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Embolic Potential of the Atrial Flutter

Garcés Eduardo; Eggers Germán; Sagardia Mauricio; Raposo Luis; Riquelme Herminia; Lanas Fernando*; Schwencke Ana María.

Unidad de Cardiología, Hospital Clínico Regional Valdivia,
Facultad de Medicina Universidad Austral de Chile, Valdivia, Chile.
*Facultad de Medicina, Universidad la Frontera, Temuco, Chile

Introduction
Objectives
Material and Methods
Results
Discussion
Conclusions

Introduction
Traditionally, a low embolic risk has been attributed to Atrial Flutter (FL). In relationship to the electrical cardioversion (EC), The American College of Chest Physicians did not consider, within the recommendations of its 1989 consensus, the anticoagulation as necessary prior to EC for patients with FL. Recent reports using the Transesophageal Echocardiography techniques (TEE), have shown however, a variable but high frequency of Thrombi (TR), and/or Spontaneous Echo Contrast (SC) in the Left Atrium (LA) of patients with FL prior to the EC. In addition, thromboembolic events in patients with AF are being reported more frequently than the early estimation .

Objetives
Based on the data described above, the aim of this study was to evaluate the embolic potential ( presence of TR and / or SC ) in patients with FL and the clinical and echocardiographic associated variables.

Material and Methods
Forty three patients giving formal consent, were prospectively studied between April 1997 and March 1999. Patients who could not have a TEE or it was not possible to clearly see the left atrial appendage were excluded from the study. Thirty two men and eleven women with an average age of 59,9 ± 14,9 years (range 23 to 83 years) were studied according to the protocol ( Fig. 1), prior to any attempt of the arrhythmia cardioversion. Following the patient admittance and participation in the study, the treatment of the patient was left to the treating doctor criteria, and during the follow up the presence of embolic events, flutter recurrence and atrial fibrillation were recorded. The Holter recording was carried out using Circadian three channel analogue recorders, the transthoracic and transesophageal echocardiography, were carried out in a VingMed CFM 750 Echocardiograph with a 3,5 Mhz transthoracic transducer and a 5Mhz multiplane transesophageal transducer. The statistical analysis was done using the Epi Info 5.01 programme, and depending on the cases, proportions, means and standard deviation , T test, Chi square, Fisher and Odds Ratio test were used.

Figure 1. Study Protocol


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Results
The main aetiologies associated to the arrhythmia were Arterial Hypertension (20 cases), Rheumatic Valvular Disease ( 8 cases), unknown aetiology (5 cases) and the remaining 10 cases corresponded to miscellaneous aetiology . Twenty nine patients had a reported first FL episode, and the remaining 14 had an average of 2,57
± 1.1 previous episodes ( between 1 - 4). The duration of the episode was unknown in 11 patients and the remaining 32 patients showed a wide range (1 - 3650 days) with an average of 297 ± 771 days. Ten patients (23%) showed Atrial Fibrillation (AF), 3 prior to admittance, 6 in the holter at admittance and 1 in the follow up holter ( Fig 2). Nine patients were taking Aspirin and other 5 were taking oral anticoagulant agents at admittance. Three patients had predominant Mitral Stenosis (MS) and 19 had Mitral Regurgitation (MR), 8 were diagnosed as mild , 9 as moderate and 2 as severe. Fifteen patients showed spontaneous echo contrast in LA and or left atrial appendage and 5 thrombi at TEE (Fig 3) and (Fig 4). The factors associated to SC or TR are shown in table 1.

Figure 2
fig2.jpg (49068 bytes)

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Figure 3

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Figure 4

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Patients with SC showed a significantly more deteriorated LV systolic function. Patients with TR showed the same tendency but without reaching statistical significance. The moderate and severe MR was , in our study, a protective factor of SC with a similar tendency in relation to the presence of TR but without reaching statistical significance. Two out of 3 patients with predominant MS showed TR in the LA vs 3 out of 40 patients without MS, thus the presence of this valvulopathy became a risk factor for the presence of thrombus.

Table 1.- Clínical and Echocardiographics factors associated to the presence of trombi
and spontaneous echo contrast in patients with atrial flutter
.

LA dimens= Left Atrial dimension, LVEF = Left Ventricular Eyection Fraction,
W/Mitral S. = With Mitral Stenoses, Wt/Mitral S. = Without Mitral Stenoses,
W/Mitral R.= With Mitral Regurgitation, Wt/Mitral R.= Without Mitral Regurgitation,
W/Anticoag.= With Anticoagulant, Wt/Anticoagulant= Without Anticoagulant,
W/SechoC= With Spontaneous Echo Contrast, Wt/SechoC= Without Spontaneous Echo Contrast
W/Thrombi= With Thrombi , Wt/Thrombi= Without Thrombi

None of the 5 patients under anticoagulant therapy at admittance showed TR however, 5 out of 38 patients without the treatment showed TR thus, this treatment became a protective factor for the presence of thrombus but not for the presence of SC. The presence of SC seems to be a predictive factor for the presence of TR since all the patients showing TR had SC but none of the 28 patients without SC. The AF record at admittance , the use of Aspirin and the presence of Cardiac Failure were not associated, in this study, to the presence of either TR or SC. Twenty four patients underwent EC, being successful in 20 (91%), 6 patients underwent pharmacological cardioversion being successful in 5 cases and in 13 patients cardioversion was not attempted due to either the presence of thrombus, previously failed cardioversion or the chronicity of the flutter. Only one case in the long term follow up showed an ischemic cerebrovascular event of a presumably embolic origin.

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Discussion
The use of transesophageal echocardiography has allowed to demonstrate the presence of spontaneous echo contrast and thrombi in the LA of patients carrying an atrial flutter, and this study confirms early reports showing the high frequency of these findings in this group of patients. In our series of 43 consecutive unselected patients, 5 of them (11,6%) showed thrombus and 15 (35%) showed spontaneous contrast in the LA. Orsinelli et al (7) studying 8 patients with flutter found thrombi in one (12%) and spontaneous contrast in 2 (24%) prior to the EC. Bikkina et al (8) studied 24 hospitalised patients with FL with TEE, excluding those patients with AF antecedents, anticoagulant therapy and prosthetic valves, and found a thrombi prevalence of 21% and 8% for spontaneous echo contrast. Gilligan et al (9) found prevalence of 12% for thrombi in 82 patients carrying FL and important LV systolic dysfunction. Black et al detected 3 patients (43%) with spontaneous echo contrast and 1 (14%) with thrombus in 7 patients with atrial flutter. Despite the clinical differences in the studied groups, the prevalence of thrombi and spontaneous echo contrast is high in patients with FL and this evidence becomes relevant since the electrical cardioversion considered as an effective treatment in the restoration of the rhythm, could be potentially associated to a high embolic risk.

Initially, the anticoagulant therapy prior to the EC of this arrhythmia was not considered necessary (2-3) and this medical strategy was supported by the study of Arnold et al (4) who did not report embolic events in 122 patients submitted to EC by FL with only 26% of them under anticoagulant therapy. This studied group however, included a great proportion of patients with postsurgical arrhythmia and therefore of a recent onset. Other studies however, report systemic embolic events following the EC of patients with FL. Metha et al (10) submitted 41 patients in FL to EC, 2 of them under anticoagulant treatment and 16 with previous TEE, in 3 patients (7%) ischemic neurological episodes post EC were developed. Wood et al (11) in a retrospective study of 86 patients found an historical embolic records in 12 patients (14%). Lanzarotti et al (13) studied the effectiveness of anticoagulant treatment in 100 patients with FL submitted to EC and 6 of them had a documented embolic episode attributed to a deficient anticoagulant therapy and those patients effectively anticoagulated did not show embolic events. These data enhance the relevance of determining the predisposing conditions to embolic events in patients carrying FL. The presence of TR and SC are well defined as embolic risk markers (15 - 16) however, their detection requires the transesophageal echocardiography techniques, which is not always widely available, therefore, it is necessary to count with clinical or transthoracic echocardiographic factors associated to these markers. In our study the presence of a more deteriorated LV function as in the studies of Bikkina (8) and Gilligan (9) was associated to these markers. In addition, the presence of Mitral Stenosis is relevant and it is not reported in other studies probably due to its lower prevalence . The presence of moderate or severe Mitral Regurgitation has not been a factor studied , and in this work it became a protective factor for EC. The protective role of the anticoagulant therapy is well known in the none valvular AF and specially associated to mitral stenosis, less clear is its role in the atrial flutter however, its use is progressively becoming more evident (13). In our study none of the patients under anticoagulant treatment showed thrombus.

The embolic events in our study were low (1 in the follow up period) in comparison with the previously reported data however, our result are probably biased due to the use of TEE in all the patients and the therapeutical induction towards and effective anticoagulation prior EC in all those with thrombus or considered high risk patients.

Conclusions
Our data confirm the high prevalence of TR and CE in non selected patients carrying Atrial Flutter. A LV systolic dysfunction and the presence of mitral stenosis were associated to a greater embolic potential, however, the anticoagulant therapy and the significant mitral regurgitation appears like a protective factors.

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Bibliografy
[1] Olshansky B., Wliber D., Hariman R. Atrial flutter, update on the mecanism and treatment. Pace 1992; 15: 2308
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[9] Gilligan D., Burch M., Fuller I., Prinz A., Kwane O. et al. High prevalence of left atrial thrombi in patients with typical Atrial Flutter and left ventricular systolic dysfunction. Abstract 1084-146 from the 48th Annual Scientific Session of ACC Congress. March 1999. http://ex2.excerptamedica.com/99acc/abstracts/abs1084-153.html.
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[11] Wood K., Eisenberg S., Kalman J., Drew S. et al. Risk of thromboembolism in chronic atrial flutter. Am. J. Cardiol 1997; 79(8): 1043.
[12] Black I., Hopkins A., Lincoln C., Lee C., Walsh W. Thromboembolic risk of atrial flutter (abstract). J. Am. Coll. Cardiol 1993; 19: 314ª.
[13] Lanzarotti Ch., Olshansky B. Thromboembolism in Chronic Atrial Flutter: Is the Risk Underestimated? J. Am. Coll. Cardiol 1997; 30(5): 1506.
[14] Black I., Hopkins A., Lee L. et al. Evaluation of transesophageal echocardiography before and during direct direct current cardioversion of atrial fibrillation and flutter in non anticoagulated patients. Am. Heart J. 1993; 126: 375.
[15] Tsai L., Fang C., Lin L et al. Clinical implications of left atrial spontaneous echo contrast in non rheumatic atrial fibrillation. Am. J. Cardiol. 1992; 70:327.
[16] Fatkin D., Kelly R., Feneley M. Relations between left atrial appendage blood flow velocity, spontaneous echo contrast and thromboembolic risk in vivo. J. Am. Coll Cardiol. 1994;23: 307.

 

Questions, contributions and commentaries to the Authors: send an e-mail message (up to 15 lines, without attachments) to ARRITMIAS@listserv.rediris.es , written either in English, Spanish, or Portuguese.

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Update
Nov/01/1999