REVIEW ARTICLE
Epidemiology and natural history of atrial fibrillation: clinical implications
Sumeet S. Chugh, MD, FACC*,
Joseph L. Blackshear, MD, FACC ,
Win-Kuang Shen, MD, FACC*,
Stephen C. Hammill, MD, FACC* and
Bernard J. Gersh, MB, DPhil, ChB, FACC*
* Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
Division of Cardiovascular Diseases, Mayo Clinic Jacksonville, Jacksonville, Florida, USA
Manuscript received March 29, 2000;
revised manuscript received August 24, 2000,
accepted October 4, 2000.
Reprint requests and correspondence: Dr. Bernard J. Gersh, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905
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Abstract
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With a substantial impact on morbidity and mortality, the growing "epidemic" of atrial fibrillation (AF) intersects with a number of conditions, including aging, thromboembolism, hemorrhage, hypertension and left ventricular dysfunction. Currently, the epidemiology and natural history of AF govern all aspects of its clinical management. The ongoing global investigative efforts toward understanding AF are also driven by epidemiologic findings. New developments, by affecting the natural history of the disease, could eventually alter the nature of decision making in patients with AF. The crucial issue of rate versus rhythm control awaits completion of the AF Follow-up Investigation of Rhythm Management trial. The processes of electrical and structural remodeling that perpetuate AF appear to be reversible. In the era of functional genomics, the molecular basis of this ubiquitous arrhythmia is in the process of being defined. Unraveling the molecular genetics of AF might provide new insights into the structural and electrical phenotypes resulting from genetic mutations and, as such, new approaches to treatment of this arrhythmia at the ion channel and cellular levels. Thus, current adverse trends are superimposed on a background of a rapidly developing knowledge base and potentially exciting new therapeutic options. Consequently, an understanding of the epidemiology and natural history of AF is crucial to the future allocation of resources and the utilization of an expanding range of therapies aimed at reducing the impact of this disease on a changing patient population.
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Abbreviations and Acronyms
| | AF | = atrial fibrillation | | CHF | = congestive heart failure | | LV | = left ventricle, left ventricular | | SOLVD | = Studies Of Left Ventricular Dysfunction | | SPAF | = Stroke Prevention in Atrial Fibrillation trial |
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Incidence and prevalence
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As we enter the 21st century, atrial fibrillation (AF), an "old" arrhythmia that was first identified in 1909 (1), has assumed increasing importance as the global demographic tide results in a burgeoning population of elderly individuals. Indeed, Braunwald, in his Shattuck lecture (2), referred to the growing "epidemic" of AF. The impact of AF on mortality and morbidity is substantial, as are the socioeconomic consequences in relationship to hospital admissions, chronic disease management and disabilities. These adverse trends, nonetheless, are superimposed on a background of potentially exciting new therapeutic options. Consequently, an understanding of the epidemiology and natural history of AF is crucial to the future allocation of resources and the utilization of an expanding range of therapies aimed at reducing the impact of this disease on a changing patient population (3).
Atrial fibrillation currently affects approximately 2.2 million patients in the U.S. (4) and is the most common rhythm disorder among U.S. patients hospitalized with a primary diagnosis of an arrhythmia (5). The median age of patients is 75 years; approximately 70% of patients are between the ages of 65 and 85 years, and 84% are older than 65 years (4) (Fig. 1). Pooled data from studies of chronic AF in North America, Britain and Iceland suggest a prevalence of 0.5% to 1% in the general population (6–9). In two separate studies restricted to patients older than 60 years, the prevalence was 5% to 9% after 5 to 15 years of follow-up (10,11). Thus, the genesis of this epidemic was initially attributed to alterations in the age-related composition of the population, with an expanding elderly population accounting for the increasing incidence and prevalence of AF. However, during the past two decades, additional factors seem to have influenced the frequency of this disease. The Framingham study found an increasing prevalence of AF even after adjusting for age, gender and other comorbidities (Fig. 2) (12); but underlying explanations are unclear, and further studies in other populations are needed. From a recent population-based study in subjects older than 65 years, the prevalence in men (9.1%) was greater than that in women (4.8%) (13). In the Framingham study, after adjustment for age and other risk factors, AF developed in men at 1.5 times the rate in women. The reason for the greater susceptibility to AF in men is unexplained (14).
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Figure 1 Prevalence of atrial fibrillation in four natural history studies. CHS = Cardiovascular Health Study; W Australia = Western Australia. (From Feinberg et al. [4]; by permission of the American Medical Association).
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Figure 2 Secular trends in the prevalence (percentage) of atrial fibrillation in subjects 65 to 84 years old in the Framingham study. (Data from Wolf et al. [13]).
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Evidence for underestimation of AF.
Significant increases in numbers notwithstanding, there is a strong likelihood that the incidence and prevalence of AF may be substantially underestimated. Underdetection due to absence of symptoms and undersampling in patients with paroxysmal AF are significant constraints to the clarification of the epidemiology of AF. Thirty percent of patients enrolled in the Cardiovascular Health Study (13) and approximately 45% of patients in the Stroke Prevention in Atrial Fibrillation (SPAF-III) study had AF detected incidentally (15) when electrocardiography was performed for an unrelated reason. In patients with symptomatic paroxysmal AF, there is a 12:1 ratio of asymptomatic versus symptomatic episodes (16).
The bulk of our knowledge of the epidemiology of AF is based predominantly on white populations. In the Cardiovascular Health study, there was a trend toward a lower incidence of AF during follow-up in blacks, but they made up only 5% of the total population in that study (17).
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Direct relationship of AF to mortality
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Until recently, the status of AF as an independent predictor of mortality in myocardial infarction, heart failure or stroke was unclear (18–23). New information from the Framingham study, however, may have put this controversy to rest (24). Even among low-risk subjects without clinically relevant cardiovascular disease, AF was still associated with an excess mortality. In subjects age 55 to 94 years from the original cohort of the Framingham study, the presence of AF independently increased the risk of death in men (odds ratio [OR]: 1.5; 95% confidence interval [CI]: 1.2 to 1.8) and women (OR: 1.9; 95% CI: 1.5 to 2.2). When subjects who died within 30 days of diagnosis were excluded, the OR decreased to 1.1 in men but was unchanged in women. Consequently, the presence of AF limited the advantage that women have over men in regard to longevity. Mechanisms remain speculative, and, in this study, data were insufficient to examine the role of anticoagulants or antiarrhythmic agents on mortality (24).
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Incidence of stroke and hemorrhage
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Atrial fibrillation is an independent risk factor for stroke; it is associated with a four- to five-fold higher risk than in the unaffected population (9,25–27). Overall, this rhythm disorder is implicated in approximately 75,000 strokes per year and is probably the major cause of embolic stroke (28). Patients with paroxysmal or intermittent AF have an annualized stroke rate (3.2%) similar to that in patients with chronic or sustained AF (3.3%) (29). The coexistence of other factors in patients with AF may compound the risk of stroke. For instance, the risk of stroke attributable to AF increases with age (28). Thus, older patients are not only more prone to AF but their risk of stroke is considerably increased compared with younger patients with AF. The propensity of the elderly for stroke may be related to a higher prevalence of comorbid conditions and to the dual factors of age and chronicity. Both increasing age and chronicity of AF correlate strongly with increased left atrial size (30).
Do predictors of stroke risk explain mechanisms of stroke occurrence?.
Traditional concepts of the pathophysiology of stroke and AF implicate stasis and thrombus formation in a structurally abnormal and dilated atrium or ventricle (31) (Fig. 3). More recent investigations suggest that AF may independently confer a hypercoagulable state (32,33). Considerable interest currently focuses on an expanded paradigm in which AF is not a putative risk factor for stroke but rather a "marker" for other conditions predisposing to stroke, including aortic atherosclerosis, cerebrovascular disease and mitral annular calcification (34–37) (Fig. 3).
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Figure 3 Pathophysiologic mechanisms and associations between atrial fibrillation and stroke. EF = ejection fraction; LA = left atrium; LV = left ventricle. (From Gersh [3]; by permission of Futura Publishing Company. Original figure, courtesy of J. H. Chesebro, MD).
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Hypertension is a powerful independent predictor of stroke in patients with nonrheumatic AF (36,37) (Table 1). In a recent large trial, a history of hypertension was strongly associated with findings of left atrial stasis and thrombi on transesophageal echocardiography (38) and the presence or absence of complex aortic plaque, which determined high or moderate risk of thromboembolism, respectively. Perhaps in some patients the presence of hypertension acts as a marker of a noncompliant atherosclerotic aorta, which increases the impedance to left atrial and left ventricular (LV) emptying, promoting chamber dilatation and stasis, in addition to the potential for atheroembolic cerebrovascular disease. The strong association between hypertension and stroke in patients with nonrheumatic AF needs further clarification. Determination of the precise relationships among severity of hypertension, extent of blood pressure control and stroke in patients with AF could also have important implications for clinical management. Diabetes emerged as a risk factor for stroke in some studies (39), but this has not been a consistent observation.
The importance of age as a risk factor.
When a group of 344 patients were stratified for stroke risk on the basis of clinical criteria, 75% of patients younger than 65 years were at low risk, but approximately 70% of patients older than 65 were at moderate risk and a third were at high risk (40). In the elderly, the epidemiologic evidence supporting an increased risk of stroke is strongest, but this has to be offset by the increased risk of bleeding. A recent analysis from the Stroke Prevention in Atrial Fibrillation (SPAF) trial showed that high-risk patients are identifiable with the same clinical criteria in both intermittent and sustained AF (29).
Benefit of warfarin for stroke prophylaxis.
A recent meta-analysis evaluated the effectiveness of stroke prevention in AF from all published randomized trials of antithrombotic therapy (41). Sixteen trials involving approximately 10,000 participants were analyzed (mean follow-up, 1.7 years). The superiority of adjusted-dose warfarin over aspirin was unequivocal. When warfarin and aspirin were individually compared with placebo, the occurrence of stroke was decreased by 60% and 20%, respectively. Although warfarin confers a relative risk reduction of 40% to 50% in all patients with stroke compared with aspirin, the magnitude of benefit is directly proportional to an increase in the inherent risk of stroke. This finding has important clinical implications. Because the concern for bleeding complications is understandably greater among the elderly high-risk subgroup, these patients are also at higher risk for stroke and may be less likely to receive warfarin (42,43). In this respect, risk stratification on the basis of the SPAF-III criteria might identify subgroups of older patients who can be treated with aspirin alone, particularly in the absence of a history of hypertension (37). In addition to its proven effectiveness for stroke prevention, warfarin therapy may have an impact on multi-infarct dementia and so may also benefit cognitive function in the elderly; however, this effect is purely speculative (43,44). Eventually, anticoagulation in the elderly may be facilitated by tight control of the International Normalized Ratio with simpler methods, such as finger-stick collection as opposed to venous blood samples (43,45).
From the randomized trials of nonrheumatic AF (5,46), the overall risk of hemorrhage attributable to this arrhythmia was low. Established risk factors for intracranial hemorrhage in anticoagulated patients include age, uncontrolled hypertension and anticoagulation level above target range.
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Lone AF
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By definition, lone AF occurs in the absence of structural heart disease, as determined by the physical examination, electrocardiography, chest radiography and echocardiography. The prevalence of lone AF depends on the age of the population under consideration and whether AF is paroxysmal or chronic; it ranges from 2% to 31% (47–49).
Stroke risk in lone AF.
The risk of stroke in subjects with lone AF is governed largely by the presence and extent of additional risk factors (Fig. 4, Table 1). In an early study of the Framingham population (47), an approximately fourfold risk of stroke was demonstrated in subjects with lone AF compared with an age- and gender-matched population. These patients had one or more risk factors for stroke; 56% were older than 70 years, and 32% had a history of hypertension. A subsequent study from Olmsted County, Minnesota (48), included subjects with no risk factors, limited to patients younger than 60 years. During a mean follow-up of approximately 17 years, the risk of stroke was very low (0.55/100 patient-years). The most recent experience from the Olmsted County population is in lone AF with one risk factor (i.e., age older than 60 years) (50). The combined risk of stroke and transient ischemic attack was intermediate, being increased compared with that in controls but substantially less than that described for the original Framingham population (47). Another difference between younger and older patients lies in the proportion in which chronic AF has developed at follow-up (Fig. 5).
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Figure 4 Analysis of thromboembolic risk in three studies of patients with lone atrial fibrillation according to the number of risk factors for stroke and age. (From Gersh BJ, Antithrombotic therapy in nonrheumatic/nonvalvular atrial fibrillation. J Cardiovasc Electrophysiol 1999;10:461–71. By permission of Futura Publishing Company).
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Figure 5 Type of atrial fibrillation (Afib) at diagnosis and at last follow-up in Olmsted County patients age 60 years or younger and those older than 60 years. Among younger patients, 20% never had a recurrence, 58% had recurrent disease, and only 22% had chronic atrial fibrillation at follow-up. Among older patients, 67% were in chronic Afib at follow-up. (Data from Kopecky et al. [48,50]).
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Chronicity of AF and stroke risk.
In a recent study of patients younger than 50 years from Trieste, Italy, most patients (66%) remained in paroxysmal AF during a 10-year follow-up (49). This group experienced a low thromboembolism rate of 0.36/100 patient-years. In contrast, the 34% of patients with chronic AF had a significantly higher rate of thromboembolism, 1.3/100 patient-years, suggesting that in addition to age, chronicity may be a risk factor for stroke in the lone AF population. In the Olmsted County study (48), the risk of thromboembolism was not significantly different in the young (<60 years) patients with chronic AF, who made up 22% of the population at the end of follow-up (0.51 vs. 0.55/100 patient-years overall). An explanation for chronicity as a risk factor may be provided by the echocardiographic documentation of increased left atrial dimensions in patients with chronic versus paroxysmal AF. An increased left atrial dimension previously has been shown to be a risk factor for stroke (51). Although patients younger than 50 years who have chronic AF are the minority, the decision to use anticoagulation in this group may be justified. The impact of warfarin on lifestyle, occupational hazard and patient compliance is critical to the judicious tailoring of therapy to the individual patient (52).
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AF and LV dysfunction
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Atrial fibrillation coexists with LV dysfunction in a significant proportion of the population with congestive heart failure (CHF). Atrial fibrillation is diagnosed in 10% to 35% of patients with CHF during the course of the disease and is related to the clinical severity of its symptoms (14,18,21,23,53,54). Congestive heart failure was a powerful independent predictor of the occurrence of AF in the Framingham study, in both symptomatic and asymptomatic LV dysfunction (55).
AF: cause as well as effect of LV dysfunction.
In most patients with CHF, AF is attributed to the pathophysiologic mechanism of stretch-mediated arrhythmogenesis, with larger left atrial volumes in those patients with AF than in those with AF in the absence of LV dysfunction (56,57). In at least a subset of the population with CHF, AF is a precursor, and the etiologic mechanism, of LV dysfunction. The entity of AF-induced cardiomyopathy, first described more than 50 years ago, is currently experiencing a resurgence of interest (58,59).
Tachycardia-induced cardiomyopathy.
Clinically, patients with this syndrome may present with marked LV dysfunction, which is often disproportionate to the severity of symptoms, but the importance is that ejection fraction and LV dimensions may revert to normal after the establishment of sinus rhythm or effective rate control. The frequency of this entity is not established, but in a series of 106 patients undergoing atrioventricular nodal ablation and permanent pacemaker implantation, LV dysfunction was noted before ablation in 45%. Three months after ablation, there was an approximately 30% improvement in ejection fraction for the group as a whole, but a dramatic improvement (ejection fraction 30% to approximately 60%) was noted in approximately 20% of patients (60). These data suggest that a heightened suspicion for a diagnosis of AF-induced cardiomyopathy should be maintained. Given its potential for reversibility, its relative infrequency belies its importance.
Detrimental effects in heart failure.
In patients with "preexisting" LV dysfunction, the detrimental role of AF on LV function and clinical CHF is probably much more common than initially suspected. In the Studies Of Left Ventricular Dysfunction (SOLVD) trials of symptomatic and asymptomatic patients with LV dysfunction, the presence of AF at baseline was a powerful independent predictor of death due to pump failure and rehospitalization for CHF. Almost identical rates of sudden cardiac death for patients with AF and those with sinus rhythm provide highly suggestive evidence that AF is the cause and not just a "marker" of more severe LV dysfunction and CHF. If AF were solely a "marker," one would have expected sudden death rates to be increased in addition to mortality associated with pump failure. Moreover, in a series of patients with stable CHF, the development of paroxysmal AF and a reduction in the contribution of the left atrium to LV filling predicted the subsequent development of AF. This, in turn, was followed by clinical and hemodynamic deterioration and a worse prognosis (61).
Mechanisms of increased mortality.
The mechanisms whereby AF adversely affects mortality may be multifactorial. The presence of an irregular ventricular rhythm has adverse hemodynamic consequences, which may have an impact on pump failure in the long term (62). Well-described repolarization abnormalities in CHF are known to increase the risk of fatal arrhythmogenesis in both humans and animal models (63,64). In addition, the increased propensity for proarrhythmia in subjects with CHF has been documented in several large series (65,66), which may be related to significant modulation of antiarrhythmic drug effects in heart failure (67,68).
Clinical implications of two epidemics (AF and CHF).
Clearly, therefore, the importance of the association of AF and LV dysfunction extends well beyond the unusual, but eminently curable, entity of tachycardia-induced cardiomyopathy. Atrial fibrillation and heart failure represent the intersection of two common diseases, both of which have been labeled "new epidemics" (2,69). The clinical management is complex, but natural history studies suggest that the maintenance of sinus rhythm and, at the very least, meticulous rate control of the ventricular response during AF are key components of the therapeutic strategy in patients with CHF. Rate control cannot be assessed solely at rest, and it is relevant that in the SOLVD database the adverse impact of AF on subsequent mortality was independent of resting heart rates (53). Adequate rate control, therefore, is defined as a heart rate of 60 to 90 beats/min on a 24-h ambulatory monitor or as an appropriate increase in response to exercise (70).
Lack of improvement in ejection fraction may be related to relatively high ejection fractions at baseline. The Ablate and Pace trial studied a similar cohort of patients but without a control group. In patients with decreased LV function at baseline (mean ejection fraction, 31%), ejection fraction increased to 41% at three months of follow-up, and the improvement was sustained at one year (60). Thus, although AF-induced cardiomyopathy is probably rare, worsening of LV dysfunction by AF may be a relatively common indication for intervention, either pharmacologic or electrical.
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Electrical and structural remodeling in AF
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Until recently, factors responsible for the maintenance of AF in prone subjects were poorly understood. A significant amount of information is now available regarding the role of electrical and anatomical changes in the atria, which result in the perpetuation of AF. Wijffels et al. (71) studied lone AF in a goat model and demonstrated that once initiated, AF tends to promote itself. It is likely that "AF begets more AF" by the process of electrophysiologic remodeling, probably related to remodeling at the ion channel level (72,73).
What requires further clarification is the extent to which these changes alter the clinical picture and the natural history in patients with AF. The implications for prevention of remodeling with early cardioversion are self-evident and could provide a strong theoretical basis for therapeutic strategies such as the implantable atrial defibrillator, transesophageal echocardiographically guided cardioversion, preventive atrial pacing methods and the use of medications to foster reverse remodeling.
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Familial AF (the genetic risk factor: hypothesis for lone AF)
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As we enter the era of functional genomics, it is relevant to consider the entity of "familial" AF. Several families with AF have been documented (74,75), but it appears that occurrence in the general population is uncommon. Nonetheless, its frequency belies its importance as a key to our understanding of factors that initiate AF. The identification by Brugada et al. (76) of a chromosome mutation in subjects with familial AF has uncovered exciting possibilities, but a culprit gene or genes have not yet been identified. Hence, continued investigation of families with hereditary AF and genotyping to identify mutations intrinsically related to a normal versus abnormal substrate is important. In regard to the functional genomics of AF, we are still in the infancy stage, but the potential is exciting.
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Who should make clinical decisions for patients with AF?
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With a condition as ubiquitous as AF, one of a variety of physicians including cardiologists, internists, neurologists, geriatricians or arrhythmia experts may be the first to come in contact with the patient. Prerequisites for management of such patients on an outpatient basis include knowledge of agents that control heart rate, antiarrhythmic drugs, anticoagulants and electrical cardioversion. Interventions such as device implantation and atrioventricular junction ablation require an arrhythmia expert and a hospital-based specialized facility. The increasing incidence of AF may necessitate the establishment of special AF clinics staffed by individuals equipped with the requisite knowledge and facilities. In the near future, anticoagulation follow-up will be simplified by the use of patient-based testing.
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Central role of epidemiology and natural history in clinical decision making: conclusions
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Currently, the epidemiology and natural history of AF govern all aspects of the clinical management of the disease. We are in the midst of an epidemic of AF, which is not entirely explained on the basis of an aging population. Age and the existence or development of concomitant heart disease determines the decision to use anticoagulation for stroke prophylaxis. Accordingly, warfarin is recommended for patients older than 65 years or in the presence of heart disease. A case has been made for aspirin alone in patients younger than 75 years without other risk factors for stroke such as hypertension or fractional shortening <28% (77). Recent data also suggest that the small subset of young patients (<50 years) with chronic lone AF has a stroke risk high enough to necessitate institution of warfarin therapy. Young patients with paroxysmal lone AF still enjoy a very low risk of stroke with no effect on mortality and do not require anticoagulation. For unknown reasons, AF is an independent predictor of hemorrhage, the occurrence of which is associated with increasing age and stroke. Of necessity, this translates into stringent control of anticoagulation, especially in these subgroups.
Chronic AF and uncontrolled ventricular rate can both result in LV dysfunction or contribute to its progression. In either case, it may worsen mortality in patients with CHF, the incidence and prevalence of which are continually increasing. Radiofrequency ablation of the atrioventricular junction with pacemaker implantation can improve symptoms and LV function in some patients, but the potential for decrease in mortality needs to be proved. The critical issue of rate versus rhythm control awaits completion of the AF Follow-up Investigation of Rhythm Management trial, which plans to enroll 5,300 patients, but results may not be available for several years (78). Finally, the syndrome of AF is an independent predictor of all-cause mortality, irrespective of age or cardiac or other comorbid conditions, for reasons that remain poorly understood.
Recent developments, by affecting the natural history of the disease, could eventually alter the nature of decision making in patients with AF. The processes of electrical and structural remodeling that perpetuate AF are reversible. Trials of reverse remodeling of atrial structure and electrophysiology with drugs such as beta-adrenergic blocking agents are awaited. If sinus rhythm can be achieved, it appears to beget sinus rhythm. The molecular basis of familial AF is in the process of being defined. There is likely a spectrum of molecular defects that predispose to familial AF. The eventual goal is identification of the specific functions of the mutant genes, which, in turn, promises a range of new and specific therapeutic targets in the future.
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R. R Kasliwal, S. Mukesh, G. Manohar, N. Aggarwal, and A. Bhatia
Pharmacotherapy of Atrial Fibrillation
Asian Cardiovasc Thorac Ann,
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11(4):
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[Abstract]
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M. S. Maurer
Age: a nonmodifiable risk factor?
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P. A Gould, M. D Esler, and D. M Kaye
Chronic atrial fibrillation does not influence the magnitude of sympathetic overactivity in patients with heart failure
Eur. Heart J.,
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[Abstract]
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D. S. Likosky, B. J. Leavitt, C. A. S. Marrin, D. J. Malenka, A. G. Reeves, R. M. Weintraub, L. R. Caplan, Y. R. Baribeau, D. C. Charlesworth, C. S. Ross, et al.
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[Abstract]
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L. Mestroni
Genomic medicine and atrial fibrillation
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P. T. Ellinor, J. T. Shin, R. K. Moore, D. M. Yoerger, and C. A. MacRae
Locus for Atrial Fibrillation Maps to Chromosome 6q14-16
Circulation,
June 17, 2003;
107(23):
2880 - 2883.
[Abstract]
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V. Essebag, T. Hadjis, R. W. Platt, and L. Pilote
Amiodarone and the risk of bradyarrhythmia requiring permanent pacemaker in elderly patients with atrial fibrillation and prior myocardial infarction
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January 15, 2003;
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[Abstract]
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Y.-H. Chen, S.-J. Xu, S. Bendahhou, X.-L. Wang, Y. Wang, W.-Y. Xu, H.-W. Jin, H. Sun, X.-Y. Su, Q.-N. Zhuang, et al.
KCNQ1 Gain-of-Function Mutation in Familial Atrial Fibrillation
Science,
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[Abstract]
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B. Gorenek, G. Kudaiberdieva, O. Goktekin, Y. Cavusoglu, A. Birdane, A. Unalir, N. Ata, and B. Timuralp
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[Abstract]
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T. S. M. Tsang, B. J. Gersh, C. P. Appleton, A. J. Tajik, M. E. Barnes, K. R. Bailey, J. K. Oh, C. Leibson, S. C. Montgomery, and J. B. Seward
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C. P. Williams, N. Hu, W. Shen, A. B. Mashburn, and K. T. Murray
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K. M. Stein, D. E. Euler, R. Mehra, K. Seidl, D. J. Slotwiner, S. Mittal, S. M. Markowitz, B. B. Lerman, and Jewel AF Worldwide Investigators
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E. MARBAN, H.B. NUSS, and J.K. DONAHUE
Gene Therapy for Cardiac Arrhythmias
Cold Spring Harb Symp Quant Biol,
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A. Palinkas, E. Antonielli, E. Picano, A. Pizzuti, A. Varga, B. Nyuzo, J.M. Alegret, A. Bonzano, M. Tanga, A. Coppolino, et al.
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M. Arndt, U. Lendeckel, C. Rocken, K. Nepple, C. Wolke, A. Spiess, C. Huth, S. Ansorge, H. U. Klein, and A. Goette
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W. Xu, H.-F. Tse, F. H.Y. Chan, P. C. W. Fung, K. L.-F. Lee, and C.-P. Lau
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Top
Abstract
Incidence and prevalence