SemOpenAlex |

SemOpenAlex

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1967121574> ?p ?o ?g. }

Showing items 1 to 100 of ±186 with 100 items per page.

W1967121574 endingPage "1277" @default.
W1967121574 startingPage "1262" @default.
W1967121574 abstract "HomeCirculationVol. 93, No. 6Management of Patients With Atrial Fibrillation Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBManagement of Patients With Atrial Fibrillation A Statement for Healthcare Professionals From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association Eric N. Prystowsky, D. Woodrow BensonJr, Valentin Fuster, Robert G. Hart, G. Neal Kay, Robert J. Myerburg, Gerald V. Naccarelli and D. George Wyse Eric N. PrystowskyEric N. Prystowsky Search for more papers by this author , D. Woodrow BensonJrD. Woodrow BensonJr Search for more papers by this author , Valentin FusterValentin Fuster Search for more papers by this author , Robert G. HartRobert G. Hart Search for more papers by this author , G. Neal KayG. Neal Kay Search for more papers by this author , Robert J. MyerburgRobert J. Myerburg Search for more papers by this author , Gerald V. NaccarelliGerald V. Naccarelli Search for more papers by this author and D. George WyseD. George Wyse Search for more papers by this author Originally published15 Mar 1996https://doi.org/10.1161/01.CIR.93.6.1262Circulation. 1996;93:1262–1277Executive Summary Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Its incidence increases with age and the presence of structural heart disease. It is a major cause of stroke, especially in the elderly. Although the causes are diverse, hypertension is common. Most patients experience palpitations, but fatigue, dyspnea, and dizziness are not uncommon. Patients with an uncontrolled ventricular response during AF may occasionally develop a tachycardia-induced cardiomyopathy. There are three therapeutic goals to consider for patients with AF: rate control, maintenance of sinus rhythm, and prevention of thromboembolism. The risks and benefits of each treatment must be considered for each patient. Restoration and Maintenance of Sinus Rhythm Several drugs effectively restore and maintain sinus rhythm in patients with AF. To date few data are available to confirm superiority of any particular drug over another for this purpose. Agents such as digitalis, verapamil, diltiazem, and β-adrenergic blockers may be useful during AF to decrease the ventricular response that occurs over the atrioventricular (AV) node, but they rarely terminate AF. Intravenous procainamide is the treatment of choice for patients with Wolff-Parkinson-White syndrome who have a preexcited ventricular response during AF, provided they are hemodynamically stable. Patients who are unstable (eg, those with hypotension or significant heart failure) may require immediate cardioversion. Drugs selected for long-term oral therapy should be given initially in low to moderate doses and titrated upward, depending on effectiveness and side effects. Drug interactions with warfarin and digoxin should be monitored. Proarrhythmia is the most important risk associated with antiarrhythmic drug therapy. Bradyarrhythmias, especially sinus bradycardia, and ventricular tachyarrhythmias, especially torsade de pointes, can occur. Proarrhythmia often occurs during initiation of antiarrhythmic drug treatment. In patients without heart disease who have a normal baseline QT interval, ventricular proarrhythmia is relatively rare, and outpatient initiation of treatment is reasonable. However, patients with structural heart disease, especially those with a history of congestive heart failure, are at highest risk for proarrhythmia. Inpatient initiation of antiarrhythmic drug therapy is recommended for these patients. Nonpharmacological approaches to prevention of AF include surgery, atrial pacing, and endocardial catheter ablation. Too few data are available to make any specific recommendations. Control of Ventricular Rate In patients without ventricular preexcitation, acute rate control is most effective with intravenous verapamil, diltiazem, or β-blockers. β-Adrenergic blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone. Verapamil, diltiazem, and β-blockers are more effective than digoxin when given orally for long-term rate control and should be the initial drugs of choice. Digoxin should be considered as first-line treatment in patients with congestive heart failure secondary to impaired systolic ventricular function. Some patients may require combinations of digoxin, calcium channel blockers, and β-adrenergic blockers to control ventricular response during AF. Intravenous procainamide is the treatment of choice if conduction is over an accessory pathway. Nonpharmacological methods to control ventricular rate include endocardial catheter ablation or modification of the AV junction and surgically induced AV block. Surgery, however, is rarely indicated. Catheter ablation is effective and is recommended in patients who have not responded to or are intolerant of drugs used for rate control. Prevention of Thromboembolism Patients at “low risk” may be given aspirin 325 mg/d to prevent stroke. “High-risk” patients who can safely receive anticoagulation should be treated with warfarin. For high-risk AF patients aged 75 years or younger, an International Normalized Ratio (INR) range of 2.0 to 3.0 is safe and effective; for those older than 75, close surveillance of INR levels is recommended because of the apparently greater likelihood of bleeding complications. Patients with AF who cannot safely receive anticoagulation should be given aspirin. The long-term recurrence rate for stroke is high, and warfarin anticoagulation is recommended; aspirin is an alternative therapy for those who cannot take anticoagulants. Regarding cardioversion, in patients who have AF of unknown duration or for more than 48 hours, anticoagulation should be given for 3 weeks before electrical or pharmacological cardioversion and continued for 4 weeks after cardioversion. An alternative approach involves use of intravenous heparin and subsequent transesophageal echocardiography (TEE). Patients without atrial thrombi may undergo cardioversion and be given warfarin for 4 weeks. Minimal data are available about embolic risk and the need for anticoagulation in patients with AF of 48 hours’ duration or less. Epidemiology Atrial fibrillation is the most common sustained arrhythmia encountered in clinical practice. Recent data suggest that hospital stays for AF are markedly greater than for any other arrhythmia.1 Nevertheless, information about its incidence and prevalence in a general population is rather sparse. There are fewer data on atrial flutter. Data from clinical populations are subject to the influence of a number of factors that tend to introduce bias. The single best sources of data are reports from the Framingham Study.2345 It should be noted that the Framingham population may not be representative of the ethnic and racial diversity found in other parts of the country. Atrial fibrillation commonly occurs with rheumatic heart disease, particularly mitral stenosis. It also occurs with many other cardiac disorders, including coronary heart disease, congestive or hypertrophic cardiomyopathy, mitral valve prolapse, and mitral valve annular calcification. In the setting of acute myocardial infarction or following cardiac surgery, AF is a common but usually self-limited problem. A number of potentially reversible, noncardiac factors are also associated with transient AF. The latter include hyperthyroidism, acute alcohol intoxication, cholinergic drugs, noncardiac surgery or diagnostic procedures, and pulmonary conditions leading to hypoxemia. Continuing problems with AF are most commonly associated with rheumatic heart disease; hypertension, especially when left ventricular hypertrophy is present; and chronic coronary heart disease.2 Of course, AF can also occur in the absence of other preexisting conditions; in this situation it is called lone or primary AF.367The reported frequency of lone AF, usually about 10% or less,367 may be lower than that currently observed in an office-based setting. At least two factors could be responsible: a referral bias caused by patients seen at tertiary medical centers, from which most data are reported, who are more sick; a change in the epidemiology of AF; or both. Other data (E.N. Prystowsky, unpublished data, 1996) demonstrate that approximately 28% of 172 consecutive outpatients referred for evaluation of AF had lone AF, defined as the absence of any known etiologic factors plus normal ventricular function by echocardiography. The majority of patients were younger than 65 years, although age was not used to define lone AF. Future investigations involving patients of various ages and from various types of practices should clarify this issue. Prevalence of AF increases with age and is slightly more common in men than in women.2 The prevalence of AF is 0.5% for the group aged 50 to 59 years and rises to 8.8% in the group aged 80 to 89 years.5 In 1982 the cumulative incidence of development of AF over 22 years in the Framingham Study was 2.2% in men and 1.7% in women.2 Excluding persons with rheumatic heart disease, the 2-year incidence of development of AF in 1987 in Framingham was 0.04% for men and 0% for women aged 30 to 39 years; the corresponding figures in the 80-to-89 age group were 4.6% and 3.6%.4 In the more recently initiated Cardiovascular Health Study, a cross-sectional population study of Americans older than 65 years, the prevalence of AF on a 24-hour electrocardiographic (ECG) recording was approximately 5%.78 Because women have a greater life expectancy than men, the actual number of cases in elderly women (older than 75) is greater than it is in elderly men. Based on biennial examination in the Framingham Study, the age-adjusted prevalence of AF has increased substantially, particularly in men, over a 30-year period beginning in the mid 1950s (unpublished data, P.A. Wolf, 1995). The importance of this observation, if it can be generalized to the nation, is that the impact of AF with respect to stroke and other consequences may actually be much greater than estimated. The cardiac precursors of AF were slightly different in men and women in the 1982 report from Framingham.2 In men the significant associations were stroke, cardiac failure, rheumatic heart disease, and hypertensive cardiovascular disease. The strongest associations of these were cardiac failure and rheumatic heart disease. In women the only two significant precursors were cardiac failure and rheumatic heart disease, and the latter was much stronger than in men. Echocardiographic correlates of these clinical features included left atrial enlargement, increased left ventricular wall thickness, and reduced left ventricular shortening.9 Cardiovascular risk factors significantly associated with AF in Framingham were diabetes and left ventricular hypertrophy.2The importance of AF in a general population is that its appearance heralds a mortality rate double that of control subjects. Much of the morbidity and some of the mortality from AF are due to stroke. The risk of stroke is not due solely to AF, and it substantially increases in the presence of other cardiovascular disease. The attributable risk of stroke from AF is estimated to be 1.5% for the 50-to-59-year age group and approaches 30% for those aged 80 to 89.45There is conflict in the literature concerning prognosis for lone or primary AF. In a 1985 report from Framingham, lone AF accounted for 11.4% of all cases of AF. Importantly, in these persons the relative risk for development of stroke was 4.1% compared with control subjects, whereas incidences for coronary heart disease events and congestive heart failure were the same in both groups.3 In Olmsted County, Minnesota, 2.7% of all patients aged 60 years or younger with AF were identified as having lone AF, and among these patients there was no increased risk of stroke.6 The major difference between the two studies is that the latter6 restricted observations to younger patients free of diabetes or hypertension, whereas in the former3 the majority of the cases of AF occurred in those older than 60 years, 31.5% of whom had hypertension, an important risk factor for stroke in patients with AF.3 Thus, it appears that there is an increased risk of stroke with lone AF in those older than 60 but not in younger patients. In the Cardiovascular Health Study, which included only patients over 65, 6% of cases of AF in women were categorized as lone AF; 9% of cases of AF in men were lone AF.7 The investigators have questioned the clinical usefulness of this diagnosis in the elderly. Atrial fibrillation is relatively rare in the first 2 decades of life. It has been reported in the fetus, neonate, child, and adolescent, but except for the study by Radford and Izukawa,10 the reports have usually been single case. The rarity of cases has resulted in a limited clinical experience, which has hindered understanding of the etiology of AF, development of management strategies, and characterization of prognosis in the young patient. Despite the rarity of cases, a few generalizations can be made. In the fetus and neonate, AF is almost always associated with an accessory AV connection.111213 In this setting it is postulated that rapid AV reentry degenerates into AF14 ; the natural history favors spontaneous resolution of tachycardia during the first year of life.15 A similar mechanism has been proposed for development of AF during paroxysmal supraventricular tachycardia in adolescents.16 Atrial fibrillation has been reported in association with dilated and hypertrophic cardiomyopathy. The precise reason for this association has not been established, but it may be related to other aspects of the heart disease rather than as a consequence of the hemodynamic derangement. For example, Spirito et al17 noted that patients with hypertrophic cardiomyopathy and AF usually have the unobstructed type with mild left ventricular hypertrophy. Long-standing, severe AV valve disease is a risk factor for development of AF. Such a problem is unusual in young persons in the industrialized world, but in areas in which rheumatic heart disease is prevalent, AF is common in young patients. Of note, AF is uncommon in young patients with tachycardia-bradycardia or sick sinus syndrome, which is relatively common following atrial surgery for congenital heart defects.18 Atrial fibrillation may occur in an adult with previous surgery to correct congenital heart disease. In this setting the tachycardia is usually atrial with some features of atrial flutter.19 Furthermore, when such patients undergo pacing conversion of atrial tachycardia, AF develops in about 25% of them, but this is transient and supervened by sinus rhythm within minutes.20 Finally, in ostensibly normal adolescents AF is rare, but in such cases hyperthyroidism has been noted.21 Atrial fibrillation has infrequently been reported in association with intracardiac tumor and muscular dystrophy. Pathophysiology Atrial tachyarrhythmias in general and AF in particular occur in three distinct clinical circumstances: (1) as a primary arrhythmia in the absence of identifiable structural heart disease; (2) as a secondary arrhythmia in the absence of structural heart disease but the presence of a systemic abnormality that predisposes the individual to the arrhythmia; and (3) as a secondary arrhythmia associated with cardiac disease that affects the atria. At this time it is unclear whether the pathophysiological factors responsible for maintaining AF after it has been induced are common to all three, but it is likely that the initiating factors differ. There are distinct differences between pathological findings in AF secondary to cardiac disorders and other forms of AF. Atrial dilatation and patchy fibrosis ranging from scattered foci to diffuse involvement, including evidence of destruction of the sinoatrial node, are commonly present when AF is associated with structural heart disease.2223 In contrast, AF secondary to systemic disorders, such as thyrotoxicosis or electrolyte disturbances, is usually unaccompanied by pathological abnormalities or at most by nonspecific scattered fibrosis. From the limited information available, paroxysmal AF in otherwise healthy persons has no pathological correlate and has its basis in either abnormal function of atrial myocyte ion channels, a functional disorder of atrial myocardium, or is associated with unidentified nonpathological structural abnormalities. In some patients AF may be the earliest manifestation of sick sinus syndrome, often a panatrial disease. There are defined clinical associations between patterns of AF and pathophysiology based on underlying cause. In the presence of heart disease, AF may be paroxysmal at onset and appears to begin when the disease has progressed to clinically significant levels. Over time it has a tendency to become chronic and fixed, rather than remaining paroxysmal. In contrast, systemic conditions that predispose a person to AF are usually associated with persistence of arrhythmia during the period of time that the abnormality persists, which is then followed by either spontaneous reversion after treatment of the predisposing condition or ability to maintain sinus rhythm after cardioversion. In the absence of cardiac or noncardiac disorders, AF is most commonly paroxysmal and recurrent and only occasionally more persistent.24Electrophysiology of Atrial Fibrillation The most widely accepted theory of the mechanism of AF is the multiple wavelet hypothesis of Moe.25 This hypothesis envisions multiple reentrant impulses of various sizes wandering through the atria, creating continuous electrical activity. The wavelets are of the leading circle type, with a functionally determined area of conduction block at the center of the circle preventing its collapse and extinction.26 The critical number of wavelets required for the perpetuation of AF is approximately six26 ; the number of wavelets appears to be smaller with longer wavelengths in coarse AF and greater with smaller wavelengths in fine AF. The wavelength, or the product of conduction velocity and refractory period, is a critical determinant for maintaining AF. Influences that increase the wavelength tend to prevent or terminate AF, whereas those that tend to shorten the wavelength of the atrial impulse tend to favor the onset and perpetuation of AF. Wavelength can be prolonged by antiarrhythmic drugs and shortened by increased parasympathetic tone, rapid atrial pacing, or intra-atrial conduction abnormalities. Recent data suggest that AF may cause electrical changes in the atria, which may lead to persistence or recurrence of AF.27 In a chronic instrumented goat model, Wijffels et al27 noted that (1) artificial maintenance of AF resulted in a prolonged duration of subsequent episodes of AF; (2) atrial refractoriness was shortened markedly during the first 24 hours of AF; and (3) an inverse rate adaptation of atrial refractoriness was manifested by shortening of the effective refractory period at slower paced rates. Anatomic and genetic correlates of these findings remain to be elucidated. However, these exciting new observations may explain, in part, the clinical observation that maintenance of sinus rhythm is more difficult in patients who have had persistent AF for many months. Functional Mechanisms of Atrial Fibrillation It has long been recognized that increased parasympathetic tone predisposes otherwise normal hearts to the onset of AF.28 This may occur through several mechanisms, but it is clear that increased parasympathetic activity, as well as the muscarinic agonist acetylcholine, can abruptly shorten the time course of repolarization through activation of a muscarinic potassium channel in atrial muscle.29 This action shortens the refractory period of atrial tissue and therefore shortens the wavelength of the atrial impulse. Increased sympathetic tone may also lead to AF. In addition, a “maladaptation” of atrial refractory periods to variations in heart rate has been associated with a propensity to AF.30 The absence of physiological shortening of the refractory period in response to an increased heart rate has been observed and found highly predictive for atrial tachyarrhythmias. This correlation appears to be at variance with the mechanism related to the response to parasympathetic stimulation, since maladaptation produces the reverse effect of the shortening induced by acetylcholine. It is possible that two fundamentally different mechanisms can both be responsible for potentiation of atrial tachyarrhythmias under different conditions, or that maladaptation to pacing may correlate with increased response to parasympathetic surges, a possibility that has not yet been studied. Furthermore, it is possible that changes in refractoriness may differ in various parts of the atria. Regardless, present knowledge suggests that one feature common to all patterns is the requirement for multiple wavelets of activation to sustain AF in normal and abnormal hearts. The possibility that multiple areas of focal automaticity could produce the same pattern should not be dismissed, particularly in the presence of underlying structural heart disease and the systemic abnormalities associated with AF. In this regard, a recent observation in a small group of patients suggests that a unifocal atrial mechanism may be the initiating factor in some patients with apparent lone AF. Such a mechanism could also produce multiple wavelets of activation, although by different pathophysiological mechanisms. Atrioventricular Node Conduction The AV node exhibits several properties that tend to limit ventricular rate during AF. First, the excitability of cells within the AV node is significantly less than the adjacent atrial myocardium.31 The inexcitable period of AV nodal cells is delayed beyond the repolarization phase of the action potential. Thus, the refractory period of the AV node tends to be relatively prolonged. Second, the AV node demonstrates decremental conduction properties; that is, the amplitude and rate of rise of cardiac action potentials decrease progressively from cell to cell. Therefore, as action potentials are conducted along the course of the AV node, there is a progressive decrease in their ability to induce new action potentials in the cells that lie ahead.32 Because of this property of decremental conduction, impulses may traverse a portion of the AV node before encountering conduction block. Among the clinical manifestations of this property is the phenomenon of concealed conduction, in which an atrial impulse that itself does not conduct to the ventricles may impair conduction of subsequent impulses.33 Thus, a premature electrical impulse may slow conduction of another impulse through the AV node, blocking an impulse that otherwise would have conducted.34 The conduction interval through the AV node is inversely related to the coupling interval of the preceding atrial impulses, with short atrial cycles resulting in longer AV nodal conduction intervals than longer atrial cycles. Moe and colleagues35 observed that when the atrial rate during AF was relatively slow, there was a tendency for the ventricular rate to increase; conversely, when the atrial rate increased, the ventricular rate slowed. The combined properties of concealed conduction, delayed refractoriness, and the rapid, variable cycle length of the wavelets of atrial activation tend to slow conduction of impulses through the AV node in AF. The result is a significantly slower ventricular rate than atrial rate. Accessory AV pathways typically do not share these electrophysiological properties of the normal AV node, and patients with Wolff-Parkinson-White syndrome require special therapeutic considerations. The electrophysiological properties of the AV node are profoundly affected by autonomic influences. Withdrawal of vagal inhibition or an increase in sympathetic stimulation facilitates AV nodal conduction. Exercise is associated with both of these changes in autonomic tone, and the ventricular response during AF may substantially increase along with the metabolic demands of the individual. Changes in AV nodal conduction will reflect the adequacy of heart rate control in patients with AF during varying levels of exertion, emotion, and other metabolic stresses. The marked variation in AV nodal conduction properties as a consequence of varying autonomic tone often presents a therapeutic dilemma for physicians treating patients with AF in whom the ventricular rate may be excessively rapid during exercise, yet inappropriately slow during rest. Hemodynamic Effects Related to Loss of Atrioventricular Synchrony and Irregular RR Intervals In addition to an inappropriately rapid heart rate, patients with AF experience the loss of normal AV synchrony and an irregular ventricular rhythm. The loss of effective atrial contraction may result in a marked decrease in cardiac output, especially for persons with impaired diastolic filling of the ventricles. Patients with mitral stenosis, restrictive or hypertrophic cardiomyopathy, pericardial diseases, or ventricular hypertrophy are especially likely to experience hemodynamic deterioration with development of AF. In contrast, patients with impaired systolic function with elevated filling pressures and dilated, compliant ventricles may experience only minor hemodynamic deterioration as a consequence of losing AV synchrony. The random variation in RR intervals during AF results in a constantly changing diastolic filling interval. This fluctuation in diastolic filling interval results in a widely varying stroke volume. Naito and colleagues36 studied the effects of an irregular ventricular rhythm on cardiac output in dogs with complete AV block during ventricular pacing. These investigators found that an irregular ventricular rhythm was associated with a 15% decline in cardiac output compared with a regular rhythm at the same average pacing rate. Mitral regurgitation was observed in these animals during an irregular paced rhythm but not with constant-rate pacing. Thus, it appears that both loss of AV synchrony and irregularity of the ventricular rhythm have an adverse impact on cardiac output. It is quite likely that many symptoms related to AF are due to the variation in left ventricular stroke volume as a result of irregular RR intervals. Chronically elevated ventricular rates during AF or any supraventricular tachycardia may result in a reversible form of ventricular dysfunction characterized by global hypokinesis and dilatation. Persons with continuously elevated ventricular rates (usually greater than 130 beats/min) for a period of several months are at risk of developing a tachycardia-induced cardiomyopathy.37 This form of cardiomyopathy is often reversible following effective control of the ventricular rate. In fact, several investigators have found this to be true in patients with AF when pharmacological or nonpharmacological methods are used to control ventricular rate.383940Clinical Presentations Symptoms associated with AF vary and depend on several factors, including ventricular rate, cardiac function, concomitant medical problems, and individual patient perceptions. Most patients experience palpitations, but presyncope, dizziness, fatigue, and dyspnea are not uncommon. Furthermore, a minority of patients are asymptomatic and AF is discovered by chance. Although asymptomatic patients usually have a relatively controlled ventricular rate, even in the absence of drugs, in some instances the ventricular rate is greater than 100 beats/min. Some patients may have left ventricular dysfunction presumably secondary to a persistently fast ventricular rate during AF.38 Three specific, although relatively uncommon clinical presentations, are noted below. Tachycardia-Induced Tachycardia Tachycardia-induced tachycardia is the phenomenon in which one tachycardia degenerates into another.14 For example, atrial flutter and certain atrial tachycardias often degenerate into AF. More interesting is the induction of AF as a result of a nonatrial tachycardia; for example, AV or AV node reentry.1441424344 Even ventricular tachycardia, with or without ventriculoatrial conduction, can initiate AF.14 The mechanism of tachycardia-induced tachycardia in nonatrial arrhythmias is unclear and probably multifactorial. Rate of tachycardia, accessory pathway electrophysiological properties, intrinsic atrial vulnerability, and contraction-excitation feedback45 may be causative. In patients who underwent surgery for Wolff-Parkinson-White syndrome, Chen et al42 reported that cycle length of AV reentry was shorter in patients with a history of AF. Spach et al46 showed that micro-reentry based on anisotropy can occur in very small muscle bundles in the atrial appendage, and in patients with AV reentry, spontaneous degeneration into AF during electrophysiological study commonly occurs first on the high right atrial recording.1447 Sudden dilatation of the atria, which can be observed at surgery after onset of AV reentry, can affect cardiac membrane potential45 and lead to development of AF. Whatever the exact mechanism for tachycardia-induced tachycardia in patients with otherwise normal atria, it is important to be aware of its occurrence. In patients with a history of regular palpitations preceding AF, AV or AV node reentry may be a cause of AF. In these persons, elimination of the primary arrhythmia almost always prevents further episodes of AF.14Atrial Fibrillation in Wolff-Parkinson-White SyndromeAtrioventri" @default.
W1967121574 created "2016-06-24" @default.
W1967121574 creator A5004242309 @default.
W1967121574 creator A5017912011 @default.
W1967121574 creator A5020566430 @default.
W1967121574 creator A5024440653 @default.
W1967121574 creator A5046539743 @default.
W1967121574 creator A5066655594 @default.
W1967121574 creator A5074727212 @default.
W1967121574 creator A5086609118 @default.
W1967121574 date "1996-03-15" @default.
W1967121574 modified "2023-10-17" @default.
W1967121574 title "Management of Patients With Atrial Fibrillation" @default.
W1967121574 cites W1512926192 @default.
W1967121574 cites W1823456243 @default.
W1967121574 cites W1952704118 @default.
W1967121574 cites W1968687951 @default.
W1967121574 cites W1971570107 @default.
W1967121574 cites W1973215845 @default.
W1967121574 cites W1976539643 @default.
W1967121574 cites W1980413398 @default.
W1967121574 cites W1981622404 @default.
W1967121574 cites W1984171219 @default.
W1967121574 cites W1984516185 @default.
W1967121574 cites W1987936575 @default.
W1967121574 cites W1989988938 @default.
W1967121574 cites W1993324690 @default.
W1967121574 cites W1994407295 @default.
W1967121574 cites W1997974761 @default.
W1967121574 cites W1998994470 @default.
W1967121574 cites W1999199829 @default.
W1967121574 cites W2002374666 @default.
W1967121574 cites W2003648920 @default.
W1967121574 cites W2005308598 @default.
W1967121574 cites W2006297977 @default.
W1967121574 cites W2013188129 @default.
W1967121574 cites W2013832146 @default.
W1967121574 cites W2014876946 @default.
W1967121574 cites W2019290393 @default.
W1967121574 cites W2024031605 @default.
W1967121574 cites W2025136043 @default.
W1967121574 cites W2025600253 @default.
W1967121574 cites W2029045834 @default.
W1967121574 cites W2029583033 @default.
W1967121574 cites W2031119712 @default.
W1967121574 cites W2031156936 @default.
W1967121574 cites W2033088301 @default.
W1967121574 cites W2033104269 @default.
W1967121574 cites W2033232925 @default.
W1967121574 cites W2036415059 @default.
W1967121574 cites W2036783406 @default.
W1967121574 cites W2037878459 @default.
W1967121574 cites W2040452288 @default.
W1967121574 cites W2045059300 @default.
W1967121574 cites W2045783302 @default.
W1967121574 cites W2049130774 @default.
W1967121574 cites W2049614660 @default.
W1967121574 cites W2051487731 @default.
W1967121574 cites W2051513183 @default.
W1967121574 cites W2052755535 @default.
W1967121574 cites W2053535889 @default.
W1967121574 cites W2053623462 @default.
W1967121574 cites W2063589187 @default.
W1967121574 cites W2065421515 @default.
W1967121574 cites W2066507239 @default.
W1967121574 cites W2066941747 @default.
W1967121574 cites W2067111847 @default.
W1967121574 cites W2067176571 @default.
W1967121574 cites W2072470433 @default.
W1967121574 cites W2072959339 @default.
W1967121574 cites W2073396391 @default.
W1967121574 cites W2074462354 @default.
W1967121574 cites W2075650482 @default.
W1967121574 cites W2076534662 @default.
W1967121574 cites W2081517567 @default.
W1967121574 cites W2083164318 @default.
W1967121574 cites W2084719078 @default.
W1967121574 cites W2086164929 @default.
W1967121574 cites W2086637755 @default.
W1967121574 cites W2087828360 @default.
W1967121574 cites W2090021728 @default.
W1967121574 cites W2090865854 @default.
W1967121574 cites W2094339929 @default.
W1967121574 cites W2095484942 @default.
W1967121574 cites W2097258336 @default.
W1967121574 cites W2097362535 @default.
W1967121574 cites W2104674675 @default.
W1967121574 cites W2110506257 @default.
W1967121574 cites W2112058034 @default.
W1967121574 cites W2116017164 @default.
W1967121574 cites W2119473125 @default.
W1967121574 cites W2119553073 @default.
W1967121574 cites W2125137491 @default.
W1967121574 cites W2126596713 @default.
W1967121574 cites W2126789285 @default.
W1967121574 cites W2127337963 @default.
W1967121574 cites W2151184079 @default.
W1967121574 cites W2153581717 @default.