Atrial fibrillation: epidemiology, mechanisms, and management

The incidence of AF, the most common sustained arrhythmia in clinical practice, increases with age, and coronary artery disease, hypertension, and valvular heart disease are common underlying substrates. Occasionally, however, AF may occur without any underlying heart disease. The most widely accepted theory of its mechanism is Moe's multiple wavelet hypothesis, although recent studies are helping to shed light on other mechanisms, including the focal origin of AF in some patients. Most patients experience palpitations, but fatigue, dyspnea, and dizziness may also occur.Therapy includes prevention of thromboembolism, control of rate, and restoration and maintenance of sinus rhythm. The risks and benefits of each treatment modality need to be assessed according to each patient's circumstances. Unlike other arrhythmias, there is still no highly successful therapy for treating AF. However, significant advances are being made using nonpharmacologic approaches to either prevent or cure this troublesome arrhythmia.     

Atrial fibrillation: guiding lessons from epidemiology

The epidemiology of AF is a challenging and surprising area of medical knowledge. The prevalence of AF may be not changing despite the common perception. It is possible that being earlier disease of the middle age, and because of changing etiology and successful treatment of underlying vascular conditions, AF is shifting to the elderly population. In this population, it becomes more clinically significant, and increasingly leads to disability and death. Screening procedures for silent AF likely are underimplemented and may change understanding of AF epidemiology significantly. Hypertension may be the most common primary etiology of AF, and the possibility of effective primary prevention of AF by strict control of hypertension needs to be evaluated adequately.     

Atrial fibrillation in patients with systolic heart failure: pathophysiology mechanisms and management

Heart failure (HF) and atrial fibrillation (AF) demonstrate a constantly increasing prevalence during the 21^st century worldwide, as a result of the aging population and the successful interventions of the clinical practice in the deterioration of adverse cardiovascular outcomes. HF and AF share common risk factors and pathophysiological mechanisms, creating the base of a constant interrelation. AF impairs systolic and diastolic function, resulting in the increasing incidence of HF, whereas the structural and neurohormonal changes in HF with preserved or reduced ejection fraction increase the possibility of the AF development. The temporal relationship of the development of either condition affects the diagnostic algorithms, the prognosis and the ideal therapeutic strategy that leads to euvolaemia, management of non-cardiovascular comorbidities, control of heart rate or restoration of sinus rate, ventricular synchronization, prevention of sudden death, stroke, embolism, or major bleeding and maintenance of a sustainable quality of life. The indicated treatment for the concomitant HF and AF includes rate or/and rhythm control as well as thromboembolism prophylaxis, while the progress in the understanding of their pathophysiological interdependence and the introduction of the genetic profiling, create new paths in the diagnosis, the prognosis and the prevention of these diseases.

Heart failure (HF) and atrial fibrillation (AF) have become epidemics of the 21st century, as a result of the increased longevity and the successful reduction of the cardiovascular (CV) mortality.^[1] The prevalence of both conditions is constantly rising, increasing significantly the cost of treatment to the healthcare systems worldwide.^[2-4] It is estimated that the incidence of AF (2%) is double compared to the last decade. AF is present in 0.12%−0.16% of those < 49 years of age, in 3.7%−4.2% of those aged 60−70 years, and in 10%−17% of those aged ≥ 80 years, occurring more frequently in males, with a male to female ratio of 1.2: 1.^[5] By the year 2030 in Europe alone it is estimated that the patients with AF will be 14−17 million, with an annual number of 120−215,000 new cases,^[5] while the prevalence in the American population will be 12 million.^[6] HF affects approximately 1%−2% of adults in developed countries.^[7] Few individuals under 50 years of age are diagnosed with HF, whereas the prevalence in those aged 75 years or above is more than 10%.^[7,8] The prevalence of HF globally in AF individuals is 33% in patients with paroxysmal AF, 44% in those with persistent and 56% in those with permanent AF.^[9] Among the 5.8 million US adults with heart failure with reduced ejection fraction (HFrEF) or preserved EF (HFpEF), the prevalence of AF is up to 40%.^[10,11] It is clear that the combination of these two conditions will have a significant impact on healthcare and the management of cardiovascular (CV) disease as it is performed so far.^[12,13] The pathophysiology and risk factors for HF and AF are closely related and the coexistence of HF and AF affects elderly patients with a significant burden of comorbidities.^{[9, 14]} The development of AF is connected with complex interactions that lead to impairment of systolic and diastolic function, that are not present in sinus rhythm (SR), resulting in a three-fold increased risk of HF incidence compared with SR.^[15] Conversely, the structural and neurohormonal changes in HF increase the possibility of the AF incidence^[16] both in HFrEF and in HFpEF.^[1] Previous studies have also demonstrated differences in atrial remodeling, prognosis and outcomes^[17] associated with AF development among the HF subtypes,^[18] with greater eccentric LA remodeling in HFrEF, and increased LA stiffness in HFpEF predisposing more evidently in AF.^[19] Regardless which condition develops first, their combined incidence is associated with a worse prognosis than either condition alone.^[20-22] Concerning the adverse outcomes that are associated with HF and AF, an important target of clinical studies is the development of effective therapies for these patients but also an arduous one as the so far applied treatments on either of these conditions alone are shown to be effective or provoke safety concerns in patients with HF and AF.^{[23, 24]}     

Atrial tachycardia: mechanisms, diagnosis, and management

Atrial tachycardia is an uncommon arrhythmia and may be focal or macroreentrant. This review concentrates on focal atrial tachycardia. Over the last decade there have been a number of advances in delineating the mechanism and anatomic locations of focal atrial tachycardia. The lack of efficacy of antiarrhythmic therapy and the advent of radiofrequency ablation have altered our primary approach to the treatment of focal atrial tachycardia. This review discusses the clinical features, diagnosis, and treatment of focal atrial tachycardia. There is particular focus on the mechanisms, anatomic locations, and P wave morphology, as well as the techniques of mapping and radiofrequency ablation.     

Atrial fibrillation post-myocardial infarction: Frequency,consequences, and management

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is a frequent complication of acute myocardial infarction (MI). AF occurs in 5% to 10% of patients who have received fibrinolysis. Post-MI AF is more common in older patients, in patients with heart failure, and after more extensive infarction. Postinfarction prognosis is worse among patients complicated by AF—indeed, mortality and morbid events including stroke, thromboembolism, and heart failure are increased in this group. It is unclear as to whether AF directly reduces survival or merely demarcates patients at higher overall risk. Despite its frequent occurrence and deleterious influence on outcomes, randomized data regarding management of AF after acute MI are scarce. This review summarizes recent data charting the incidence of AF after acute MI and describes features associated with its occurrence. Clinical sequelae and current principles in treatment are also discussed.     

Atrial fibrillation and congestive heart failure: risk factors, mechanisms, and treatment

Atrial fibrillation (AF) and congestive heart failure (CHF) are commonly encountered together, and either condition predisposes to the other. Risk factors for AF and CHF include age, hypertension, valve disease, and myocardial infarction, as well as a variety of medical conditions and genetic variants. Congestive heart failure and AF share common mechanisms, including myocardial fibrosis and dysregulation of intracellular calcium and neuroendocrine function. Pharmacological treatments including beta-blockers, digoxin, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can be useful in treating both of these conditions. Antiarrhythmic medications intended to achieve and maintain sinus rhythm may be beneficial in some patients with AF and CHF. Advances in pacemaker and defibrillator therapy, including cardiac resynchronization therapy, may also benefit patients with AF and CHF. Surgical and catheter-based ablation therapy can restore sinus rhythm in patients with AF, with proven benefit in patients with concommitant CHF. Investigational biologic therapy, including cell and gene based therapy, offers promise for the future of reversing the pathophysiological mechanisms that underlie AF and CHF.     

Atrial fibrillation pathophysiology: implications for management

Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is an important contributor to population morbidity and mortality. An arrhythmia that is particularly common in the elderly, AF is growing in prevalence with the aging of the population. Our understanding of the basic mechanisms that govern AF occurrence and persistence has been increasing rapidly. This article reviews the basic pathophysiology of AF over a broad range of levels, touching on the tissue mechanisms that maintain the arrhythmia, the relationship between clinical presentation and basic mechanisms, ion channel and transporter abnormalities that lead to ectopic impulse formation, basic models and tissue determinants of reentry, ion channel determinants of reentry, the nature and roles of electric and structural remodeling, autonomic neural components, anatomic factors, interactions between atrial and ventricular functional consequences of AF, and the basic determinants of atrial thromboembolism. We then review the potential implications of the basic pathophysiology of the arrhythmia for its management. We first discuss consequences for improved rhythm control pharmacotherapy: targeting underlying conditions, new atrium-selective drug targets, new targets for focal ectopic source suppression, and upstream therapy aiming to prevent remodeling. We then review the implications of basic mechanistic considerations for rate control therapy, AF ablation, and the prevention of thromboembolic events. We conclude with some thoughts about the future of translational research related to AF mechanisms.     

Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation

Atrial fibrillation (AF) is the most common arrhythmia in the clinical setting, and traditional pharmacological approaches have proved to have important weaknesses. Structural remodeling has been observed in both clinical and experimental AF paradigms, and is an important feature of the AF substrate, producing fibrosis that alters atrial tissue composition and function. The precise mechanisms underlying atrial fibrosis are not fully elucidated, but recent experimental studies and clinical investigations have provided valuable insights. A variety of signaling systems, particularly involving angiotensin II and related mediators, seem to be centrally involved in the promotion of fibrosis. This paper reviews the current understanding of how atrial fibrosis creates a substrate for AF, summarizes what is known about the mechanisms underlying fibrosis and its progression, and highlights emerging therapeutic approaches aimed at attenuating structural remodeling to prevent AF.     

Atrial fibrillation: current knowledge and recommendations for management

Atrial fibrillation, a commonly encountered arrhythmia, hasin recent years, been the subject of increased interest andintensive clinical research. There is also increasing awarenessthat atrial fibrillation is a major cause of embolic eventswhich in 75% of cases are complicated by cerebrovascular accidents^[1,2].Atrial fibrillation is often associated with heart disease buta significant proportion of patients (about 30%) have no detectableheart disease^[3]. Symptoms, occasionally disabling, haemo-dynamicimpairment and a decrease in life expectancy are among the untowardeffects of atrial fibrillation, resulting in an important morbidity,mortality and an increased cost for the health care provider^[4]. The Working Group of Arrhythmias of the European Society ofCardiology created a Study Group on Atrial Fibrillation in orderto establish recommen-dations for the better management of thisarrhythmia and to promote multicentre studies. The purpose ofthis paper is to briefly outline the state of our knowledgeon the clinical presentation, the causes, the mechanisms andtherapeutic approaches currently available and to propose recommendationsfor management. Although atrial flutter can coexist with atrialfibrillation, it is considered a different arrhythmia and willnot be covered in the present paper.     

肥厚型心肌病心房颤动:决定因素、临床进程与处理

Atrial fibrillation(AF)is the most common sustained arrhythmia in patients with hypertrophic cardiomyopathy(HCM),and represents an important complication in the clinical COUlee of the disease,with adverse consequences on functional status and outcome.Studies on community-based HCM patient populations have shown that AF is associated with long-term clinical deterioration,cardioembolic stroke and increaeed cardiovascular mortality due to heart failure and stroke.Moreover.acute onset of AF may cause severe hemodynamic impairment and represent a trigger of potentially lethal ventricular arrhythmias.However,the consequences of AF on the long-term prognosis of HCM patients are not uniformly unfavorable,and may be compatible with an uneventful course,when properly managed.Management of AF in HCM is challenging,particularly when onset occurs at a young age.Both paroxysmal and permanent AF represent clear indications for oral anticoagulation.In moat patients,maintenance of sinus rhythm is highly desirable but made difficult by the limited long-term efficacy and potentially hazardous side effects of available pharmacological options.In selected patients with HCM and severely symptomatic AF,radiofrequency catheter ablation may represent an effective therapeutic ahemative,improving functional status,and reducing or postponing the need for antiarrhythmic drugs. In patients with persistent AF,in whom maintenance of sinus rhythm is not feasible.adequate ventricular rate control should be pursued aggressively by atrio-ventricular node blocking agents.     

Atrial fibrillation: management for the geriatric patient

Atrial fibrillation is one of the most common rhythm disorders encountered in the geriatric population. The diagnosis is well established, but the treatment has undergone many changes. Many long-held notions have been challenged and new treatment options, both medical and procedural, have offered new hope in the management of this disease in the elderly. This review will describe atrial fibrillation from its diagnosis to the common and more cutting-edge treatment modalities with special focus on the elderly population.