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Ann Thorac Surg 1998;65:1566-1569
© 1998 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Is Atrial Fibrillation Resulting From Rheumatic Mitral Valve Disease a Proper Indication for the Maze Procedure?

^a Department of Thoracic and Cardiovascular Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan

Accepted for publication November 15, 1997.

Address reprint requests to Dr Fukada, Department of Thoracic and Cardiovascular Surgery, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060, Japan
e-mail: (fukada{at}pop.pitt.edu)

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. There are a few patients without detectable atrial contraction despite restoration of atrial rhythm after the maze procedure for atrial fibrillation (AF) associated with mitral valve disease.

Methods. From January 1995 to March 1997, 29 consecutive patients with AF associated with mitral valve disease underwent our modified maze procedure combined with mitral or other valve operations. The causes of mitral valve disease were rheumatic mitral stenosis (n = 22) and nonrheumatic mitral regurgitation (n = 7). The 17 patients with postoperative atrial rhythm were divided into group I with rheumatic mitral stenosis (n = 10), and group II with mitral regurgitation of nonrheumatic origins (n = 7).

Results. Seventeen patients regained atrial rhythm, 2 patients had junctional rhythm, and another 10 remained in AF. Between the group of patients with restoration of atrial rhythm and that of patients remaining in AF, significant differences were found in the percentage with rheumatic disease, history of AF, and maximum f-wave voltage. The postoperative peak velocity of the atrial filling wave to peak velocity of early filling wave ratio for the left atrium measured using Doppler echocardiography was 0.25 in group I, which was significantly lower than that (0.42) in group II.

Conclusions. Reconsideration of the indications for the maze procedure for AF associated with rheumatic mitral stenosis may thus be reasonable, particularly for cases in which replacement using a prosthetic valve is necessary, but we believe that patients with nonrheumatic mitral valve disease, especially those able to undergo reconstructive operations, are the best candidates for the maze procedure.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
The maze procedure was initially reported by Cox and colleagues [1]. They indicated that this procedure improved hemodynamics and decreased the risk of systemic thromboembolism by restoring atrioventricular synchrony [2]. Whereas they operated mainly for lone atrial fibrillation (AF), Kosakai and associates [3] found that the maze procedure was also effective for secondary AF associated with mitral valve disease. They also noted that an atrial A wave was detected in 71% for transmitral flow on Doppler echocardiography. This finding indicates that after combined maze procedure and mitral operation atrial contractility is not recovered in 30% of patients, and that patients without recovery of atrial contraction therefore are not at decreased risk of thromboembolism. We postulated that there are two groups of patients, those who easily recover atrial contractility after the maze procedure and those who do so only with difficulty. This study examined recovery of atrial function after this operation as a function of origin of mitral valve disease.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
From January 1995 to March 1997, 29 consecutive patients with AF associated with mitral valve disease underwent our modified maze procedure combined with mitral or other valve operations. Associated valve procedures were as follows: aortic, mitral, and tricuspid valve operations in 4 patients, aortic and mitral operations in 4, mitral and tricuspid operations in 13, and mitral operation alone in 8. The causes of mitral valve disease were as follows: rheumatic mitral stenosis with or without mitral regurgitation in 22 patients, and nonrheumatic origin in 7. There were 14 men and 15 women, with a mean age of 59.8 ± 10.5 years (range, 34 to 74 years). The 17 patients who regained atrial rhythm after operation were divided into two groups. Group I consisted of 10 patients who had rheumatic mitral valve disease, and group II consisted of 7 patients with mitral valve regurgitation of nonrheumatic origins. The nonrheumatic causes were annular dilatation in 2 patients, leaflet prolapse in 4, and chordal rupture in 1.

Our modification of the maze procedure is illustrated in Figure 1. Cardiopulmonary bypass is instituted with bicaval venous drainage, direct cannulation of the superior vena cava and cannulation of the inferior vena cava through the lower right atrium. With the patient supported by total bypass, the right atrial appendage is amputated. A lateral incision, parallel to the right atrioventricular groove, is made from the base of the excised right atrial appendage toward the inferior vena cava, which is cryoablated (-60°C for 1 minute) after institution of cardiac arrest. From the midpoint of this atriotomy, a T incision is begun toward the tricuspid annulus, which is cryoablated later. A posterior longitudinal line from the superior vena cava to the inferior vena cava is then cryoablated. A left vertical atriotomy is extended to the left margin of the left pulmonary veins. After excision of the left atrial appendage, the cryoablation is directed toward the incisional ridge between the upper and lower left pulmonary veins, from the base of the excised left atrial appendage to the left upper atrial incisional edge, and from the edge of the left lower atrial incision into the posterior mitral valvular annulus. After completion of this procedure, the mitral and other valve operations are performed.

View larger version (65K): [in this window] [in a new window]   Fig 1. Schematic representation of our modification of the maze procedure (surgical view). The cryoablating lines are illustrated by thick black lines. (IVC = inferior vena cava; LAA = left atrial appendage; MV = mitral valve; PV = pulmonary vein; RAA = right atrial appendage; SVC = superior vena cava; TV = tricuspid valve.)

Cardiac catheterization was performed for hemodynamic assessment before and 1 month after operation. Transthoracic echocardiography was performed to measure left and right atrial contractile function at a mean of 3.8 ± 3.5 months (range, 1 to 11 months) after operation. Using apical four-chamber view for left atrial outflow and parasternal four-chamber view for right atrial outflow, the Doppler signal was recorded at the annulus of the atrioventricular valves. Grades of atrial contractility were determined by measurement of peak velocity of atrial filling (A) wave to the peak velocity of early filling (E) wave ratio (A/E) using Doppler echocardiography.

Results were recorded as means ± standard deviations, and statistical significance was determined using Student’s t test and ² analysis with p values less than 0.05 considered significant.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
All of the patients survived without serious complications. Cardiac arrest time ranged from 88 to 201 minutes, with a mean of 149.5 ± 32.2 minutes, necessitating cardiopulmonary bypass runs varying from 139 to 270 minutes, with a mean of 209.0 ± 34.0 minutes. Seventeen patients (59%) regained atrial rhythm, 2 patients (7%) had junctional rhythm, and another 10 (34%) remained in AF.

The 17 patients with postoperative atrial rhythm were compared with the other 12 patients. Significant differences were noted between these two groups in the percentage of patients with rheumatic disease, history of AF, and maximum f-wave voltage in the V₁ lead. On the other hand, there were no differences in patient age, sex, echocardiographic left atrial dimension, or sinus node artery variation (Table 1).

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
Cox and colleagues [4] initially designed the maze procedure based on results of experimental studies of dogs and studies of patients with Wolff-Parkinson-White syndrome. They designed the incision lines of this procedure to be placed in such a manner that a sinus node impulse would be "directed" to the atrioventricular node while allowing the entire atrial myocardium to be activated by the electrical activity traveling along confined paths throughout the atria, and such that no macroreentrant circuits could form without crossing one of the incision lines [1]. Although they demonstrated the safety and efficacy of the maze procedure mainly for patients with isolated AF, Kosakai and associates [3] reported that it was also effective in controlling secondary AF with mitral valve disease. On the other hand, Harada and coworkers [5], using computerized intraoperative mapping, found that chronic AF associated with isolated mitral valve disease in the majority of patients featured regular and repetitive activation in the left atrium. Sueda and colleagues [6] also found that patients with AF associated with isolated mitral valve disease had areas with the shortest cycle length at the base of the left atrial appendage and the posterior wall lateral to the left pulmonary veins. They therefore insisted that an operation to eliminate chronic AF should be applied to the left atrium, but is not required in the right atrium. After all, the mechanism of AF is not completely understood, and the appropriate surgical procedure for elimination of AF has not yet been established.

On the basis of the excellent results of the maze procedure obtained by Cox and associates [4] and Kosakai and colleagues [3], we have performed our modification of the maze procedure. To reduce operating time and blood loss, we replaced atriotomy and reanastomosis with cryoablation. However, our results were not entirely satisfactory, because the rate of recovery to atrial rhythm was only 59%. The cause of mitral valve disease in all 12 patients without restoration of atrial rhythm was rheumatic mitral stenosis, whereas all of the patients without rheumatic disease regained atrial rhythm. Moreover, the left atrial contractility determined as the A/E ratio by Doppler echocardiography in group I was significantly reduced compared with that in group II, and there were 7 patients in group I with undetectable left atrial contraction. On the other hand, one patient in group II had restoration of excellent left atrial contraction, with an A/E of 0.69. Therefore, patients with rheumatic mitral stenosis may have difficulty regaining not only atrial rhythm but also left atrial contractility, whereas patients without rheumatic valve disease readily regain left atrial contractility.

Goldstein and coworkers [7] reported the important finding that group A streptococci have antigens that cross-react with the structural glycoprotein of heart valves, thus directly linking these organisms with valvular disease, and Waller and associates [8] noted that nonrheumatic causes of valvular mitral stenosis were extremely uncommon, although there are some aspects encountered in patients who have no history of rheumatic fever [9]. Dekker and associates [10] found that patients with mitral valve restenosis frequently exhibited focal calcification and thickening in the left atrial endocardium. We believe that there is a relationship between calcification in the left atrial endocardium and persisting rheumatic inflammatory activity. Therefore, the contractility of the left atrium, which has less compliance because the wall is thickened or calcified by the influence of rheumatic disease, seems to be able to exhibit little improvement. Ueshima and coworkers [11] noted that delayed recovery of atrial function might occur; however, they did not consider possible effects of rheumatic disease. Although we might have missed patients who would regain left atrial contractility because the range of interval between the operation and postoperative echocardiography was broad (1 to 11 months), we doubt whether the left atrium of mitral stenosis affected by rheumatic disease can exhibit late recovery of contraction.

We cannot conclude that rheumatic disease is a main cause of the poor outcome in the patients with rheumatic mitral stenosis because the long duration of AF after low electrical activity in the left atrium in patients with rheumatic disease may make them less likely to return to sinus rhythm. And, although we have confirmed the efficacy of cryoablation by postoperative catheter mapping of the right atrium for 6 rheumatic patients with postoperative atrial rhythm, it is still possible that our modification may leave the area available for the development of a macroreentrant circuit around the left atrial posterior wall between the upper and lower left pulmonary veins, in which cryoablation is used instead of transection. Thus, incision and resuture might be more successful in the thickened left atrium of rheumatic patients, particularly if there is persistent rheumatic inflammatory activity.

The combined maze procedure required significantly longer aortic clamping time than the mitral valve operations with or without other valve operations performed from January 1990 to December 1991 in our institution (149.5 ± 32.2 minutes versus 124.3 ± 43.3 minutes; p = 0.016), whereas our modification was simplified by the use of cryoablation. Although the combined maze procedure is performed to lessen the risk of thromboembolism and increase the cardiac output by atrial kick, if left atrial contractility is not regained despite restoration of atrial rhythm, it is possible that this procedure may only increase the operative risk without elimination of thromboembolic episodes and hemodynamic improvement. In fact, it is quite possible that elimination of the left atrial appendage, which is a portion of the maze procedure, removes the major locus of thrombus formation in the noncontractile atrium, and so decreases the risk of thromboembolic complications despite the lack of contraction.

We believe that the factors affecting atrial function and restoration of sinus rhythm after the maze procedure have relation not only to the fibrosis of atrial muscle caused by the long duration of AF but also to the rheumatic inflammatory activity. In conclusion, reconsideration of the indications for the maze procedure for AF associated with rheumatic mitral stenosis may be reasonable, particularly for cases in which replacement using a prosthetic valve is necessary, but we believe that patients with nonrheumatic mitral valve disease, especially those able to undergo reconstructive operations, are the best candidates for the maze procedure.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

1. Cox J.L., Schuessler R.B., D’Agostino H.J., Jr, et al. The surgical treatment of atrial fibrillation. III. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569-583.[Abstract]
2. Cox J.L., Boineau J.P., Schuessler R.B., Kater K.M., Lappas D.G. Five-year experience with the maze procedure for atrial fibrillation. Ann Thorac Surg 1993;56:814-824.[Abstract]
3. Kosakai Y., Kawagushi A., Isobe F., et al. Cox maze procedure for chronic atrial fibrillation associated with mitral valve disease. J Thorac Cardiovasc Surg 1994;108:1049-1055.[Abstract/Free Full Text]
4. Cox J.L., Canavan T.E., Schuessler R.B., et al. The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiological mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:402-426.[Abstract]
5. Harada A., Sasaki K., Fukushima T., et al. Atrial activation during chronic atrial fibrillation in patients with isolated mitral valve disease. Ann Thorac Surg 1996;61:104-112.[Abstract/Free Full Text]
6. Sueda T., Nagata H., Shikata H., et al. Simple left atrial procedure for chronic atrial fibrillation associated with mitral valve disease. Ann Thorac Surg 1996;62:1796-1800.[Abstract/Free Full Text]
7. Goldstein I., Halpern B., Robert L. Immunological relationship between streptococcus polysaccharide and the structural glycoproteins of heart valve. Nature 1967;213:44-47.
8. Waller B., Howard J., Fess S. Pathology of mitral valve stenosis and pure mitral regurgitation—part I. Clin Cardiol 1994;17:330-336.[Medline]
9. Selzer A.S., Cohn K.E. Natural history of mitral stenosis: a review. Circulation 1972;45:878-890.[Free Full Text]
10. Dekker A., Black H., Von Lichtenberg F. Mitral valve restenosis. J Thorac Cardiovasc Surg 1968;55:434-446.[Medline]
11. Ueshima K., Hashimoto K., Chiba M., et al. Recovery of atrial function after combined treatment with surgical repair for organic heart disease and maze procedure for atrial fibrillation. J Thorac Cardiovasc Surg 1997;113:214-215.[Free Full Text]

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