HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sagie, A. Articles by Levine, R. A. Search for Related Content PubMed PubMed Citation Articles by Sagie, A. Articles by Levine, R. A.

J Thorac Cardiovasc Surg 1994;108:727-735
© 1994 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

Significant tricuspid regurgitation does not resolve after percutaneous balloon mitral valvotomy

Boston, Mass.

Dr. Sagie was a Visiting Research Fellow from Beilinson Medical Center, Petah Tikva and Tel Aviv University Sackler School of Medicine, Tel Aviv, Israel. He was supported in part by a research grant of American Physician Fellowship (APF) for Medicine in Israel, Brookline, Mass. This study was supported in part by a grant of the American Heart Association, Dallas, Texas. Dr. Levine is an Established Investigator of the American Heart Association, Dallas, with funds contributed in part by its Massachusetts Affiliate, Natick, Mass. Dr. Schwammenthal was a Visiting Scientist and Research Fellow from the Westfalische Wilhelms-Universitat, Munster, Germany, and supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn, Germany.

Received for publication Jan. 27, 1994. Accepted for publication May 17, 1994. Address for reprints: Alex A. Sagie, MD, Cardiac Unit, Vincent Burnham 5, Massachusetts General Hospital, Boston, MA 02114.

Abstract

A total of 318 consecutive patients with mitral stenosis underwent percutaneous mitral valvotomy at our institution from 1987 to 1993. Of those, 98 patients had color Doppler echocardiographic studies performed before, 24 hours after, and late after the intervention. On the basis of color Doppler echocardiographic grading of tricuspid regurgitation, 32 patients (32%; mean age 57 ± 15 years) had significant (moderate or severe) tricuspid regurgitation before the intervention and were the subject of this study. The follow-up study was performed 18.4 ± 13 months after the procedure. Successful percutaneous mitral valvotomy (1.5 cm²valve area or50% increase after valvotomy) with no restenosis at follow-up was achieved in 20 patients. Tricuspid regurgitation decreased by one grade (from severe to moderate) in only four subjects in this group and in none of the 12 patients who did not meet the criteria for successful percutaneous mitral valvotomy or who had restenosis. Thus tricuspid regurgitation did not improve in 88% of all patients studied. On average, no significant change was observed in the ratio of maximal tricuspid regurgitant jet area to right atrial area 24 hours after percutaneous mitral valvotomy and at late follow-up (37% vs 33% vs 34%, respectively) or in any of the right heart dimensions, even in patients who underwent successful percutaneous mitral valvotomy. Right ventricular systolic pressure also did not change significantly on average in those patients (46 ± 15 versus 42 ± 14 versus 48 ± 18 mm Hg, respectively). However, right ventricular dimensions did not decrease and tricuspid regurgitation did not resolve even in a subgroup of patients in whom right ventricular systolic pressure fell by more than 10 mm Hg (up to 41 mm Hg). (J THORACCARDIOVASCSURG1994;108:727-35)

Mitral stenosis is commonly associated with tricuspid regurgitation (TR) of varying degrees. ^1-5 The decision regarding whether to repair or replace the tricuspid valve in patients with significant TR during mitral valve operations is of great clinical importance, because TR (functional or organic) can persist and contribute to increased morbidity and mortality despite adequate correction of the mitral valve. ^6-10 Because current methods cannot predict in which patients significant TR may or may not resolve after mitral valve surgery, simultaneous repair of the tricuspid valve is generally advised. Recently, percutaneous balloon mitral valvotomy has become the procedure of choice for selected patients with mitral stenosis. ^11-14 Like the closed mitral valvotomy procedure performed in the early days of cardiac surgery, it has the potential disadvantage of leaving the associated tricuspid valve disease untreated. The patient group undergoing percutaneous mitral valvotomy constitutes a unique population that allows us to evaluate the changes in TR severity after relief of mitral stenosis, because there is no selection introduced by the surgeon's decision to correct the tricuspid valve when it appears necessary during the operation. These patients, therefore, provide valuable information as to whether mitral balloon valvuloplasty should be generally performed in patients with associated significant TR, or whether they instead should undergo mitral valve surgery with concomitant tricuspid valve repair.

The objectives of the present study are as follows: (1) to investigate whether TR resolves, persists, or progresses after percutaneous mitral valvotomy and (2) to explore whether changes in TR severity after percutaneous mitral valvotomy are related to changes in right heart dimensions and systolic pressure.

METHODS

A total of 318 consecutive patients with mitral stenosis underwent percutaneous mitral valvotomy at our institution from 1987 to 1993. Of those, 98 patients had color Doppler echocardiographic studies performed before, 24 hours after, and late after the intervention. On the basis of color Doppler echocardiographic grading of TR (described later), 32 patients (32%) had significant (moderate or severe) TR before intervention and were the subject of this study. The group included 26 (81%) women and six men with a mean age of 57 ± 15 years (range 30 to 80 years). The follow-up study was performed 18.4 ± 13 months after the procedure. Important clinical characteristics of the study group are presented in Table I. The study group was divided into two subgroups: group 1, comprising 20 patients in whom percutaneous mitral valvotomy resulted in sustained success and no evidence for restenosis (as defined later) at follow-up echocardiographic study, and group 2, comprising 12 patients in whom percutaneous mitral valvotomy initially failed or restenosis subsequently occurred (defined as loss of 50% or more of gain in the mitral valve area produced by percutaneous mitral valvotomy).

Clinical follow-up
Clinical follow-up ranged from 6 to 62 months (mean 26.7 ± 18 months). Data were obtained during patient visits to the clinic or by telephone interviews conducted by a trained nurse or cardiologist with the referring physician, the patients, or both. The clinical end points included (1) mitral valve replacement or repair, (2) repeat percutaneous mitral valvotomy, (3) development of symptomatic heart failure (New York Heart Association functional class III or IV), and (4) death unrelated to the valve operation. Causes of death were obtained from the patient's physician or from medical records.

Echocardiographic analysis.
In all 32 patients a complete two-dimensional and color Doppler flow examination was performed less than 24 hours before percutaneous mitral valvotomy, 24 hours after valvotomy, and a mean of 18.4 ± 13 months (range 2 to 43 months) after valvotomy. In 21 patients the follow-up was more than 1 year. A Hewlett-Packard 77020A ultrasound imaging system (Hewlett-Packard Company, Andover, Mass.) equipped with a 2.5 MHz phased-array transducer was used.

Mitral valve.
A previously described semiquantitative echocardiographic assessment of mitral valve score ¹⁷ was obtained in each patient by assigning values of 0 to 4 (with increasing abnormality) to each of four morphologic characteristics of the valve, namely, leaflet mobility, thickening, calcification, and subvalvular thickening (score range from 0 to 16). Mitral valve area was measured by direct planimetry in the standard manner. ¹⁸ Technically satisfactory images suitable for planimetry could not be obtained at follow-up in three patients, in whom the pressure half-time method was used to assess mitral valve area. ¹⁹

Assessment of TR and right ventricular pressure.
TR was assessed by integrating both Doppler color flow mapping images of the regurgitant jet and pulsed wave Doppler evidence of systolic flow reversal in the inferior vena cava or hepatic veins. ²⁰ Careful Doppler evaluation of the jet was performed in all obtainable views of the right ventricle and atrium, including the parasternal short-axis view at the aortic valve level, the right ventricular inflow view, the apical four-chamber view, and subcostal views. The color flow mapping display of reversed or mosaic signals originating from the tricuspid valve and extending into the right atrium during systole identified the presence of TR. The narrowest sector angle encompassing the regurgitant jet was used to obtain maximal frame rate. The area of disturbed flow that was traced (using a calibrated Sony off-line analysis system; Sony Medical Systems, Montvale, N.J.); included the aliased signals as well as the immediately contiguous nonturbulent velocities that were moving in the same direction as the jet. Right atrial area was traced from the same frame as the maximal jet area. TR was then graded as mild, moderate, or severe according to the following algorithm: (1) The view in which the spatial distribution of the jet was maximal was selected. (2) The severity of regurgitation was graded as mild if jet area occupied less than 20% of right atrial area, as moderate if this value was between 20% and 33%, and as severe if this value exceeded 33%, based on correlations with surgical and angiographic severity in previous studies. ^21-23 (3) If the ratio of jet area to right atrial area was close to a cutoff point, jet eccentricity increased the grade above that cutoff to the next higher grade because eccentric wall jets appear smaller than comparable free jets. ^24,25 (4) Systolic flow reversal in the inferior vena cava or hepatic veins by pulsed wave Doppler echocardiography was considered as indicating at least moderate TR, regardless of the other findings. ²² TR was defined as organic if thickening, doming, or restricted motion of the valve leaflets was present.

Right ventricular systolic pressures were estimated by continuous wave Doppler ultrasonography by means of the modified Bernoulli equation (4 X [peak TR velocity]²), with 10 mm Hg added for the estimated right atrial pressure. ²⁶

Right heart dimensions.
Measurements were made from the apical four-chamber view. The right ventricular long axis was measured from the apex to the midpoint of the tricuspid anulus at end-diastole; the right ventricular minor axis was measured from the septum to the free wall at the mid-cavity level; right atrial area was traced in the same systolic frame used for jet area measurements. ²⁷ The maximal tricuspid valve anulus diameter during diastole was measured from the insertion of the septal tricuspid leaflet to the insertion of the anterior tricuspid leaflet; the minimal tricuspid anulus diameter was measured during systole using the same beat and plane in which the maximal diameter was taken. ²⁷ The percent shortening of the tricuspid anulus was calculated as (maximal diastolic diameter minimal systolic diameter)/maximal diastolic diameter. ²¹

Statistics
Data were expressed as mean ± standard deviation. Changes in two-dimensional echocardiographic, Doppler color flow mapping, and angiographic findings were assessed by the paired Student's t test (two-tailed).

Observer variability
Two independent observers repeated 10 measurements of jet and right atrial areas. The measurements of the two observers were subtracted and the standard deviation of the differences was used to express interobserver variability.

RESULTS

Clinical characteristics and hemodynamics before percutaneous mitral valvotomy (Tables I and II)
Fifteen (47%) patients had moderate TR and 17 (53%) had severe TR. Six (20%) were in New York Heart Association class II, 21 (67%) in class III, and 5 (13%) in class IV. The study group had a high prevalence (75%) of atrial fibrillation and a high mean mitral valve score (8 in 63% of the studied patients) on echocardiography. In 6 (19%) patients the TR was considered as organic in origin. The study group was characterized by a high mean right atrial pressure (11.1 ± 4.7 mm Hg) and markedly elevated pulmonary artery resistance (309 ± 330 dyne·sec·cm^-5).

View larger version (14K): [in this window] [in a new window]   Fig. 1. Change in TR grade at late follow-up in 20 patients who underwent successful percutaneous mitral valvotomy (PMV).

View larger version (14K): [in this window] [in a new window]   Fig. 2. Change in TR grade at late follow-up in 12 patients who had unsuccessful percutaneous mitral valvotomy (PMV).

View larger version (28K): [in this window] [in a new window]   Fig. 3. Percent ratio of maximal TR jet area to right atrial area in 20 patients who underwent successful percutaneous mitral valvotomy at three times: before the procedure, 24 hours after it, and at mean follow-up of 18.4 months.

Right ventricular systolic pressure (see Table V)
On average, right ventricular systolic pressure estimated from the TR jet velocity decreased slightly 24 hours after percutaneous mitral valvotomy but was slightly higher at late follow-up (46 ± 15 versus 42 ± 14 versus 48 ± 18 mm Hg, respectively). None of these changes reached statistical significance. Despite reduction of more than 10 mm Hg (up to 41 mm Hg) in right ventricular systolic pressure (before percutaneous mitral valvotomy versus follow-up) in five patients with successful percutaneous mitral valvotomy, TR grade did not change in any of these patients. In those five patients the ratio of TR jet area to right atrial area averaged 41% before and 38% late after percutaneous mitral valvotomy (p = NS).

Right-sided dimensions (see Table V)
Right atrial area, right ventricular length and width, maximal and minimal annular dimensions, and the percent shortening of the tricuspid valve anulus did not change significantly 24 hours and at late follow-up after percutaneous mitral valvotomy. They also did not change in the subgroup of patients whose right ventricular systolic pressure decreased more than 10 mm Hg after percutaneous mitral valvotomy.

Clinical follow-up (Table VI)
Follow-up data were available for all patients in the study group. At a mean follow-up of 27 months, the rate of late complications was relatively high, such as the need for mitral valve surgery (28%), restenosis (22%), the development of symptomatic heart failure (18%), and cardiac death (12.5%). (These complications are not mutually exclusive.)

DISCUSSION

TR, whether organic or functional, is an important factor in the surgical management of patients with rheumatic mitral valve disease. Although earlier reports had suggested that TR can resolve once the diseased mitral valve is replaced, ² more recently, surgical experience has indicated that the degree of resolution of significant TR after correction of mitral stenosis is not predictable, and failure to repair severe TR lesions seriously compromises the results of mitral valve operations and is associated with increased morbidity and mortality despite adequate mitral valve area. ^5-10 Therefore, in an effort to ensure optimal outcome, it has become common surgical practice—although still controversial—to correct significant residual TR routinely at the time of the mitral valve operation, ^5-7,9,10 particularly after the introduction of the De Vega annuloplasty. ^6,7,28,29 The intraoperative decision to perform tricuspid annuloplasty when deemed necessary has intervened in the course of the disease so that the fate of untreated significant TR after successful repair of the mitral valve can now be studied only in patients not selected for tricuspid valve repair. Recently, however, percutaneous mitral balloon valvotomy has emerged as an attractive therapeutic alternative for patients with mitral stenosis. ^11-14 Although safe, economical, and efficacious, it has the potential disadvantage of leaving associated tricuspid valve disease untreated. Therefore, patients undergoing percutaneous mitral valvotomy constitute a unique population that can allow us to evaluate the fate of significant TR after relieving the mitral stenosis prospectively and without the selection introduced by the surgical decision to correct the tricuspid lesion at the time of the mitral valve operation.

Despite the relatively high prevalence of significant TR in this population (32%), the late follow-up of this lesion after percutaneous mitral valvotomy has not been established. The results of this study show that significant TR does not substantially decrease or resolve after the procedure in the majority of patients at late follow-up. These data are consistent with those reported by Shafie, Hayat, and Majid ⁸ in 23 patients with variable degrees of TR after closed mitral valvotomy, which like percutaneous mitral valvotomy cannot directly correct the tricuspid valve disease. They found that despite successful operation on the mitral valve, eight patients with initially severe TR did not show significant improvement at 1 year's follow-up. Three to 5 years later, four of these patients had to be recatheterized for persistent right ventricular failure and were found to have an adequate mitral valve area, good left ventricular function, but significant TR. Their findings highlight the clinical significance of such persistent TR.

Potential mechanisms for these observations
Several mechanisms may explain the lack of substantial improvement in significant TR after percutaneous mitral valvotomy in this study population:

1. Rheumatic involvement of the tricuspid valve or degenerative changes could lead to organic TR that is not entirely related to the presence or severity of mitral stenosis. For example, this may be the mechanism of persistent TR in the four patients with organic tricuspid valve disease and successful percutaneous mitral valvotomy.
   
2. Elevated pulmonary artery pressure can persist despite successful percutaneous mitral valvotomy, an important finding by itself. In this study, right ventricular systolic pressure did not decrease substantially at late follow-up in 15 (75%) patients with successful percutaneous mitral valvotomy despite the initial decreases described previously. This maintains the driving pressure for TR and can also potentially play a role in keeping the right ventricle and tricuspid anulus dilated. Recently, Georgeson and associates ³⁰ found similar results for pulmonary hypertension after percutaneous mitral valvotomy evaluated by Doppler TR velocities, which provided good correlation with pressures measured at cardiac catheterization. They found that initial decreases in right ventricular systolic pressure did not persist at 17 months of follow-up, and in fact right ventricular pressure increased almost to preprocedural values. In that and other studies, ^31,32 restenosis and significant MR were the most important contributors to persistent adverse hemodynamics. In our study restenosis occurred in six patients of the 12 with initial failure or restenosis and in none of the 20 patients with initial successful percutaneous mitral valvotomy. New significant mitral regurgitation developed in none. Thus it must be assumed that in the majority of patients long-standing mitral stenosis caused irreversible pulmonary vascular disease. ³³ The fact that pulmonary resistance did not decrease significantly immediately after successful percutaneous mitral valvotomy supports this view. In those 12 patients with initial failure or restenosis, the absence of improvement in TR and right heart measurements is probably related to the status of the mitral valve (persistent stenosis or late restenosis) because of unsuccessful percutaneous mitral valvotomy.
   
3. Persistent right ventricular and tricuspid annular dilatation despite significant relief of pulmonary hypertension could maintain TR. In five of our patients, although right ventricular systolic pressure decreased more than 10 mm Hg (up to 41 mm Hg) at follow-up, TR was not relieved and right heart dimensions did not decrease. This suggests that right ventricular and tricuspid annular dilatation caused by long-standing pressure overload may become irreversible, causing significant functional TR to persist even after relief of the initial cause of dilatation (high pulmonary artery pressure). It further suggests that it is right heart dilatation (and not high pulmonary artery pressure) that directly causes the tricuspid valve to become incompetent. This is also consistent with a preliminary report of Skudick and coworkers ³⁴ from South Africa in 18 young patients (mean age 18 years), all in sinus rhythm, whose initial TR severity ranged from mild to severe before percutaneous mitral valvotomy. Their patients, who were significantly younger than all of the patients in our study, showed a reduction of both right ventricular pressure and tricuspid annular diameter along with decreases in TR. It is likely that in these patients with shorter-term disease, right-sided changes are still reversible, in contrast to the patients in our study, whose age is comparable to that of our entire percutaneous mitral valvotomy population and who had evidence of long-standing disease (discussed later).
   

Clinical follow-up
Our patients with mitral stenosis associated with significant TR were characterized by relatively older age, high prevalence of atrial fibrillation, symptomatic heart failure, and a high echocardiographic score. These findings show that significant TR is associated with a poor baseline clinical status and extensive structural and functional abnormalities of the mitral apparatus, reflecting long-standing disease. Consistent with these characteristics is a high rate of adverse outcomes. Clinical follow-up in these patients is in agreement with the poor immediate and late results reported in patients with significant TR who underwent mitral valve operations. ^3,5-10 (Of course, TR itself, although a marker for adverse outcome, is not a cause of restenosis or mitral valve surgery and may be only one contributing factor to clinical heart failure.) In fact, analysis of our database has also revealed that the severity of prevalvotomy TR is an independent predictor for adverse outcome in patients undergoing percutaneous mitral valvotomy for mitral stenosis. ³⁵

Limitations
A potential limitation of the present study is that we could study only those patients in whom follow-up echocardiographic studies were performed at our institution. Assuming that more severely symptomatic patients were more likely to be referred for follow-up, a selection bias might have been introduced. However, because our institution is a referral center for percutaneous mitral valvotomy, the main reason for patients not to be examined at our hospital for follow-up was that they lived in distant states or foreign countries. In addition, when we compared the baseline clinical and hemodynamic characteristics of those patients with moderate and severe TR in whom follow-up echocardiographic study was not available with the study group, we found no significant differences in any of the preprocedural variables. More important, late clinical outcome, such as death rate and the need for mitral valve surgery or repeat percutaneous mitral valvotomy, was not significantly different from that of the study group. Therefore, this study group constitutes a representative sample of patients with mitral stenosis and associated significant TR from our population having percutaneous mitral valvotomy.

Currently, no ideal quantitative method—invasive or noninvasive—is available to estimate the degree of TR accurately. Angiographic estimation of TR requires positioning of the catheter across the tricuspid valve, which interferes with valve competence. ³⁶ Therefore, despite its known limitations, color Doppler echocardiography, especially when integrating information from both the pulsed wave and color techniques, seems the most appropriate and readily available tool to assess the severity of TR. ^21-23 In addition, the high mean atrial pressure found in this group confirms that color Doppler echocardiographic assessment of significant TR correctly predicted hemodynamically important disease.

The patient population in the present study is a unique group with a relatively high mean age, which represents those patients with mitral stenosis and advanced disease. Therefore, the results of this study leave open the possibility that the natural history may be different in a considerably younger or different population, ³⁴ because abnormalities causing persistent TR may still be reversible, as discussed earlier.

CONCLUSIONS AND CLINICAL IMPLICATIONS

The present study demonstrates that significant TR is commonly associated with mitral stenosis in patients undergoing percutaneous mitral valvotomy. Regardless of the outcome of percutaneous mitral valvotomy, significant TR did not substantially decrease or resolve after the procedure in the majority of patients in our population. These findings are consistent with and support the current policy of correcting associated significant TR during mitral valve operations. In selected patients with significant TR, mitral valve surgery, which allows simultaneous tricuspid valve repair, can be considered an alternative therapeutic option, particularly if long-term survival can be shown to be improved.

Acknowledgments

We thank Lari Harrell for her expert assistance with maintenance of the percutaneous mitral valotomy database and John B. Newell for his assistance with the statistical analysis.

References

1. Sepulveda G, Luks DS. Diagnosis of tricuspid insufficiency. Circulation 1955;11:552-9.[Medline]
   
2. Braunwald NS, Ross J, Morrow AG. Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation 1967;35(Suppl):I63-9.
   
3. Farid L, Dayem KA, Guindy R, Shabetai R, Dittrich HC. The importance of tricuspid valve structure and function in the surgical treatment of rheumatic mitral and aortic disease. Eur Heart J 1992;13:366-72.[Abstract/Free Full Text]
   
4. Hauck AJ, Freeman DP, Ackerman DM, Danielson GK, Edwards WD. Surgical pathology of the tricuspid valve: a study of 363 cases spanning 25 years. Mayo Clin Proc 1988;63:851-63.[Medline]
   
5. Pluth JR, Ellis FH. Tricuspid insufficiency in patients undergoing mitral valve replacement. J THORAC CARDIOVASC SURG 1969;58:484-9.
   
6. King RM, Schaff HV, Danielson GK, et al. Surgery for tricuspid regurgitation late after mitral valve replacement. Circulation 1984;70(suppl):II193-7.
   
7. Breyer RM, McClenathan JH, Michaelis LL, McIntosh CL, Morrow GM. Tricuspid regurgitation: a comparison of nonoperative management, tricuspid annuloplasty, and tricuspid valve replacement. J THORAC CARDIOVASC SURG 1976;72:867-74.[Abstract]
   
8. Shafie MZ, Hayat N, Majid OA. Fate of tricuspid regurgitation after closed valvotomy for mitral stenosis. Chest 1985;88:870-3.[Abstract/Free Full Text]
   
9. Groves PH, Lewis NP, Ikaram S, Maire R, Hall RJC. Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease. Br Heart J 1991;66:295-301.[Abstract/Free Full Text]
   
10. Groves PH, Ikaram S, Ingold U, Hall RJC. Tricuspid regurgitation following mitral valve replacement: an echocardiographic study. J Heart Valve Dis 1993;2:273-8.[Medline]
    
11. Lock JE, Khalilullah M, Shirivastava S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in patients with rheumatic mitral stenosis. N Engl J Med 1985;313:1515-8.[Abstract]
    
12. Palacios J, Block PC, Brandi S, et al. Percutaneous balloon valvotomy for patients with severe mitral stenosis. Circulation 1987;75:778-84.[Abstract/Free Full Text]
    
13. Palacios IF, Block PC, Wilkins GT, Weyman AE. Follow-up of patients undergoing percutaneous mitral balloon valvotomy: analysis of factors determining restenosis. Circulation 1989;79:573-9.[Abstract/Free Full Text]
    
14. Cohen JC, Kuntz RE, Gordon SPF, et al. Predictors of long-term outcome after percutaneous balloon mitral valvuloplasty. N Engl J Med 1992;327:1329-35.[Abstract]
    
15. Carabello BA, Grossman W. Calculation of stenotic valve orifice area. In Grossman W, ed. Cardiac catheterization and angiography. Philadelphia: Lea & Febiger, 1986:143-54.
    
16. Sellers RD, Levy MJ, Amplatz K, Lillehei CW. Left retrograde cardioangiography in acquired cardiac disease. Am J Cardiol 1964;14:437-47.[Medline]
    
17. Wilkins GT, Weyman AE, Abascal VM, Block PC, Palacios IF. Percutaneous mitral valvotomy: an analysis of echocardiographic variables related to outcome and mechanism of dilatation. Br Heart J 1988;60:299-308.[Abstract/Free Full Text]
    
18. Wann LS, Weyman AE, Feingenbaum H, Dillon JC, Johnston KW, Eggleston RC. Determination of mitral valve area by cross-sectional echocardiography. Ann Intern Med 1978;88:337-41.
    
19. Hatle L, Angelsen B, Tromsdal A. Noninvasive assessment of atrioventricular pressure half-time by Doppler ultrasound. Circulation 1979;60:1096-104.[Abstract/Free Full Text]
    
20. Mintz GS, Kotler MN, Parry WR, Iskandrian AS, Kane SA. Real time inferior vena caval ultrasonography: normal and abnormal findings and its use in assessing right-heart function. Circulation 1981;64:1018-85.[Abstract/Free Full Text]
    
21. Chopra HK, Nanda NC, Fan P, et al. Can two-dimensional echocardiography and Doppler color flow mapping identify the need for tricuspid valve repair. J Am Coll Cardiol 1989;14:1266-74.[Abstract]
    
22. Cooper JW, Nanda NC, Philpot E, Fan P. Evaluation of valvular regurgitation by color Doppler. J Am Soc Echocardiogr 1989;2:56-66.[Medline]
    
23. Mugge A, Daniel WG, Herrmann G, Simon R, Lichtlen PR. Quantification of tricuspid regurgitation by Doppler color flow mapping after cardiac transplant. Am J Cardiol 1990;66:884-7.[Medline]
    
24. Chen C, Thomas JD, Anconina J, et al. Impact of impinging wall jet on color Doppler quantification of mitral regurgitation. Circulation 1991;84:712-20.[Abstract/Free Full Text]
    
25. Cape EG, Yoganathan AP, Weyman AE, Levine RA. Adjacent solid boundaries alter the size of regurgitation jets on Doppler color flow maps. J Am Coll Cardiol 1991;17:1094-102.[Abstract]
    
26. Currie PJ, Seward JB, Chan K, et al. Continuous wave Doppler determination of right ventricular systolic pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750-6.[Abstract]
    
27. Triulzi M, Gillam LD, Gentile F, Newell JB, Weyman AE. Normal adult cross-sectional echocardiographic values: linear dimensions and chamber areas. Echocardiography 1984;4:403-26.
    
28. Minale C, Lambertz H, Nikol S, Gerich N, Messemer BJ. Selective annuloplasty of the tricuspid valve: two-year experience. J THORAC CARDIOVASC SURG 1990;99:846-51.[Abstract]
    
29. Chidambara M, Abdulali SA, Baliga BG, Ionescu MI. Long term results of DeVega tricuspid annuloplasty. Ann Thorac Surg 1987;43:185-8.[Abstract]
    
30. Georgeson S, Panidis IP, Kleaveland JP, Heilbrunn S, Gonzales R. Effect of percutaneous balloon valvuloplasty on pulmonary hypertension in mitral stenosis. Am Heart J 1993;125:1374.[Medline]
    
31. Levine MJ, Weinstein JS, Diver DJ, et al. Progressive improvement in pulmonary vascular resistance after percutaneous mitral valvuloplasty. Circulation 1989;79:1061-7.[Abstract/Free Full Text]
    
32. Dev V, Shrivastava S. Time course of changes in pulmonary vascular resistance and the mechanism of regression pulmonary arterial hypertension after balloon mitral valvuloplasty. Am J Cardiol 1991;67:439-42.[Medline]
    
33. Foltz BD, Hessel EA, Ivey TD. The early course of pulmonary artery hypertension in patients undergoing mitral valve replacement with cardioplegic arrest. J THORAC CARDIOVASC SURG 1984;88:238-47.[Abstract]
    
34. Skudick D, Mohammed RE, Thomas W, Rothlisberger C, Skoularigis J. Does tricuspid regurgitation improve following successful mitral balloon valvotomy? [Abstract] Circulation 1992;86(Suppl):I594.
    
35. Sagie A, Schwammenthal E, Newell JB, et al. Significant tricuspid regurgitation is a marker for adverse outcome in patients undergoing mitral balloon valvotomy [Abstract]. Circulation 1993;88(Suppl):I340.
    
36. Ahn AJ, Segal BL. Isolated tricuspid insufficiency: clinical features, diagnosis and management. Prog Cardiovasc Dis 1967;9:166-93.
    

This article has been cited by other articles:

				S. Agarwal, E. M. Tuzcu, E. R. Rodriguez, C. D. Tan, L. L. Rodriguez, and S. R. Kapadia Interventional Cardiology Perspective of Functional Tricuspid Regurgitation Circ Cardiovasc Interv, December 1, 2009; 2(6): 565 - 573. [Full Text] [PDF]

				A. Shiran and A. Sagie Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. J. Am. Coll. Cardiol., February 3, 2009; 53(5): 401 - 408. [Abstract] [Full Text] [PDF]

				H. Song, D.-H. Kang, J. H. Kim, K.-M. Park, J.-M. Song, K.-J. Choi, M.-K. Hong, C. H. Chung, J.-K. Song, J.-W. Lee, et al. Percutaneous Mitral Valvuloplasty Versus Surgical Treatment in Mitral Stenosis With Severe Tricuspid Regurgitation Circulation, September 11, 2007; 116(11_suppl): I-246 - I-250. [Abstract] [Full Text] [PDF]

				A. Boyaci, V. Gokce, S. Topaloglu, S. Korkmaz, and S. Goksel Outcome of Significant Functional Tricuspid Regurgitation Late After Mitral Valve Replacement for Predominant Rheumatic Mitral Stenosis Angiology, June 1, 2007; 58(3): 336 - 342. [Abstract] [PDF]

				A. Matsunaga and C. M. G. Duran Progression of Tricuspid Regurgitation After Repaired Functional Ischemic Mitral Regurgitation Circulation, August 30, 2005; 112(9_suppl): I-453 - I-457. [Abstract] [Full Text] [PDF]

				K. Matsuyama, M. Matsumoto, T. Sugita, J. Nishizawa, Y. Tokuda, and T. Matsuo Predictors of residual tricuspid regurgitation after mitral valve surgery Ann. Thorac. Surg., June 1, 2003; 75(6): 1826 - 1828. [Abstract] [Full Text] [PDF]

				T. Treasure, M. Chandra, O. F. Sogade, I. A. Alhaddad, A. R. Conrad, B. Dalvi, T. O. Cheng, Z. G. Turi, B. S. Raju, B. A. Carabello, et al. Treatment of Mitral Stenosis N. Engl. J. Med., March 16, 1995; 332(11): 748 - 750. [Full Text]

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sagie, A. Articles by Levine, R. A. Search for Related Content PubMed PubMed Citation Articles by Sagie, A. Articles by Levine, R. A.