The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 328:750-755 March 18, 1993 Number 11
NextNext

Cardioversion from Atrial Fibrillation without Prolonged Anticoagulation with Use of Transesophageal Echocardiography to Exclude the Presence of Atrial Thrombi
Warren J. Manning, David I. Silverman, Stephen Gordon, Harlan M. Krumholz, and Pamela S. Douglas

 

This Article
-Abstract

Commentary
-Letters

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
ABSTRACT

Background Because atrial thrombi are poorly detected by conventional noninvasive techniques such as transthoracic echocardiography, patients with prolonged atrial fibrillation usually receive several weeks of oral anticoagulation therapy before cardioversion is attempted. We wondered whether transesophageal echocardiography, an accurate method of detecting atrial thrombi, would allow early cardioversion to be performed safely if no thrombi were identified.

Methods A total of 669 consecutive patients admitted with the diagnosis of atrial fibrillation were screened. Patients were excluded if they were receiving long-term anticoagulation, if the duration of atrial fibrillation was two days or less, if they were not candidates for cardioversion, or if transesophageal echocardiography was contraindicated. Of 119 qualifying patients, 94 agreed to participate; the average duration of atrial fibrillation was 4.5 weeks. Participating patients underwent transthoracic echocardiography and transesophageal echocardiography followed by cardioversion if no thrombi were seen. Short-term anticoagulation with heparin was used in 80 patients before cardioversion, and 60 patients received warfarin for one month after cardioversion.

Results Fourteen atrial thrombi were identified in 12 patients (13 percent), and 12 of the 14 thrombi were visualized only on transesophageal echocardiography. Cardioversion was deferred in all 12 patients. Two of these 12 patients died suddenly; 4 of the 10 surviving patients underwent uneventful cardioversion after prolonged oral anticoagulation. Seventy-eight of the 82 patients without thrombi underwent successful cardioversion to sinus rhythm (47 by means of antiarrhythmic drugs and 31 by electrical cardioversion), all without long-term oral anticoagulation. None of these patients (95 percent confidence interval, 0 to 4.6 percent) had an embolic event.

Conclusions In patients with atrial fibrillation of unknown or prolonged duration who are not receiving long-term anticoagulation, atrial thrombi are detected by transesophageal echocardiography in only a small minority (13 percent in our study). Our preliminary data suggest that if transesophageal echocardiography excludes the presence of thrombi, early cardioversion can be performed safely without the need for prolonged oral anticoagulation before the procedure.

Atrial fibrillation is one of the most common types of arrhythmia, occurring in up to 4 percent of patients over 60 years of age1,2,3. This arrhythmia is characterized by a lack of organized atrial electrical and mechanical activity, and the resulting blood stasis favors the formation of atrial thrombi. Atrial fibrillation has been identified as the rhythm responsible for more than half of all instances of systemic thromboembolism from the heart4; the brain is the primary target5,6. In addition, atrial fibrillation is associated with a decrease in cardiac output because of the loss of the atrial contribution to ventricular filling7.

Cardioversion is performed in patients with atrial fibrillation in an effort to improve cardiac function, relieve symptoms, and decrease the risk of thrombus formation8. Unfortunately, successful cardioversion is associated with a 5 to 7 percent incidence of embolism among patients who have not received anticoagulant therapy9,10,11,12,13,14. Because atrial thrombi are poorly detected by conventional noninvasive techniques, such as transthoracic echocardiography, the standard care of patients with atrial fibrillation of unknown or prolonged duration (longer than two days) usually includes several weeks of oral anticoagulation before cardioversion is attempted8,15. Anticoagulation decreases the risk of an embolic event after cardioversion to less than 1.6 percent,10,12,16 but it carries its own risks, and the patient must be hospitalized a second time for cardioversion.

Transesophageal echocardiography is a highly accurate method of detecting atrial thrombi17,18,19. We evaluated the efficacy of transesophageal echocardiography to exclude the presence of atrial thrombi in patients with atrial fibrillation of prolonged or unknown duration, thereby allowing early, safe cardioversion if no thrombi were found.

Methods

Study Patients

We evaluated 669 consecutive adults admitted to Beth Israel Hospital from January 1, 1990, through September 15, 1992, or to the University of Connecticut Health Center from January 1, 1991, through September 15, 1992, with diagnoses that included atrial fibrillation. Patients were excluded if they were receiving long-term anticoagulation, if the duration of atrial fibrillation was two days or less, if their physicians thought that cardioversion was not indicated, or if transesophageal echocardiography was contraindicated (because of esophageal stricture in one patient and because of a large esophageal diverticulum in one patient)20. A previous embolic event was not grounds for exclusion. Of the 119 eligible patients, 25 declined to participate.

Of the remaining 94 patients, 43 were men and 51 were women; their mean age (±SD) was 72 ±13 years (range, 30 to 98). The underlying disorder predisposing these patients to atrial fibrillation included one or more of the following: hypertension (in 46 patients), ischemic heart disease (in 15), rheumatic heart disease (in 4, including mild mitral stenosis in 2), pneumonia (in 4), alcoholism (in 6), and pulmonary embolism (in 1). No predisposing condition was identified for 26 patients (28 percent). The estimated duration of atrial fibrillation was 4.5 ±8.3 weeks (3 to 7 days in 17 patients; 8 to 28 days in 55 patients; and more than 28 days in 10 patients). In 12 patients (13 percent), the duration of atrial fibrillation was unknown. Twelve patients had a history of neurologic events.

Anticoagulation

After they gave informed consent, 80 patients were given an intravenous bolus of heparin (3000 to 5000 units) followed by continuous intravenous heparin to maintain a partial thromboplastin time of 1.4 to 1.7 times the control value. The mean (±SD) duration of heparin therapy before cardioversion was 2.1 ±1.2 days (range, 0.9 to 4.5). Fourteen patients were thought by their primary physicians not to be candidates for short-term heparin therapy because of a history of gastrointestinal bleeding (seven patients), advanced age (five patients), or a recent stroke (two patients). Treatment with oral warfarin was also begun in 60 patients thought to be suitable for anticoagulation after cardioversion, with a target prothrombin time of 1.3 to 1.5 times control. Warfarin was continued for one month. Heparin was continued for 24 hours after cardioversion in those who were not receiving warfarin and until the prothrombin time was in the therapeutic range for those who were receiving warfarin.

Echocardiographic Studies

Conventional transthoracic echocardiography was performed in all patients; this procedure was followed within 48 hours by transesophageal echocardiography if no thrombus was seen.

Two-dimensional imaging and transthoracic Doppler studies were performed with use of an HP Sonos 500, 1000, or 1500 echocardiograph with a 2.5- or 3.5-MHz transducer (Hewlett-Packard, Andover, Mass.). The left atrial dimension was measured in the parasternal long-axis view21. The extent of mitral regurgitation was assessed by pulsed and color Doppler echocardiography and graded from 0 (none) to 3 (severe)22. Left ventricular systolic function was defined as abnormal if there was evidence of global or regional hypokinesis.

After an overnight fast, the patients underwent transesophageal echocardiography under anesthesia with 10 percent lidocaine spray to the posterior pharynx and mild sedation with intravenous meperidine, midazolam, or fentanyl, if needed. Prophylactic antibiotics were given to patients with clinically important valvular abnormalities23. For transesophageal echocardiography we used a 5.0-MHz single-plane probe (in 39 patients -- all those studied at the University of Connecticut Medical Center, and those studied at Beth Israel Hospital before May 24, 1991) or biplane probe (55 patients). An atrial thrombus was reported when a well-circumscribed echo-reflective mass different in texture from the atrial wall and uniform in consistency was identified24. Spontaneous echo contrast (an indication of stasis) was defined as dynamic "smoke-like" echoes within the atria25. Images and Doppler echocardiographic data were recorded on videotape for review by two experienced observers (the presence or absence of thrombi was determined by consensus).

Cardioversion

If no atrial thrombi were seen, pharmacologic cardioversion with antiarrhythmic agents was attempted in patients who had received heparin; such patients received quinidine, procainamide, disopyramide, or flecainide at the discretion of the primary physician. If sinus rhythm was not restored within 12 to 36 hours, then direct-current cardioversion was performed26. (One patient declined electrical cardioversion after attempted pharmacologic cardioversion was unsuccessful.) Because of the potential for thrombi to form during the interval between transesophageal echocardiography and cardioversion, patients in whom thrombi were not seen and who did not receive anticoagulation with heparin underwent direct-current cardioversion immediately after transesophageal echocardiography. Patients were followed daily during their hospitalization and were contacted by telephone one month after cardioversion. No patient was lost to follow-up.

Patients in whom transthoracic echocardiography or transesophageal echocardiography indicated the presence of an atrial thrombus received prolonged warfarin therapy with a target prothrombin time of 1.5 to 1.8 times control. Repeat transesophageal echocardiography was then recommended, and cardioversion was performed if no thrombus was visualized.

Statistical Analysis

All data are expressed as means ±1 SD. Comparisons of categorical variables in the two groups were made by Fisher's exact test with SAS software (SAS Institute, Cary, N.C.). Continuous variables were compared with the Mann-Whitney U test for unpaired samples (with use of StatView II; Abacus Concepts, Berkeley, Calif.). A confidence interval for the percentage of patients in whom an embolic event occurred after cardioversion was calculated with an exact binomial procedure. In all cases, tests were two-tailed, and a P value of less than 0.05 was considered to indicate statistical significance.

The protocol was approved by the investigational review boards at both institutions, and informed consent was obtained from all participants.

Results

All 94 patients underwent transthoracic echocardiography and transesophageal echocardiography without complication. Fourteen atrial thrombi were identified in 12 patients (13 percent), of which 12 (86 percent) were visualized only with transesophageal echocardiography (Figure 1). The predisposing disorders associated with atrial fibrillation in this group included rheumatic heart disease in two patients, hypertension in two, ischemic heart disease in two, alcoholism in one, and pulmonary embolism in one. No predisposing condition was identified for four patients. Atrial thrombi varied in size from 3 to 15 mm (maximal length), and all involved the atrial appendages (the left in 10 cases and the right in 4). Of six thrombi detected during biplane transesophageal echocardiography, all left atrial thrombi were seen in both imaging planes, whereas one of two right atrial thrombi was visualized only in the vertical plane.


View larger version (165K):
[in this window]
[in a new window]
  		Figure 1. Transesophageal Echocardiograms (Horizontal Plane) of the Left Atrium (LA) and Left Atrial Appendage (White Arrow).

Panel A shows a normal left atrial appendage with apical pectinate muscles (small black arrows). Panel B shows the left atrium and appendage in an 82-year-old woman with a one-week history of palpitations, new right-sided weakness, and new atrial fibrillation. Note the thrombus (large black arrow) at the mouth of the left atrial appendage.

 
The left atrial dimension was greater in the group with left atrial thrombi than in those without thrombi (P = 0.024) (Table 1), but there was substantial overlap between the two groups (Figure 2). The incidence of spontaneous echo contrast was also higher in the group with left atrial thrombi (P = 0.015) (Table 1). The group with left atrial thrombi and the group without them did not differ significantly in terms of sex, age, the duration of atrial fibrillation, the severity of mitral regurgitation, or the percentage with abnormal left ventricular systolic function (Table 1). As compared with spontaneous left atrial contrast, there was evidence on transesophageal echocardiography of spontaneous right atrial contrast in only 10 study patients, including all 4 patients with right atrial thrombi (100 percent vs. 7 percent of patients without thrombi, P<0.001).

View this table:
[in this window]
[in a new window]
  		Table 1. Characteristics and Echocardiographic Data of 94 Patients with Atrial Fibrillation.

 

View larger version (12K):
[in this window]
[in a new window]
  		Figure 2. Transthoracic Left Atrial Dimensions in Patients with and Those without Left Atrial Thrombi.

The left atrial dimension was measured in the parasternal long-axis view. The group means (±SD) are indicated by the bars. P = 0.024 for the difference between the groups.

 
Despite the deferment of cardioversion and anticoagulation in the 12 patients with atrial thrombi, 2 of them died suddenly; both had left atrial thrombi. One was an 81-year-old woman with mild mitral stenosis who had been admitted with atrial fibrillation of one week's duration. Transthoracic echocardiography revealed a 10-mm thrombus in the left atrial appendage, and treatment with heparin was initiated. On the fourth hospital day the patient suddenly became unresponsive and had a flaccid right arm and leg. An electrocardiogram demonstrated the persistence of atrial fibrillation, and she died shortly thereafter. The family declined an autopsy. The second patient was an 85-year-old man with coronary artery disease and hypertension who had been admitted with a four-day history of atrial fibrillation. Treatment with heparin was begun; transthoracic echocardiography demonstrated an enlarged left atrium, and transesophageal echocardiography identified an 8-mm thrombus in the left atrial appendage. Cardioversion was deferred, but five days later the patient was found to be unresponsive. An electrocardiogram revealed asystole, and attempted resuscitation was unsuccessful. An autopsy limited to the thorax revealed no left atrial thrombus. Four of the 10 surviving patients with thrombi have undergone uneventful cardioversion after prolonged anticoagulation: 3 after repeat transesophageal echocardiography documented no residual thrombus, and 1 without repeat transesophageal echocardiography, in accordance with the decision of her primary physician. One of the six remaining patients underwent transesophageal echocardiography after five weeks of anticoagulation; the procedure demonstrated the persistence of a 3-mm thrombus, and she continues to receive anticoagulation. Five patients have not undergone repeat transesophageal echocardiography. In most cases the primary physician has deferred transesophageal echocardiography and cardioversion because of the large left-atrial dimension and the belief that sinus rhythm would not be maintained even if cardioversion were successful.

In 82 patients (87 percent), no atrial thrombi were visualized on transesophageal echocardiography. Of these patients, 78 (95 percent) underwent successful cardioversion to sinus rhythm, all without long-term anticoagulation, and none (95 percent confidence interval, 0 to 4.6 percent) had an embolic event. Pharmacologic cardioversion was achieved in 47 patients, with quinidine (29 patients), procainamide (13 patients), disopyramide (2 patients), or flecainide (3 patients). Thirty-one patients underwent successful direct-current cardioversion either immediately after transesophageal echocardiography (11 patients) or after unsuccessful attempts at pharmacologic cardioversion. In four patients, atrial fibrillation was refractory to pharmacologic or electrical cardioversion, or both, and they continued to receive anticoagulant therapy without evidence of an embolic event. One patient had guaiac-positive stool while he was receiving warfarin, and he received a transfusion of one unit of blood. The results of colonoscopy and upper-gastrointestinal series were normal.

Discussion

In the past, no methods were available to determine reliably which patients with atrial fibrillation had atrial thrombi and were thus at risk of thromboembolism. The substantial morbidity associated with thromboembolism, however, demanded that all patients with atrial fibrillation receive several weeks of oral anticoagulation before cardioversion, followed by anticoagulation after cardioversion during the recovery of atrial mechanical function15,26,27. Although studies have proved the efficacy of prophylactic anticoagulation in decreasing the incidence of embolic events to 1.6 percent or less,10,12,16 this incidence is achieved at the cost of eight weeks of oral anticoagulation with its attendant risks, a delay in cardioversion, and a second hospitalization for cardioversion. This prospective study demonstrates the potential role of transesophageal echocardiography as a tool for guiding safe, early cardioversion in patients with atrial fibrillation of unknown or prolonged duration. The results show that the majority of such patients do not have atrial thrombi as assessed by transesophageal echocardiography. Transesophageal echocardiography has the potential not only to shorten the duration of anticoagulation, therefore, but also to eliminate the need for hospitalization one month later for cardioversion; it may also further reduce the incidence of embolic events.

Conventional transthoracic echocardiography is a sensitive and specific test for the presence of left ventricular thrombi,28 but the posterior location of the left atrium and the frequent inability to visualize the atrial appendages17 make it an inadequate method for excluding the presence of atrial thrombi. Transesophageal echocardiography, however, is safe,29 even in elderly30 and critically ill31 patients, and it is highly accurate in detecting atrial thrombi17,18,19.

Mugge and colleagues18 reported on a series of 75 left atrial thrombi detected by transesophageal echocardiography. Sixty percent of their study patients had a history compatible with arterial embolism. Twelve patients underwent cardiac surgery, during which the presence of thrombi was confirmed. The true sensitivity of transesophageal echocardiography for detecting atrial thrombi is unknown, though presumably it is related to the size of the thrombus and the capacity to obtain an adequate image of the atria. Unfortunately, embolization of very small thrombi may cause considerable morbidity. For this reason, our protocol stipulated that patients eligible for anticoagulation receive intravenous heparin until 24 hours after cardioversion. We presumed that anticoagulation during this period would serve to minimize the development of small thrombi. Patients in whom there is inadequate visualization of the atria or in whom transesophageal echocardiography is inconclusive should be treated conservatively with prolonged oral anticoagulation before cardioversion. Our data on patients who did not receive anticoagulation with heparin are not of sufficient power for us to advocate cardioversion guided by transesophageal echocardiography without short-term anticoagulation. Atrial fibrillation in patients who are poor candidates for any anticoagulation, however, can best be managed with transesophageal echocardiography before cardioversion. If a thrombus is seen, then the risks and benefits of anticoagulation can be reassessed.

Historically, patients with atrial fibrillation who have undergone cardioversion without previous anticoagulation have had an incidence of clinical emboli that is lower than the 13 percent incidence of thrombi in our study. This disparity may be explained by the likelihood that not all atrial thrombi embolize after cardioversion or that in some cases thromboembolism may be clinically silent.

Eliminating the need for prolonged anticoagulation before cardioversion would lower the costs of medication and monitoring and reduce the morbidity associated with anticoagulation. Patients would still require anticoagulant therapy after cardioversion to prevent the formation of a thrombus during the recovery of atrial mechanical function,26 but the total duration of anticoagulation should be substantially shorter than at present. A recent review of the use of anticoagulation for atrial fibrillation over a 10-year period12 confirmed the benefit of anticoagulation of intermediate length in reducing the incidence of embolic events, but 14 percent of the patients had a bleeding event, including 2 percent in whom it was considered life-threatening. No bleeding events were seen among the patients who received anticoagulation for less than one month. The use of transesophageal echocardiography as described in this study would allow the 87 percent of patients without atrial thrombi to undergo early cardioversion safely, thereby shortening the duration of anticoagulation to less than one month.

Earlier cardioversion would also have the benefit of allowing a more rapid return of atrial mechanical function. Studies of patients with atrial fibrillation of less than one week in duration who have undergone cardioversion have documented a more prompt return of atrial mechanical function,27 as compared with patients who have had atrial fibrillation for five months26. Shortening the overall duration of atrial fibrillation may also permit an abbreviated course of anticoagulation after cardioversion, though this possibility remains to be clarified by future study. Morever, the likelihood of maintaining sinus rhythm is inversely related to the duration of atrial fibrillation32,33. The use of transesophageal echocardiography to minimize the duration of atrial fibrillation may enhance the long-term success of cardioversion.

Few data are available on the incidence of embolic events in patients with atrial fibrillation who undergo systemic anticoagulation in preparation for later cardioversion. In this study two patients with left atrial thrombi identified echocardiographically died suddenly despite anticoagulation. One patient's clinical course was highly suggestive of an embolic event, whereas the limited autopsy of the second patient demonstrated the absence of the recently visualized atrial thrombus. No patient died within 24 hours of transesophageal echocardiography; thus, it is unlikely that the procedure contributed to the migration of a thrombus.

Over half the patients in this study had spontaneous left atrial contrast on transesophageal echocardiography. This finding, often seen with higher-frequency transducers, is related to the formation of rouleaux by erythrocytes and to stasis34 and has been associated with the presence of left atrial thrombi35. Our data confirm these earlier findings and also highlight the importance of spontaneous right atrial contrast, a finding that was seen in every patient with right atrial thrombi but in only 7 percent of patients without right atrial thrombi.

It was not our intention in this study to examine the relative sensitivity of single-plane and biplane transesophageal echocardiography in visualizing atrial thrombi. During the course of this study, a biplane transesophageal echocardiographic probe became available at one of the study sites, and it was used for all subsequent studies. Biplane transesophageal echocardiography is thought to be superior for visualizing both the atria and the atrial appendages36,37. In patients who underwent biplane transesophageal echocardiography, left atrial thrombi were seen in both imaging planes. In one patient, however, a thrombus was visualized in the right atrial appendage only in the vertical plane. In the future, multiplane transesophageal echocardiography may further enhance the capacity of the technique to detect atrial thrombi.

A limitation of our study is that we recorded only clinical embolic events and did not perform CT or magnetic resonance imaging of the brain before and after cardioversion to detect clinically silent cerebral emboli. In addition, from our study alone it cannot be determined whether early cardioversion guided by transesophageal echocardiography is safer than conventional therapy. Assuming a risk of emboli of 1.2 percent with conventional therapy and 0.6 percent with cardioversion guided by transesophageal echocardiography, a randomized trial involving more than 6000 patients would be required to demonstrate a benefit of transesophageal echocardiography followed by cardioversion (80 percent power at a significance level of P<0.05)38. Our study does, however, suggest that the strategy we used is reasonable and safe. Preliminary studies like this one need to be performed before costly large-scale trials are undertaken.

In conclusion, atrial thrombi were detected by the combination of transthoracic and transesophageal echocardiography in 13 percent of patients with atrial fibrillation of unknown or prolonged duration who were not receiving long-term anticoagulation. If transesophageal echocardiography excludes the presence of atrial thrombi, our preliminary data support the use of transesophageal echocardiography as a tool for guiding early cardioversion.

Supported in part by a Cardiovascular Research Training Grant (HL 07374) from the National Heart, Lung, and Blood Institute. Dr. Manning is the recipient of a Physician-Scientist Award from the National Institute on Aging (AG00294), and Dr. Gordon is the recipient of a W.A. and M.G. Saw Medical Research Fellowship from the University of Western Australia.

We are indebted to Drs. Carol Waksmonski, Susan Eysmann, and Michael Lauer and to Ms. Marilyn F. Riley, Ms. Sarah E. Katz, Ms. Cindy Comstock, Ms. Rosalie M. Doherty, and Ms. Jiyl T. Munson for their assistance with the transesophageal echocardiographic studies; to the members of the medical staff and house staff at the hospitals for their assistance with the recruitment of patients; to Dr. William Grossman for his helpful review of the manuscript; and to Dr. Bernard Ransil for calculating the sample sizes.


Source Information

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

Address reprint requests to Dr. Manning at the Cardiovascular Division, Beth Israel Hospital, 330 Brookline Ave., Boston, MA 02215.

References

  1. Ostrander LD Jr, Brandt RL, Kjelsberg MO, Epstein FH. Electrocardiographic findings among the adult population of a total natural community, Tecumseh, Michigan. Circulation 1965;31:888-898. [Free Full Text]
  2. Petersen P. Thromboembolic complications in atrial fibrillation. Stroke 1990;21:4-13. [Free Full Text]
  3. Kannel WB, Wolf PA. Epidemiology of atrial fibrillation. In: Falk RH, Podrid PJ, eds. Atrial fibrillation: mechanisms and management. New York: Raven Press, 1992:81-92.
  4. Abbott WM, Maloney RD, McCabe CC, Lee CE, Wirthlin LS. Arterial embolism: a 44 year perspective. Am J Surg 1982;143:460-464. [CrossRef][Medline]
  5. Aberg H. Atrial fibrillation. I. A study of atrial thrombosis and systemic embolism in a necropsy material. Acta Med Scand 1969;185:373-379. [Medline]
  6. Hinton RC, Kistler JP, Fallon JT, Friedlich AL, Fisher CM. Influence of etiology of atrial fibrillation on incidence of systemic embolism. Am J Cardiol 1977;40:509-513. [CrossRef][Medline]
  7. Morris JJ Jr, Entman M, North WC, Kong Y, McIntosh H. The changes in cardiac output with reversion of atrial fibrillation to sinus rhythm. Circulation 1965;31:670-678. [Free Full Text]
  8. Pritchett ELC. Management of atrial fibrillation. N Engl J Med 1992;326:1264-1271. [Medline]
  9. Resnekov L, McDonald L. Complications in 220 patients with cardiac dysrhythmias treated by phased direct current shock, and indications for electroconversion. Br Heart J 1967;29:926-936. [Free Full Text]
  10. Bjerkelund CJ, Orning OM. The efficacy of anticoagulant therapy in preventing embolism related to D.C. electrical conversion of atrial fibrillation. Am J Cardiol 1969;23:208-216. [CrossRef][Medline]
  11. Lown B, Perlroth MG, Kaidbey S, Abe T, Harken DE. "Cardioversion" of atrial fibrillation: a report on the treatment of 65 episodes in 50 patients. N Engl J Med 1963;269:325-331.
  12. Weinberg DM, Mancini GBJ. Anticoagulation for cardioversion of atrial fibrillation. Am J Cardiol 1989;63:745-746. [CrossRef][Medline]
  13. Petersen P, Godtfredsen J. Embolic complications in paroxysmal atrial fibrillation. Stroke 1986;17:622-626. [Free Full Text]
  14. Rokseth R, Storstein O. Quinidine therapy of chronic auricular fibrillation: the occurrence and mechanism of syncope. Arch Intern Med 1963;111:184-189.
  15. Dunn M, Alexander J, de Silva R, Hildner F. Antithrombotic therapy in atrial fibrillation. Chest 1989;95:Suppl:118S-127S. [Free Full Text]
  16. Arnold AZ, Mick MJ, Mazurek RP, Loop FD, Trohman RG. Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter. J Am Coll Cardiol 1992;19:851-855. [Abstract]
  17. Aschenberg W, Schluter M, Kremer P, Schroder E, Siglow V, Bleifeld W. Transesophageal two-dimensional echocardiography for the detection of left atrial appendage thrombus. J Am Coll Cardiol 1986;7:163-166. [Abstract]
  18. Mugge A, Daniel WG, Hausmann D, Godke J, Wagenbreth I, Lichtlen PR. Diagnosis of left atrial appendage thrombi by transesophageal echocardiography: clinical implications and follow-up. Am J Card Imaging 1990;4:173-179.
  19. Manning WJ, Reis GJ, Douglas PS. Use of transesophageal echocardiography to detect left atrial thrombi before percutaneous balloon dilation of the mitral valve: a prospective study. Br Heart J 1992;67:170-173. [Free Full Text]
  20. Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. Mayo Clin Proc 1988;63:649-680. [Medline]
  21. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978;58:1072-1083. [Free Full Text]
  22. Helmcke F, Nanda NC, Hsiung MC, et al. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation 1987;75:175-183. [Free Full Text]
  23. Dajani AS, Bisno AL, Chung KJ, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1990;264:2919-2922. [Free Full Text]
  24. Seward JB, Khandheria BK, Oh JK, Freeman WK, Tajik AJ. Critical appraisal of transesophageal echocardiography: limitations, pitfalls, and complications. J Am Soc Echocardiogr 1992;5:288-305. [Medline]
  25. Castello R, Pearson AC, Labovitz AJ. Prevalence and clinical implications of atrial spontaneous contrast in patients undergoing transesophageal echocardiography. Am J Cardiol 1990;65:1149-1153. [CrossRef][Medline]
  26. Manning WJ, Leeman DE, Gotch PJ, Come PC. Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation. J Am Coll Cardiol 1989;13:617-623. [Abstract]
  27. Shapiro EP, Effron MB, Lima S, Ouyang P, Siu CO, Bush D. Transient atrial dysfunction after conversion of chronic atrial fibrillation to sinus rhythm. Am J Cardiol 1988;62:1202-1207. [CrossRef][Medline]
  28. Stratton JR, Lighty GW Jr, Pearlman AS, Ritchie JL. Detection of left ventricular thrombus by two-dimensional echocardiography: sensitivity, specificity, and causes of uncertainty. Circulation 1982;66:156-166. [Free Full Text]
  29. Daniel WG, Erbel R, Kasper W, et al. Safety of transesophageal echocardiography: a multicenter survey of 10,419 examinations. Circulation 1991;83:817-821. [Free Full Text]
  30. Zabalgoitia M, Gandhi DK, Evans J, Mehlman DJ, McPherson DD, Talano JV. Transesophageal echocardiography in the awake elderly patient: its role in the clinical decision-making process. Am Heart J 1990;120:1147-1153. [CrossRef][Medline]
  31. Pearson AC, Castello R, Labovitz AJ. Safety and utility of transesophageal echocardiography in the critically ill patient. Am Heart J 1990;119:1083-1089. [CrossRef][Medline]
  32. Dethy M, Chassat C, Roy D, Mercier LA. Doppler echocardiographic predictors of recurrence of atrial fibrillation after cardioversion. Am J Cardiol 1988;62:723-726. [CrossRef][Medline]
  33. Dittrich HC, Erickson JS, Schneiderman T, Blacky AR, Savides T, Nicod PH. Echocardiographic and clinical predictors for outcome of elective cardioversion of atrial fibrillation. Am J Cardiol 1989;63:193-197. [CrossRef][Medline]
  34. Wang XF, Liu L, Cheng TO, Li ZA, Deng YB, Wang JE. The relationship between intracardiovascular smoke-like echo and erythrocyte rouleaux formation. Am Heart J 1992;124:961-965. [CrossRef][Medline]
  35. Daniel WG, Nellessen U, Schroder E, et al. Left atrial spontaneous echo contrast in mitral valve disease: an indicator for an increased thromboembolic risk. J Am Coll Cardiol 1988;11:1204-1211. [Abstract]
  36. Wang XF, Li ZA, Cheng TO, Deng YB, Wang JE, Yang Y. Biplane transesophageal echocardiography: an anatomic-ultrasonic-clinical correlative study. Am Heart J 1992;123:1027-1038. [CrossRef][Medline]
  37. Seward JB, Khandheria BK, Edwards WD, Oh JK, Freeman WK, Tajik AJ. Biplanar transesophageal echocardiography: anatomic correlations, image orientation, and clinical applications. Mayo Clin Proc 1990;65:1193-1213. [Medline]
  38. Determining sample sizes needed to detect a difference between two proportions. In: Fleiss JL. Statistical methods for rates and proportions. 2nd ed. New York: John Wiley, 1981:33-49.

 

This Article
-Abstract

Commentary
-Letters

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation

Related Letters:

Transesophageal Echocardiography before Cardioversion
Grimm R. A., Black I. W., Klein A. L., Manning W. J., Silverman D. I., Douglas P. S.
Extract | Full Text  
N Engl J Med 1993; 329:577-578, Aug 19, 1993. Correspondence

This article has been cited by other articles:


HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.