjustment for age and structural heart disease.7 Hypertensive, valvular, ischaemic, and other types of structural heart disease underlie most cases of chronic atrial fibrillation. From long-term follow-up data of the Framingham study, independent risk factors for atrial
Classification
Atrial fibrillation is mostly classified according to its temporal pattern (Panel 1). A patient presenting with this disorder could have a first detected episode of atrial fibrillation, or recurrent arrhythmia if they have had previous documented episodes. Episodes are paroxysmal if they terminate spontaneously, or persistent if they require electrical or pharmacological cardioversion. Atrial fibrillation that cannot be successfully stopped by cardioversion and long-standing (>1 year) atrial
Electrophysiological effects
Several experimental and human mapping studies done over the past 30 years have shown that atrial fibrillation is characterised by multiple wavelets of excitation that propagate around the atrial myocardium, and that perpetuation of the arrhythmia is the result of an abnormal atrial tissue substrate.18 Atrial fibrillation in general results from a complex interaction between initiating triggers and development of this abnormal tissue substrate capable of maintaining the arrhythmia. Although
Genetics of atrial fibrillation
Although the rare familial occurrence of atrial fibrillation has been recognised for some time,46 the location of the gene responsible for this disorder has only recently been identified in a family in whom the arrhythmia segregated as an autosomal dominant trait (10q22–q24).47 Brugada and colleagues48 have since identified many more families who have atrial fibrillation, and found that the locus on chromosome 10 did not contain the gene responsible for atrial fibrillation in all families,
Haemodynamic and prothrombotic effects
Atrial fibrillation has many adverse haemodynamic effects that relate not only to loss of atrial contraction and thus atrioventricular synchrony, but also to the accompanying rapidity and irregularity of ventricular contraction.49 These effects are especially relevant to patients with underlying systolic ventricular dysfunction, and those with diastolic dysfunction or mitral stenosis in whom cardiac function depends more on a long diastole and active ventricular filling than a healthy heart.
The
Effect on quality of life
Although atrial fibrillation can be symptomless, up to two-thirds of patients report that the arrhythmia is disruptive to their lives.51 Cerebrovascular complications are a further important cause of functional limitation in patients with atrial fibrillation.
Diagnosis
Diagnosis of atrial fibrillation is based on history and clinical examination and confirmed with a 12-lead ECG. However, patients with atrial fibrillation do not always have symptoms. In the Cardiovascular Health Study,52 12% of new cases of atrial fibrillation were diagnosed on the basis of yearly ECG screening alone, and thus presumably had no symptoms. In recurrent atrial fibrillation, patients may have a history suggestive of a paroxysmal tachycardia, which might be perceived as episodic
Treatment
Panel 3 shows the principles of management of atrial fibrillation, with an algorithm for management of atrial fibrillation in figure 3, which should be read together with published guidelines.5
Recommendations for antithrombotic treatment in patients with atrial fibrillation
Pooled data133 from five randomised studies of patients with atrial fibrillation have shown that dose-adjusted oral anticoagulation with warfarin reduces risk of ischaemic stroke by 68%, and lowers mortality by 33%. However, since warfarin might increase haemorrhagic events, the risk-benefit ratio must be assessed for every patient individually. In patients who do not have valvular heart disease, the target international normalised ratio should be 2·0 to 3·0. Anticoagulation within this
Conclusion
The past decade has seen many advances in understanding all aspects of atrial fibrillation. We are now able to cure a small but increasingly recognised proportion of patients with this disorder, with the promise of more widespread application of the evolving treatment strategies. The recommended treatment algorithm (figure 3) has greatly changed from that proposed by Narayan and colleagues4 although anticoagulation remains a central feature in keeping morbidity and mortality to a minimum.
Search strategy and selection criteria
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2023, Hellenic Journal of CardiologyCitation Excerpt :The incidence of atrial fibrillation (AF), a common cardiac arrhythmia, is increasing because of an extended longevity of the population, the rising burden of comorbidities, and the more frequent identification of asymptomatic AF by wearable devices.1 AF is associated with a significant increase in the incidence of stroke, congestive heart failure, and mortality, with a substantial impact on quality of life and healthcare costs.2,3 Accordingly, the identification and targeting of modifiable risk factors for developing AF is important for both AF risk prediction and prevention.
Optimizing prognosis in atrial fibrillation: A call to action in Portugal
2021, Revista Portuguesa de CardiologiaThe Changing Landscape for Stroke Prevention in AF: Findings From the GLORIA-AF Registry Phase 2
2017, Journal of the American College of Cardiology