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(Circulation. 1995;92:160-163.)
© 1995 American Heart Association, Inc.

Articles

Cardioversion of Nonrheumatic Atrial Fibrillation

Reduced Thromboembolic Complications With 4 Weeks of Precardioversion Anticoagulation Are Related to Atrial Thrombus Resolution

Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994.

Laura J. Collins, MD; David I. Silverman, MD; Pamela S. Douglas, MD; Warren J. Manning, MD

From the Charles A. Dana Research Institute and the Harvard-Thorndike Laboratory of the Department of Medicine, Cardiovascular Division (L.J.C., P.S.D., W.J.M.), Beth Israel Hospital and Harvard Medical School, Boston, Mass, and the Cardiology Division of the John Dempsey Hospital and University of Connecticut Health Center, Farmington, Conn (D.I.S.).

	Abstract

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Background The use of warfarin anticoagulation for several weeks before cardioversion results in a 90% reduction in the incidence of cardioversion-related thromboembolism. The mechanism of this benefit, however, is unknown; it has been widely attributed to organization and adherence of atrial thrombi, a finding observed among pathological studies of patients with rheumatic valvular disease.

Methods and Results Serial transesophageal echocardiography was performed in 14 patients with nonrheumatic atrial fibrillation after identification of atrial thrombi on initial transesophageal study. All patients received warfarin anticoagulation and were followed clinically for signs of thromboembolism. Eighteen atrial thrombi were identified on initial transesophageal study, including 14 thrombi confined to the left atrial appendage, 2 in the body of the left atrium, 1 in the right atrial appendage, and 1 in the body of the right atrium. Thrombus size varied from 5 to 20 mm, and 6 were considered mobile. After a median of 4 weeks of warfarin, 16 of 18 atrial thrombi (89%; 95% CI, 73% to 100%) had completely resolved on transesophageal echocardiographic study. In addition, no new thrombi were identified on follow-up study, and no patient had a clinical thromboembolic event between studies.

Conclusions These data strongly support the hypothesis that among patients with nonrheumatic atrial fibrillation, the mechanism of clinical benefit with 3 to 4 weeks of warfarin before cardioversion is related to thrombus resolution and prevention of new thrombus formation rather than thrombus organization.

Key Words: echocardiography • fibrillation • electric stimulation • arrhythmia

	Introduction

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Atrial fibrillation is the most common sustained arrhythmia and is responsible for more than 180 000 hospital admissions yearly in the United States.¹ In this condition, the lack of an effective atrial contraction results in blood stasis and the formation of potentially embolic atrial thrombi. Cardioversion from atrial fibrillation to sinus rhythm is commonly performed in an effort to improve cardiac function, minimize symptoms of palpitations and dyspnea, and decrease the incidence of thrombus formation. In the absence of anticoagulation, cardioversion is associated with clinical thromboembolism in 5% to 7% of patients.^{2 3 4} The use of anticoagulation with warfarin for 3 to 4 weeks before cardioversion is associated with a reduction in cardioversion-related thromboembolism to 0% to 1.6%.^{2 3 4} This 87% improvement in the incidence of cardioversion-related embolic events has led to the widespread recommendation that anticoagulation be prescribed for several weeks before cardioversion.⁵

The mechanism by which warfarin conveys this beneficial effect on patients with atrial fibrillation is unknown. In 1960, a time when rheumatic valvular disease was commonly associated with atrial fibrillation, Goldman⁶ proposed "that recently formed atrial thrombi are likely to be dislodged at the time of conversion" and that "within 14 days there is sufficient fibroblastic infiltration to cause firm adherence of the thrombus to the atrial endocardium, thus reducing the likelihood of dislodgment." Several investigators have reported that atrial thrombi in patients with rheumatic heart disease may require several months of warfarin to resolve.^{7 8 9} In addition, a recent study demonstrated increased left atrial plasma levels of fibrinopeptide A and thrombin–antithrombin III complex activity among patients with rheumatic mitral stenosis, suggesting a state of increased coagulability in the left atrium.¹⁰ In nonrheumatic atrial fibrillation, the beneficial effects of use of warfarin for 3 to 4 weeks before cardioversion are also well established.^{2 3 4} Although the mechanism of the protective effect of warfarin against thromboembolism in this population has not been documented, enhanced thrombus organization is widely believed to be responsible.^{3 5 6 11 12 13 14}

Transesophageal echocardiography is both sensitive and specific for the premorbid identification of left atrial thrombi^{15 16 17 18 19 20} and offers the opportunity to serially evaluate left atrial thrombi before and after a 4-week course of warfarin anticoagulation. Such an assessment would help delineate the mechanism by which warfarin conveys its benefit to this group. If the majority of atrial thrombi remain present yet less mobile after 4 weeks of anticoagulation, then one could infer that the clinical benefit is probably related to thrombus organization/adherence. If a follow-up transesophageal echocardiogram documents absence of residual thrombi, however, one could infer that the benefit in this population is probably related to thrombus resolution/resorption and prevention of new thrombus formation.

	Methods

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We identified all patients with recent-onset nonrheumatic atrial fibrillation who underwent transesophageal echocardiography at our institutions from June 1, 1989, to December 31, 1994, and identified 14 consecutive patients with left atrial thrombi who had follow-up transesophageal echocardiography after warfarin therapy. Before the initial transesophageal echocardiographic study, none of the patients had been therapeutically anticoagulated with warfarin. Transesophageal echocardiography was performed after a minimum 6-hour fast. Patients received pharyngeal anesthesia with 10% lidocaine or Cetacaine spray (Cetylite Industries, Inc) and mild sedation with intravenous meperidine, midazolam, or fentanyl as necessary. Transesophageal echocardiography was performed with a commercial HP (Hewlett Packard, Medical Products Group) 5.0-MHz single-plane (n=6), biplane (n=2), or multiplane (n=6) probe. The left atrial appendage was initially viewed in the horizontal (0°) plane with the tip of the probe slightly flexed, and the probe was gently withdrawn until the bifurcation of the pulmonary artery was visualized. Imaging of the left atrium and appendage in the vertical (90°) plane was followed by posterior and anterior rotation of the probe until the coronary sinus and aorta, respectively, were visualized. Multiplane imaging was done at 0° and 90° as described above, followed by imaging of the left atrium and appendage in the horizontal (0°) plane and rotation of the imaging sector from 0° to 180° during continuous visualization of the appendage. An atrial thrombus was defined as a well-circumscribed, uniformly consistent, echo-reflective mass of different texture than the atrial wall.²¹

After identification of atrial thrombi on echocardiographic study, all patients received warfarin anticoagulation with guidelines to maintain a prothrombin time of 1.5 to 1.8 times control (international normalized ratio, 2.0 to 2.8). Follow-up transesophageal echocardiography was performed while the patients were still therapeutically anticoagulated, after review of the initial transesophageal echocardiographic data.

All data are presented as mean±SD.

	Results

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The study population included 7 women and 7 men, 69±16 years old. All patients had nonrheumatic atrial fibrillation. The clinically estimated duration of atrial fibrillation before transesophageal echocardiography was 6.1±4.2 weeks (range, 1 to 14 weeks) and was indeterminate in 4 patients. Clinical characteristics and echocardiographic data are summarized in the Table. The median interval between transesophageal echocardiographic studies was 4 weeks (mean, 5.8±3.9 weeks).

View this table: [in this window] [in a new window]   Table 1. Clinical and Echocardiographic Characteristics

Eighteen atrial thrombi were identified on initial transesophageal echocardiographic study, including 14 thrombi confined to the left atrial appendage, 2 in the body of the left atrium, 1 in the right atrial appendage, and 1 in the body of the right atrium. Patient 13 had a thrombus in both the body of the left atrium and the left atrial appendage, and patient 10 had multiple thrombi in the left atrial appendage and one in the right atrium. Thrombus size (longest dimension) ranged from 5 to 20 mm, and 6 thrombi were considered mobile.

After a median time of 4 weeks on warfarin, 16 of 18 atrial thrombi (89%; 95% CI, 73% to 100%) had completely resolved on transesophageal echocardiographic study in 12 of 14 patients (86%; 95% CI, 70% to 100%). In addition, no new thrombi were identified on follow-up transesophageal echocardiography, and no patient had clinical evidence of a thromboembolic event between echocardiographic studies. One patient (Figure) had a residual, although smaller, left atrial thrombus at transesophageal echocardiographic examination 1 and 3 weeks after the index transesophageal echocardiographic study, but no thrombus was visible at 5.5 weeks. (This patient had multiple studies because he had presented with a ventricular arrhythmia requiring electrophysiological study. This latter study was felt to be relatively contraindicated in the presence of a left atrial thrombus.) The remaining patient had follow-up transesophageal echocardiography at 4 weeks that revealed a smaller but persistent nonmobile thrombus at the tip of the left atrial appendage.

View larger version (73K): [in this window] [in a new window]   Figure 1. Serial transesophageal echocardiograms showing the left atrium (LA) and left atrial appendage (Laa) viewed in the vertical plane with a 5-MHz biplane transesophageal probe. The thrombus (arrow) is in the body of the left atrium, closely associated with the mitral annulus in the posterior portion of the left atrium. a, Initial study demonstrating a mobile 12-mm thrombus. b, Thrombus persists (arrow) but is smaller after 1 week of warfarin therapy. c, After 3 weeks of warfarin, the thrombus continues to be seen (arrow). d, Complete thrombus resolution after 5.5 weeks of warfarin.

	Discussion

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In this study, we found transesophageal echocardiographic evidence of complete atrial thrombus resolution in the vast majority of patients with nonrheumatic atrial fibrillation treated with 4 weeks of warfarin. This 89% reduction in atrial thrombi parallels historical reports of an 87% (6% to 0.8%) improvement in clinical thromboembolism afforded by 3 to 4 weeks of warfarin therapy. These data strongly suggest that in contrast to the widely held belief^{3 5 6 11 12 13 14} that the benefit of use of warfarin for several weeks before cardioversion is thrombus organization/adherence, instead, thrombus resolution and prevention of new thrombus formation during this period are the primary mechanisms of benefit for this population.

Warfarin exerts its anticoagulant activity through the inhibition of vitamin K–dependent clotting factors, thus preventing extension of existing thrombi in vivo and new thrombus formation. Although endogenous fibrinolysis probably plays a role in clot resolution, whether warfarin exerts any direct influence on clot thrombolysis is unknown. The benefit conferred by anticoagulation on left ventricular thrombi after myocardial infarction was recently demonstrated by Küpper et al,²² who found that 55% of left ventricular thrombi resolved by 12 weeks of warfarin therapy.

The ability of transesophageal echocardiography to accurately detect atrial thrombi has been demonstrated by Olson et al²³ and Hwang et al²⁴ who reported nonsimultaneous operative series using monoplane transesophageal echocardiography with sensitivities of 100% and 93% and specificities of 100% and 99%, respectively. More recently, we demonstrated left atrial thrombus sensitivity and specificity of 100% and 99%, respectively, in a simultaneous transesophageal echocardiographic intraoperative series.²⁰

Our data demonstrating that the majority (89%) of atrial thrombi resolve after 4 weeks of warfarin therapy without clinical evidence of thromboembolism do not exclude the possibility of "clinically silent" thrombus migration as a mechanism to explain our results. Patients with atrial fibrillation who are >65 years old and have a left atrial dimension >5.0 cm appear to be at highest risk for asymptomatic cerebral thromboembolism.²⁵ These represent a minority of our patients. Clinical thromboembolism among patients with atrial fibrillation and left atrial appendage thrombi has been described, despite conventional warfarin treatment and deferment of cardioversion.²⁶ The absence of any clinical event in our population, however, makes migration of thrombus an unlikely explanation for our findings.

Recently, we and others have been studying the use of transesophageal echocardiography in concert with short-term anticoagulation as a strategy for guiding early cardioversion from atrial fibrillation.^{8 26 27 28 29 30} For patients with transesophageal echocardiographic evidence of left atrial thrombi, cardioversion is generally deferred, but physicians may be reluctant to refer their patients for follow-up transesophageal echocardiography to document thrombus resolution before cardioversion, using the argument that 4 weeks of "blind" warfarin is conventional therapy before cardioversion.^{2 3 4} Our data demonstrate the persistence of residual, although smaller, "organized" thrombi in 14% of patients treated with warfarin for 4 weeks. Although we cannot conclude that cardioversion would have resulted in thromboembolism in this group, we do not recommend cardioversion if there is transesophageal echocardiographic evidence for atrial thrombi and recommend follow-up transesophageal echocardiographic study in all of these patients to document thrombus resolution before cardioversion is attempted.

In conclusion, these data strongly support the hypothesis that among patients with nonrheumatic atrial fibrillation, the mechanism of clinical benefit from use of warfarin anticoagulation for 3 to 4 weeks before cardioversion is related to atrial thrombus resolution and prevention of new thrombus formation rather than thrombus organization. In addition, the 14% prevalence of residual atrial thrombi after use of warfarin for 4 weeks suggests that precardioversion transesophageal echocardiography should be considered in all patients with evidence of atrial thrombi on initial transesophageal echocardiographic study.

	Acknowledgments

 
Dr Manning was supported in part by the Edward Mallinckrodt Jr Foundation, St Louis, Mo. Dr Silverman was supported in part by a Young Investigator Award from the Patrick and Katherine Weldon Donahue Foundation, Hartford, Conn.

	Footnotes

 
Reprint requests to Warren J. Manning, MD, Cardiovascular Division, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215.

Received March 30, 1995; revision received May 22, 1995; accepted May 25, 1995.

	References

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