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J Thorac Cardiovasc Surg 1999;117:463-471
© 1999 Mosby, Inc.

SURGERY FOR ADULT CARDIOVASCULAR DISEASE

LONG-TERM EVALUATION OF TREATMENT FOR FUNCTIONAL TRICUSPID REGURGITATION WITH REGURGITANT VOLUME: CHARACTERISTIC DIFFERENCES BASED ON PRIMARY CARDIAC LESION

From the Department of Surgery, Division II, Kobe University School of Medicine, Kobe, Japan.

Received for publication Sept 12, 1997. Revisions requested Nov 12, 1997. Revisions received Oct 5, 1998. Accepted for publication Oct 5, 1998. Address for reprints: Takaki Sugimoto, MD, Department of Surgery, Division II, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.

	Abstract

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Objectives: The aim of this study was to characterize differences in the long-term effects of treatment for functional tricuspid regurgitation based on the primary cardiac lesion.
Methods: Ninety-six patients with valvular heart disease and 32 patients with atrial septal defects associated with tricuspid regurgitation were studied. The tricuspid annular diameter was associated with evidence of right heart failure. In valvular heart disease, a Kay annuloplasty was performed in 33 patients with a tricuspid annular diameter of 40 mm to 44 mm, a modified De Vega annuloplasty in 12 patients with a tricuspid annular diameter of 45 mm to 49 mm, and a modified De Vega annuloplasty, annuloplasty using a Carpentier ring, or tricuspid valve replacement in each of 4 patients with a tricuspid annular diameter of 50 mm. In atrial septal defects, a Kay annuloplasty was performed in 11 patients with a tricuspid annular diameter of 45 mm to 49 mm, and a modified De Vega annuloplasty was performed in 5 patients with a tricuspid annular diameter of 50 mm. A mean follow-up period was 79 months after operation.
Results: In the patients with a tricuspid annular diameter of <50 mm, the hemodynamic and clinical findings and tricuspid regurgitation remarkably improved. In the patients with valvular heart disease with a tricuspid annular diameter of 50 mm, however, the right heart parameters also showed improvement but less so when compared with those patients with a tricuspid annular diameter of <50 mm. In addition, 4 patients undergoing a modified De Vega annuloplasty have had a gradual increase in tricuspid regurgitation and clinical manifestations late after the operation. In contrast, all 5 patients with atrial septal defects with a tricuspid annular diameter of 50 mm have shown remarkable improvement, similar to those with a tricuspid annular diameter of <50 mm. Preoperative analyses revealed that the right heart function in atrial septal defects had not deteriorated to the same extent as in valvular heart disease.
Conclusion: In the patients with a severely dilated tricuspid anulus (50 mm), the postoperative change of tricuspid regurgitation differed between those patients with valvular heart disease and atrial septal defects.

	Introduction

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Left-sided valvular heart disease (VHD) and left-to-right cardiac shunt disease often cause functional tricuspid regurgitation (TR) as the result of right ventricular pressure or volume overload. ^1-8 With respect to surgical treatment of functional TR, surgeons have advocated not repairing the valve, ¹ performing a variety of tricuspid annuloplasty procedures, ^2-9 or performing valve replacement. ^9-12 Because of the differences in both cause and treatment, TR may decrease gradually after correction of the primary cardiac lesion. ¹ However, in some patients, significant TR remains after annuloplasty. ^5-9 There may be differences in the degree of TR after surgical repair on the basis of the primary cardiac lesion responsible for the TR. This study presents the long-term effects of treatment for TR and shows characteristic differences on the basis of the primary cardiac lesion.

	Methods

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Patients
From April 1985 to September 1995, 276 patients underwent valve operation for acquired VHD, and 60 patients underwent repair of a secundum atrial septal defect (ASD). Among the patients with VHD, 85 patients who had organic TR or who underwent isolated aortic valve operation or concomitant cardiac procedures such as coronary artery bypass grafting were excluded from the study. Organic TR was defined as prolapse of the cusps, rheumatic valvulitis, or destruction of the valve apparatus because of infective endocarditis, diagnosed with preoperative echocardiography. Seven patients who died of cardiac complications early after the operation and 8 patients who had repeat operations because of dysfunction of the left-side valve repairs were also excluded from the study. Among the patients with ASD, 10 patients who had organic TR or who underwent concomitant coronary artery bypass grafting, mitral valve operation, or operation for anomalous pulmonary venous drainage were also excluded from the study. Among the remaining patients, 96 patients (30 men and 66 women) with a mitral valve lesion or mitral and aortic valve lesions and 32 patients (14 men and 18 women) with ASD associated with functional TR were enrolled in the study. For the patients with VHD, the main left-sided lesions were mitral stenosis in 56 patients and mitral regurgitation in 24 patients. Sixteen patients had both mitral and aortic valve lesions. Open mitral commissurotomy was performed in 4 patients; mitral valve replacement was performed in 76 patients, and combined mitral and aortic valve replacement was performed in 16 patients. All ASDs were closed with a patch.

Evaluation of TR
Echocardiographic studies were performed within 5 days before the operation when the patient was hemodynamically stable. Two-dimensional and Doppler echocardiography was performed with Toshiba SSH-65A and SSH-140A equipment (Toshiba Corp, Tokyo, Japan) with a 2.5 MHz transducer. Each patient lay quietly for 15 minutes in a supine position and underwent the procedure in the left lateral decubitus position while breathing quietly. The TR jet was observed in the following 3 cross-sectional views: parasternal long-axis view of the right ventricular inflow tract, apical 4-chamber view, and parasternal short-axis view at the level of the aortic valve.

Calculation of TR volume. First, TR was observed in the 2 right-angle cross-sectional views with 2-dimensional color Doppler echocardiography. The width of the base of the TR jet at a right angle (a,b) was measured at the tricuspid valve position in each view. The cross-sectional area (S) of the base of the TR jet was calculated as an elliptical shape (S = /4 · ab), where the major and minor axes were a and b. Next, a continuous-wave Doppler echocardiogram was recorded from the center of the base of the TR jet (the most accelerated point of the functional TR occurring as the result of dilation of the anulus). The TR volume of 1 unit area (Vu) at this point was calculated by integrating the parabolic flow velocity signal of the echocardiogram during the ejection phase (Vu = 2/3 · vt; v, peak velocity; t, duration of regurgitation). The TR volume per beat (V_TR) is equal to the sum of the volume of 1 unit area per cross-sectional area, which is assumed to build up a conical shape. This is because the volume of 1 unit area decreases in accordance with distance from the center of the TR jet. The V_TR can be calculated by the following formula: 1/3 · S · Vu = /18 · abvt (Fig. 1). Because all of the patients underwent atrial fibrillation, each value for V_TR was obtained from an average of more than 5 heart beats. In 2-dimensional color Doppler echocardiography, the Doppler gain was set at the maximum level where no background noise was seen. In the continuous-wave Doppler echocardiogram, the angle between the Doppler beam and the direction of the TR jet was provided within 20 degrees. The echocardiogram was passed through a high-pass filter (1600 Hz) to eliminate the influence of the movement of the intracardiac structure and was recorded on a stripchart at a paper speed of 50 mm/s.

View larger version (51K): [in this window] [in a new window]   Fig 1. Calculation of TR volume per beat (VTR).

Other parameters
All patients underwent preoperative right heart catheterization studies, including cineangiography at the same time as Doppler studies. The right ventricular volume was obtained from the biplane cineangiograms by the area-length method ¹³ on an average of 5 heart beats excluding premature contractions.

The degree of heart failure was based on New York Heart Association (NYHA) functional class, the degree of hepatomegaly, and indocyanine green measurement.

Treatment of TR
There was a significant correlation between preoperative TAD and V_TR in the VHD group (r = 0.87; P < .0001) and the ASD group (r = 0.88; P < .0001). The slope of the correlation line (TAD: x-axis, V_TR: y-axis) was steeper for the VHD group (y = 1.41x – 46.0) than the ASD group (y = 1.11x – 37.6; Fig. 2). In the patients with VHD with a TAD of 40 mm or more and the patients with ASD with a TAD of 45 mm or more, hepatomegaly, disappearance rate of indocyanine green (k value), right atrial mean pressure (RAMP), right ventricular end-diastolic pressure (RVEDP), and right ventricular end-diastolic volume index (RVEDVI) had deteriorated to the point that surgical repair for TR was necessary (Tables I and II).

View larger version (22K): [in this window] [in a new window]   Fig 2. Correlation of regurgitant volume per beat (VTR) and TAD at end-diastole. There is a significant correlation between preoperative TAD and VTR in the VHD group (r = 0.87) and the ASD group (r = 0.88). However, the slope of the correlation line is steeper for the VHD group than for the ASD group.

View this table: [in this window] [in a new window]   Table I. Preoperative profile of patients with VHD with a TAD of <40 mm and of 40 mm

View this table: [in this window] [in a new window]   Table II. Preoperative profile of patients with ASD with a TAD of <45 mm and of 45 mm

The disappearance of regurgitation was confirmed intraoperatively by the injection of saline solution into the right ventricle after TR repair, and recently in combination with transesophageal echocardiography. In a modified De Vega annuloplasty, the anterior anulus was also repaired in addition to obliteration of the posterior leaflet. For a Kay or a modified De Vega annuloplasty, the dilated anulus was reduced to 2.5 fingerbreadths in the patients with VHD and 3 fingerbreadths in the patients with ASD, where the volume reduction of the right ventricle was likely due to closure of the ASD.

Follow-up
Except for 1 late death in the group with VHD, all patients have been followed up, with good repair of the primary cardiac lesions. None of them have undergone repeat operation. The follow-up period ranged from 6 to 130 months (mean, 79 months; median, 84 months). A postoperative catheterization study was performed 1 month after the operation at the same time as Doppler study in all patients. Echocardiograms and physical examinations were obtained every 6 months after the operation, and the most recent values of these data were used as the postoperative values. Good repair of the primary cardiac lesions was confirmed by postoperative Doppler study, which showed a functional mitral orifice area of greater than 2.5 cm² and a pressure gradient across the aortic valve of below 30 mm Hg with no perivalvular regurgitation in patients with VHD, and no leakage of the patch repair of the ASD.

Statistical analysis
Statistical analysis was performed with the Stat View 4.11 software package (Abacus Concepts, Inc, Berkeley, Calif). Values are expressed as the mean ± standard deviation. Statistical differences were evaluated with unpaired or the paired Student t test.

	Results

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Comparisons of the methods evaluating TR with the surgical procedure
With the conventional 4-grade classification based on the distance reached by TR jet in 2-dimensional Doppler echocardiography, ¹⁴ it was difficult to decide on the treatment of TR, that is, repair or no repair, in patients with grade II and III disease. In contrast, the evaluation according to the V_TR provided a clearer guideline for requirement of TR repair (V_TR 10 cc) before the operation (Fig 3).

View larger version (24K): [in this window] [in a new window]   Fig. 3 Comparisons of the methods used to evaluate the TR with the surgical procedure. With the conventional 4-grade classification based on the distance reached by TR jet in 2-dimensional Doppler echocardiography (2-DD), 14 it is difficult to select the treatment for TR, that is, repair or no repair, in patients with grade II and III disease. The evaluation according to VTR provides a clearer guideline for TR repair (VTR 10 cc) before the operation.

Changes in degree of heart failure after operation
In the patients in whom TR was not treated, NYHA functional class has significantly improved in those patients with VHD and those patients with ASD (2.7 ± 0.5 to 1.3 ± 0.5 and 1.9 ± 0.6 to 1.1 ± 0.3; P < .0001, respectively). Hepatomegaly, RAMP, RVEDP, and RVEDVI have not shown any deterioration in both groups.

In the patients with repair of the tricuspid valve, hepatomegaly, RAMP, RVEDP, pulmonary arterial mean pressure (PAMP), RVEDVI, and NYHA functional class significantly improved in both groups. In the patients with VHD with a TAD of 50 mm or more, however, these parameters significantly improved but still remained less good than in those patients with a TAD of 40 mm to 49 mm (Table III). In addition, 4 patients who underwent a modified De Vega annuloplasty had a gradual increase in clinical manifestations; 1 of them died of right heart failure late after operation. The other 8 patients who underwent annuloplasty with a Carpentier ring or valve replacement have shown no deterioration of these parameters. In contrast, all 5 patients with ASD with a TAD of 50 mm showed significant improvement of these values to the same extent as did those patients with a TAD of 45 mm to 49 mm even after a modified De Vega annuloplasty (Table IV).

View this table: [in this window] [in a new window]   Table V. Preoperative profile of patients with VHD with a TAD of 40 mm to 49 mm and 50 mm

View this table: [in this window] [in a new window]   Table VI. Preoperative profile of patients with ASD with a TAD of 45 mm to 49 mm and 50 mm

	Discussion

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Functional TR is first originated by right ventricular pressure or volume overload, with VHD causing the former and ASD causing the latter. This is supported by the result that PAMP in the patients with insignificant TR was significantly lower in patients with ASD than in patients with VHD (Tables I and II). Furthermore, development of TR causes volume overload on the right ventricle by TR itself along with dilation of the tricuspid anulus. ^18,19 In support of this finding, the present study showed that the preoperative V_TR was directly proportional to the TAD in the VHD and ASD groups, respectively. In addition in ASD, a left-to-right shunt flow augments such volume loading. This may explain the steeper slope for the correlation line for the relationship between TAD and V_TR in VHD, when compared with in ASD. That is, the TR volume was smaller in quantity in ASD than VHD when the TAD was equal.

Regarding estimation of the TAD, the TAD proved to be reproducible regardless of the size or geometry of the right ventricle. The TAD was associated with evidence of right heart failure, and the patients with VHD with a TAD of 40 mm and the patients with ASD with a TAD of 45 mm required TR repair. Most of them experienced remarkable improvement in TR and hemodynamic and clinical findings after a Kay or a modified De Vega annuloplasty. In the patients with severely dilated anulus, however, the long-term changes of TR differed somewhat between those patients with VHD and ASD. In fact, in the patients with VHD with a TAD of 50 mm, the right heart parameters still remained less good when compared with those patients with a TAD of <50 mm. In addition, 4 patients who underwent a modified De Vega annuloplasty experienced a gradual increase in TR and clinical manifestations late after the operation. In contrast, in the patients with ASD in this category, these right heart parameters significantly improved to the same extent as in those patients with a TAD of <50 mm and have experienced no deterioration even after a modified De Vega annuloplasty. This might indicate that De Vega annuloplasty is sufficient for ASD, although a more rigid annuloplasty method or valve replacement is mandatory for VHD in this category.

The retrospective preoperative analyses revealed that the patients with VHD with a TAD of 50 mm showed lower RVSP and RVEF (Table V). However, previous studies ^20,21 have demonstrated that more severe TR is accompanied by higher RVSP. We believe that the forward flow of the right ventricle decreases with progression of TR. As a result, such a severe TR in this category would have a lower RVSP because of right ventricular dysfunction, indicative of a lower RVEF, as was proved in this study. In contrast, the patients with ASD with a TAD of 50 mm did not show such a decrease in RVSP and RVEF. This indicates that in ASD, right ventricular function did not deteriorate to the same extent as in VHD, even in this category. This would be the reason that the postoperative change of TR differed between those patients with VHD and ASD in this category.

	Acknowledgments

 
We thank Dr Yoshimasa Maniwa for statistical consultation.

	References

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1. Braunwald NS, Ross J Jr, Morrow AG. Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation 1967;35(Suppl):I63-9.
   
2. Kay JH, Maselli-Champagna G, Tsuji HK. Surgical treatment of tricuspid insufficiency. Ann Surg 1965;162:53-8. [Medline]
   
3. Boyd AD, Engelman RM, Isom OW, Reed GE, Spencer FC. Tricuspid annuloplasty: five and one-half years' experience with 78 patients. J Thorac Cardiovasc Surg 1974;68:344-51. [Medline]
   
4. Carpentier A, Deloche A, Hanania G, et al. Surgical management of acquired tricuspid valve disease. J Thorac Cardiovasc Surg 1974;67:53-65. [Medline]
   
5. Cohn LH. Tricuspid regurgitation secondary to mitral valve disease: when and how to repair. J Card Surg 1994;9(suppl):II237-41.
   
6. Cohen SR, Sell JE, McIntosh CC, Clarke RE. Tricuspid regurgitation in patients with acquired chronic, pure mitral regurgitation: nonoperative management, tricuspid annuloplasty and tricuspid valve replacement. J Thorac Cardiovasc Surg 1987;94:488-97. [Abstract]
   
7. Nakano S, Kawashima Y, Hirose H, et al. Evaluation of long-term results of bicuspidalization annuloplasty for functional tricuspid regurgitation: a seventeen-year experience with 133 consecutive patients. J Thorac Cardiovasc Surg 1988;95:340-5. [Abstract]
   
8. Kay LG, Morita S, Mendez MA, Zubiate P, Kay HJ. Tricuspid regurgitation associated with mitral valve disease: repair and replacement. Ann Thorac Surg 1989;48:593-5.
   
9. McGrath LB, Gonzalez-Lavin L, Bailey BM, Grunkemeier GL, Fernandez J, Laub GW. Tricuspid valve operations in 530 patients. J Thorac Cardiovasc Surg 1990;99:124-33. [Abstract]
   
10. Mullany CJ, Gersh BJ, Orzulak TA, et al. Repair of tricuspid valve insufficiency in patients undergoing double (aortic and mitral) valve replacement: perioperative mortality and long-term (1 to 20 years) follow-up in 109 patients. J Thorac Cardiovasc Surg 1987;94:740-8. [Abstract]
    
11. Singh AK, Feng WC, Sanofsky SJ. Long-term results of St Jude Medical valve in the tricuspid position. Ann Thorac Surg 1992;54:538-40. [Abstract/Free Full Text]
    
12. Scully HE, Armstrong CS. Tricuspid valve replacement: fifteen years of experience with mechanical prostheses and bioprostheses. J Thorac Cardiovasc Surg 1995;109:1035-41.
    
13. Ferlinz J, Gorlin R, Cohn PF, Herman M. Right ventricular performance in patients with coronary artery disease. Circulation 1975;52:608-15. [Abstract/Free Full Text]
    
14. Miyatake K, Okamoto M, Kinoshita N, et al. Evaluation of tricuspid regurgitation by pulsed Doppler and two-dimensional echocardiography. Circulation 1982;66:777-84. [Abstract/Free Full Text]
    
15. Carreras F, Borras X, Auge JM, Pons-Llado G. Pulsed Doppler assessment of tricuspid regurgitation: usefulness of regurgitant signal patterns for estimation of severity. Angiology 1988;39:788-94.
    
16. Suzuki Y, Kambara H, Kadota K, et al. Detection and evaluation of tricuspid regurgitation using a real-time, two-dimensional, color-coded, Doppler flow imaging system: comparison with contrast two-dimensional echocardiography and right ventriculography. Am J Cardiol 1986;57:811-5. [Medline]
    
17. Sugimoto T, Ota T, Nakamura K. New method quantifying tricuspid regurgitant volume by two-dimensional color and continuous wave Doppler echocardiography. J Cardiol (in Japanese) 1988;18:1069-81.
    
18. Tei C, Pilgrim JP, Shah PM, Ormiston JA, Wong M. The tricuspid valve annulus: study of size and motion in normal subjects and in patients with tricuspid regurgitation. Circulation 1982;66:665-71. [Abstract/Free Full Text]
    
19. Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H. Mechanisms for development of functional tricuspid regurgitation by pulsed Doppler and two-dimensional echocardiography. Am J Cardiol 1984;53:160-3. [Medline]
    
20. Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70:657-62. [Abstract/Free Full Text]
    
21. Morrison DA, Ovitt T, Hammermeister KE, Stovall LR. Functional tricuspid regurgitation and right ventricular dysfunction in pulmonary hypertension. Am J Cardiol 1988;62:108-12. [Medline]
    

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