Rheumatic tricuspid valve disease: two-dimensional echocardiographic, hemodynamic, and angiographic correlations

From March 1977 through April 1982, 2-dimensional echocardiography detected 372 patients with rheumatic mitral valve disease. Of these patients, 23 (6%) had tricuspid valve involvement. Two-dimensional echocardiographic criteria of rheumatic tricuspid valve disease included thickened leaflets with restriction in motion, diastolic doming, and encroachment of the leaflet tips on the ventricular inlet. These criteria provided a sensitivity of 100%, a specificity of 90%, a predictive accuracy of 21%, and a negative predictive value of 100% in diagnosing hemodynamically significant tricuspid stenosis. Hemodynamic variables in patients with rheumatic tricuspid valve disease (Group I) were compared with those in patients with no rheumatic tricuspid disease (Group II). The only significant difference was mean right atrial pressure (15 +/- 7 mm Hg versus 11 +/- 5 mm Hg, p less than 0.02). Both groups were classified into patients with (A) and without (B) significant tricuspid regurgitation (TR). There was no significant difference in any hemodynamic variable when Group IA was compared with Group IIA. In addition, there was no difference in any hemodynamic variable when patients with functional TR (Group IIA) were compared with those with rheumatic mitral valvular disease without TR (Group IIB). Two-dimensional echocardiography and cardiac catheterization provide complementary diagnostic information in these patients.     

Functional tricuspid regurgitation following replacement of the mitral valve.

In this series, the effect of replacement of the mitral valve was examined in 86/900 (9.6%) patients who had developed moderate functional tricuspid regurgitation, secondary to rheumatic mitral valvar disease. These patients were subdivided according to the severity of pulmonary hypertension and impairment of right ventricular function. Forty-six patients presented with severe pulmonary hypertension and 40 patients had moderate pulmonary hypertension (mean main pulmonary arterial pressure: 78 +/- 14 mmHg vs 41 +/- 6 mmHg; P less than 0.05). The latter had more advanced disease, greater impairment of right ventricular function and dilatation of the right heart chambers. Functional tricuspid regurgitation regressed in 38/42 survivors with severe pulmonary hypertension and persisted or progressed significantly in 22/34 survivors with impaired right ventricular function despite successful replacement of the mitral valve. The latter underwent replacement of the tricuspid valve (n = 16) or tricuspid annuloplasty (n = 6), at a mean interval of 44 +/- 4.4 months after replacement of the mitral valve, which resulted in 8/22 (23.5%) early deaths. Functional tricuspid regurgitation is more likely to persist in patients with advanced right ventricular failure. Tricuspid valvar competence should be restored in these patients at initial replacement of the mitral valve.     

Function of the right ventricle in patients with mitral valve diseases

To investigate right ventricular function in mitral valve disease, biplane cineventriculograms of the right and left ventricle were performed in 96 patients-35 with mitral stenosis, 26 with mitral regurgitation, 12 with combined mitral valve disease, 14 with mitral stenosis and tricuspid regurgitation, and nine with mitral regurgitation and tricuspid regurgitation, compared to 18 normals (N). Right ventricular enddiastolic volume index was moderately elevated in patients with mitral stenosis and concomitant tricuspid regurgitation (111.6 +/- 35.3 ml/m2, no significance compared to N: 95.9 +/- 21.8 ml/m2) and with mitral regurgitation and tricuspid regurgitation (107.9 +/- 45.1 ml/m2, no significance compared to N). A reduced right ventricular ejection fraction (RVEF less than or equal to 50%) was found in 40 of the 96 patients. Right ventricular ejection fraction was frequently reduced in patients with mitral regurgitation and tricuspid regurgitation (46.7% +/- 15.1%) and significantly reduced in patients with combined mitral valve disease (45.0 +/- 17.6%, compared to N: 58.0 +/- 7.1%, p less than 0.01). No significant correlations were found between right ventricular ejection fraction and left ventricular enddiastolic volume or left ventricular ejection fraction in patients with mitral valve disease. Moreover, right ventricular ejection fraction did not correlate with systolic pulmonary artery pressure, mean pulmonary artery pressure or mean pulmonary capillary wedge pressure. Local wall motion (mean systolic shortening) was determined for the anterior, anteroapical, and inferior segment in the RAO-projection and for the right ventricular free wall in the LAO-projection. 63% of the patients (n = 25) with reduced right ventricular function (RVEF less than of equal to 50%) showed local wall motion abnormalities, preferably in the anterior segment of the RAO- projection (48%) and the right ventricular free wall (30%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Evidence for rheumatic valve disease in patients with severe tricuspid regurgitation long after mitral valve surgery: the role of 3D echo reconstruction

BACKGROUND AND AIM OF THE STUDY: Although severe tricuspid regurgitation (TR) is a well-recognized, long-term complication of rheumatic mitral valve replacement that impairs the functional results of surgery, its exact basis remains unclear and its management is unsatisfactory. The study aim was to obtain a detailed assessment of tricuspid valve morphology and function using 2D transesophageal echocardiography (TEE) with 3D reconstruction, and to determine long-term clinical outcome in patients after surgery for rheumatic mitral valve disease. METHODS: A total of 42 patients (mean age 50 +/- 10 years) was followed up; 39 patients had mitral replacement and three had valvotomy. Thirty patients had developed impaired exercise tolerance, fluid retention and echocardiographic evidence of severe TR at 8.2 +/- 2.6 years after surgery; the remainder had mild regurgitation. RESULTS: Follow up showed greater mortality in the severe TR group, with approximately 50% survival at 60 months after diagnosis compared with mild TR. None of the patients with severe TR had a dysfunctional mitral prosthesis. In these patients, transthoracic echo-Doppler showed enlarged right atrium and right ventricle, a mean transtricuspid retrograde pressure drop of 15 +/- 4 mmHg and apparently normal leaflet anatomy. Twenty patients (15 with severe TR) underwent a TEE and 3D reconstruction study for further evaluation. Abnormal leaflet anatomy was demonstrated in all patients with severe TR, with restricted leaflet motion in 10, leaflet shortening and thickening in the remainder, and dilatation of tricuspid valve annular insertion suggestive of rheumatic involvement. Although diastolic transtricuspid velocities were increased (peak flow 0.8 +/- 0.1 m/s) in these patients due to increased stroke volume, significant tricuspid stenosis was present in only two cases (mean gradient 4 and 3 mmHg respectively). Histopathology confirmed the presence of leaflet vascularization and extensive fibrosis in two patients who underwent tricuspid valve replacement. CONCLUSION: Rheumatic leaflet involvement contributes to severe TR occurring long after mitral valve replacement, though overt stenosis is uncommon. Knowledge of the structural basis of this condition may thus improve its long-term management, possibly with early tricuspid valve repair.     

Incidence and concomitant factors of tricuspid valve insufficiency in patients with aortic and mitral valve diseases

Invasive data about the frequency and associated factors of tricuspid regurgitation in normals and in patients with aortic and mitral valve disease are still rare. Thus, right ventricular biplane angiograms (RAO/LAO projection), the mean pulmonary artery pressure and the presence of atrial fibrillation were analyzed with regard to tricuspid regurgitation in 30 normals and 165 patients with pure mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis, combined mitral valve disease or combined aortic valve disease. Patients with tricuspid stenosis or coronary artery disease were excluded. In 52 of the 195 patients tricuspid regurgitation was present. Tricuspid regurgitation occurred statistically more often in patients with mitral stenosis (33%), mitral regurgitation (48%) or combined mitral valve disease (68%) than in patients with aortic regurgitation (4%) or combined aortic valve disease (3%). In patients with aortic stenosis and in normals tricuspid regurgitation was not present. In patients with combined mitral valve disease, tricuspid regurgitation was more often present than in patients with pure mitral stenosis (p less than 0.002), despite comparable values of the mean pulmonary artery pressure, the right ventricular enddiastolic and endsystolic volume indexes, the right ventricular ejection fraction and the frequency of atrial fibrillation. Only in patients with pure mitral regurgitation tricuspid regurgitation was associated with an elevated mean pulmonary artery pressure (p less than 0.02). Differences in the right ventricular size and function did not occur between normals and patients with mitral or aortic valve disease. Therefore, the mean pulmonary artery pressure, atrial fibrillation and the size and function of the right ventricle are not major determinants for the occurrence of tricuspid regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Triple valve replacement. Evaluation of 90 surgically treated patients

Ninety patients, aged 17 to 59 years (average 39.8 yrs) underwent triple valve replacement from January 1967 to December 1979. The aetiology was rheumatic carditis in 84% of cases. There had been previous surgery in 29 cases (19 mitral commissurotomies). All patients were severely symptomatic: 68 (76%) had atrial fibrillation and the cardiothoracic ratio was 0.70 +/- 0.085. In 24 cases, triple valve stenosis (aortic, mitral and tricuspid) was observed; 13 patients had triple regurgitation and 53 patients had mixed lesions (stenosis and regurgitation). Triple mechanical valve prostheses were implanted in 35 cases (Bj?rk or Starr), triple bioprostheses were implanted in 12 cases, and 43 patients received a combination of mechanical and bioprostheses (tricuspid bioprostheses in all 43 cases). The patients were divided into two groups according to the type of valve replacement; Group I: 57 patients, subdivided into Group IA (35 cases, 39%) with triple mechanical prosthesis, and Group IB (22 cases, 25%) with mechanical aortic and mitral valve prostheses and tricuspid bioprostheses; Group II, 33 patients, subdivided into Group IIA (12 patients, 13%) with triple bioprostheses, and Group IIB (21 patients, 23%) with mitral and tricuspid bioprostheses and a mechanical aortic valve prosthesis. Techniques of myocardial protection have have improved since the beginning of this series and at present comprise cardioplegia associated with general hypothermia to 25 degrees C and pericardial irrigation with ice cold saline. The overall operative mortality was 37% (34/90) but in 1979 alone it was only 10%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical significance of incomplete tricuspid valve closure seen on two-dimensional echocardiography

Incomplete closure of the tricuspid valve without apparent cusp disease was noted on two-dimensional echocardiography in 31 patients. This abnormality was defined as a failure of the tricuspid valve leaflet tips to reach the plane of the tricuspid valve anulus by at least 1 cm in the standard apical four chamber view at the point of maximal systolic closure. This resulted in a final systolic leaflet position deeper within the right ventricular cavity than is normally seen. The finding was present in the following diagnostic subgroups: Group A, pulmonary hypertension (11 patients); Group B, rheumatic heart disease (4 patients); Group C, dilated cardiomyopathy (9 patients) and Group D, previous myocardial infarction (7 patients). Right atrial, right ventricular and tricuspid anulus measurements were made and compared with those from a group of 67 normal subjects. The results were as follows: right atrial endsystolic area = 27.2 +/- 8.6 cm2 (normal = 13.4 +/- 2.0); right ventricular end-systolic area = 25.6 +/- 8.7 cm2 (normal = 10.9 +/- 2.9); right ventricular end-diastolic area = 31.5 +/- 9.1 cm2 (normal = 20.1 +/- 4.9) and tricuspid valve anular end-systolic dimension = 4.0 +/- 0.6 cm (normal = 2.2 +/- 0.3). The differences from the normal data were all statistically significant (p less than 0.001). Incomplete closure of the tricuspid valve, although a nonspecific diagnostic finding, is primarily associated with right-sided chamber enlargement. Tricuspid regurgitation may be present. The mechanism could be related to geometric changes in valve apparatus dynamics secondary to right-sided cardiac enlargement and tricuspid valve anular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Isolated tricuspid valve regurgitation resulting from severe annular dilatation: case report.

A rare case of isolated tricuspid regurgitation (TR) in a 65-year-old man is presented. Echocardiography revealed enlargement of the right atrium, dilatation of the tricuspid valve annulus without thickening or prolapse of the leaflets, and an intact atrial septum. No downward displacement of the tricuspid septal leaflet was observed by echocardiography. Mild mitral regurgitation and severe TR were detected on color flow Doppler studies. Cardiac catheterization indicated elevated right atrial pressure, with a pronounced V-wave. No left-to-right shunt was detected at the right atrium. At surgery, severe annular dilatation of the tricuspid valve (without organically diseased or deformed tricuspid leaflets) was observed, and tricuspid annuloplasty with a prosthetic ring performed. Postoperative echocardiography and right ventriculography showed trivial TR.     

Tricuspid valve disease

The normal tricuspid valve anatomy and function have several dissimilarities to the corresponding mitral valve in the left heart, in part, based on lower pressures in the right heart chambers. The functional abnormalities resulting from tricuspid valve disease are classified as primary and secondary. Primary valve disease is any associated intrinsic valve pathology. The list of responsible conditions includes congenital, rheumatic, infective endocarditis, carcinoid heart disease, toxic effects of chemicals, tumors, blunt trauma, and myxomatous degeneration. The secondary tricuspid valve disease does not involve intrinsic anatomic abnormalities of the valve apparatus, aside from tricuspid annular dilation secondary to right ventricular dilation and dysfunction. The most common cause of tricuspid valve disease is secondary to left heart disease, either myocardial, valvular, or mixed. Although bedside diagnosis of advanced tricuspid valve disease is feasible, echocardiography provides valuable clues to the presence and severity of tricuspid valve stenosis and/or regurgitation with considerable accuracy. The tricuspid regurgitation signal using Doppler techniques is utilized for estimation of right ventricular systolic pressure, which, in the absence of right ventricular outflow obstruction, corresponds to pulmonary arterial systolic pressure. This is clinically useful since nearly 80 to 90% of patients exhibit some degree of tricuspid regurgitation. The treatment of tricuspid valve disease is guided by underlying etiology and pathology. Tricuspid valve repair is increasingly advocated for patients with advanced tricuspid regurgitation, especially when combined with surgery on the left heart pathology. Primary tricuspid valve disease is often treated by surgical approach specific to the underlying pathology.     

Clinical and anatomic observations in patients having mitral valve replacement for mitral stenosis and simultaneous tricuspid valve replacement

Certain clinical and morphologic findings are described in 67 patients (aged 23 to 76 years [mean 52]; 55 women [82%]) who had mitral valve replacement for mitral stenosis (with or without associated regurgitation), and simultaneous tricuspid valve replacement for pure tricuspid regurgitation (58 patients) or tricuspid stenosis (all with associated regurgitation; 9 patients). Of the 58 patients with pure tricuspid regurgitation, 21 had anatomically normal and 37 had anatomically abnormal (diffusely fibrotic leaflets) tricuspid valves. Among these 58 patients, no clinical or hemodynamic variable was useful before surgery in distinguishing the group without from that with anatomically abnormal tricuspid valves. All 9 patients with stenotic tricuspid valves had anatomically abnormal tricuspid valves. The latter group had a lower average right ventricular systolic pressure (tricuspid valve closing pressure) than those with pure tricuspid regurgitation, and none had severe pulmonary arterial hypertension (present in 20 [30%] of the 58 patients with pure tricuspid regurgitation).     

Effect of volume load of the left ventricle in aortic and mitral insufficiency on the geometry and function of the right ventricle

To investigate the effect of chronic left ventricular enlargement on right ventricular geometry and function, biplane cineventriculograms were analyzed in 23 patients with aortic regurgitation (AR) and in 17 patients with mitral regurgitation (MR). Left ventricular end-diastolic volume indices (LVEDVI) were elevated and significantly (p less than 0.05) different in patients with aortic regurgitation (AR) (190.2 +/- 65.2 ml/m2) and mitral regurgitation (MR) (148.7 +/- 40.1 ml/m2). Right ventricular end-diastolic volume indices (RVEDVI), however, were comparable and within the normal range (AR: 96.6 +/- 18.3 ml/m2, MR: 100.2 +/- 33.7 ml/m2). Mean pulmonary artery pressure was significantly (p less than 0.05) higher in patients with mitral regurgitation with 24.7 +/- 12.8 mm Hg (AR: 17.5 +/- 6.6 mm Hg). Six patients with mitral insufficiency had concomitant tricuspid valve insufficiency. In five out of six patients with tricuspid insufficiency, right ventricular afterload was significantly elevated. Only in patients with mitral regurgitation was a significant correlation (r) between left and right ventricular end-diastolic volume index found (RVEDVI = 0.7 X LVEDVI +1, r = 0.80). Moreover, in patients with MR, left ventricular end-diastolic volume index correlated with right ventricular end-systolic volume index (RVESVI = 0.4 X LVEDVI -8, r = 0.73). Right ventricular ejection fraction was significantly different (p less than 0.05) between patients with aortic and mitral insufficiency (AR: 53.7 +/- 8.9%, MR: 46.7 +/- 10.7%). Particularly in patients with normal left ventricular ejection fraction (greater than 50%) and mitral regurgitation, the incidence of a reduced right ventricular ejection fraction (less than 50%) was significantly higher (p less than 0.01) compared to patients with aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Can mitral regurgitation after balloon dilatation of the mitral valve be predicted?

OBJECTIVE--To determine which factors predict the occurrence of mitral regurgitation after balloon dilatation of the mitral valve for rheumatic stenosis. DESIGN--Analysis of a case series of patients with rheumatic mitral valve stenosis who had had successful balloon dilatation of the mitral valve. SETTING--A tertiary care centre with an experience of over 150 balloon dilatations of the mitral valve. PATIENTS--70 young patients with non-calcified rheumatic mitral stenosis, who had undergone successful balloon dilatation of the mitral valve. No patient had mitral regurgitation or atrial fibrillation before dilatation. INTERVENTION--Dilatation of the mitral valve by the transvenous, transatrial double balloon technique. MAIN OUTCOME MEASURE--Development of mitral regurgitation after balloon dilatation of the mitral valve and its relation to age, mitral valve area before dilatation and after dilatation, the degree of mitral subvalvar pathology, and the size of balloon used for dilatation. RESULTS--In 10 patients (14%) mitral regurgitation developed after balloon dilatation of the mitral valve. No statistically significant differences were found between patients who did not develop regurgitation and those who did in terms of age (mean (SD)) (19.9 (6.46) v 19.4 (5.5)), mitral valve area before dilatation (1.05 (0.33) v 0.94 (0.4) cm2) and after dilatation (2.52 (1.06) v 2.45 (1.1) cm2), mitral subvalvar pathology assessed by the mitral subvalvar distance ratio (0.116 (0.03) v 0.118 (2.32), or balloon diameter corrected for body surface area (21.37 (3.5) v 20.57 (2.32) mm/m2. CONCLUSIONS--In this subset of children and young adults with non-calcified mitral stenosis, none of the morphological, technical, or patient characteristics studied predicted the development of mitral regurgitation after balloon dilatation. The low incidence of mitral regurgitation may have reduced the discriminatory power of this study. None the less, the means and standard deviation for each factor in each group suggest that even in a larger sample size the variables would have little predictive capacity.     

Can mitral regurgitation after balloon dilatation of the mitral valve be predicted?

OBJECTIVE--To determine which factors predict the occurrence of mitral regurgitation after balloon dilatation of the mitral valve for rheumatic stenosis. DESIGN--Analysis of a case series of patients with rheumatic mitral valve stenosis who had had successful balloon dilatation of the mitral valve. SETTING--A tertiary care centre with an experience of over 150 balloon dilatations of the mitral valve. PATIENTS--70 young patients with non-calcified rheumatic mitral stenosis, who had undergone successful balloon dilatation of the mitral valve. No patient had mitral regurgitation or atrial fibrillation before dilatation. INTERVENTION--Dilatation of the mitral valve by the transvenous, transatrial double balloon technique. MAIN OUTCOME MEASURE--Development of mitral regurgitation after balloon dilatation of the mitral valve and its relation to age, mitral valve area before dilatation and after dilatation, the degree of mitral subvalvar pathology, and the size of balloon used for dilatation. RESULTS--In 10 patients (14%) mitral regurgitation developed after balloon dilatation of the mitral valve. No statistically significant differences were found between patients who did not develop regurgitation and those who did in terms of age (mean (SD)) (19.9 (6.46) v 19.4 (5.5)), mitral valve area before dilatation (1.05 (0.33) v 0.94 (0.4) cm2) and after dilatation (2.52 (1.06) v 2.45 (1.1) cm2), mitral subvalvar pathology assessed by the mitral subvalvar distance ratio (0.116 (0.03) v 0.118 (2.32), or balloon diameter corrected for body surface area (21.37 (3.5) v 20.57 (2.32) mm/m2. CONCLUSIONS--In this subset of children and young adults with non-calcified mitral stenosis, none of the morphological, technical, or patient characteristics studied predicted the development of mitral regurgitation after balloon dilatation. The low incidence of mitral regurgitation may have reduced the discriminatory power of this study. None the less, the means and standard deviation for each factor in each group suggest that even in a larger sample size the variables would have little predictive capacity.     

Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease.

OBJECTIVE--To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN--9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING--University Hospital of Wales, Cardiff. SUBJECTS--18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE--Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS--Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS--Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.     

Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease.

OBJECTIVE--To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN--9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING--University Hospital of Wales, Cardiff. SUBJECTS--18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE--Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS--Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS--Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.     

The importance of tricuspid valve structure and function in the surgical treatment of rheumatic mitral and aortic disease.

A significant proportion of individuals with rheumatic disease have tricuspid valve involvement which may be clinically important and alter the medical or surgical approach to treatment. Therefore 50 patients with rheumatic left-sided valvular lesions who were referred for operative treatment were studied. Thirty patients had angiographically significant tricuspid regurgitation (group I) and 20 had a competent tricuspid valve (group II). Pre-operative cardiac assessment included Doppler echocardiography and contrast ventriculography. Patients with tricuspid regurgitation more commonly had mitral valve disease or combined mitral and aortic valve lesions, (P less than 0.001) and were more likely to have atrial fibrillation than those without tricuspid regurgitation (P less than 0.001). Pulmonary arterial systolic and mean right atrial pressures were higher in group I (both P less than 0.01). A close relationship was found between the angiographic and Doppler assessment of the degree of tricuspid regurgitation (P less than 0.01). Doppler-derived measurement of the right ventricular-right atrial systolic pressure difference correlated well with the systolic trans-tricuspid pressure difference measured at cardiac catheterization (y = 0.7x + 22, r = 0.67, P less than 0.001) and the pulmonary arterial systolic pressure (y = 0.8x + 27, r = 0.71, P less than 0.001). Rheumatic involvement of the tricuspid valve identified by pre-operative echocardiography was confirmed in five patients at surgery. Of the 13 patients with functional tricuspid regurgitation at operation, only two had been diagnosed as having organic disease by echocardiography. Furthermore, in all 18 cases where Doppler suggested grade 3 or 4+ tricuspid regurgitation, surgical repair or replacement of the valve was performed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evolution of repaired and non-repaired tricuspid regurgitation in rheumatic mitral valve surgery without severe pulmonary hypertension

The aim of this study was to evaluate the usefulness of repairing significant tricuspid regurgitation (> or = grade 2) without severe pulmonary hypertension (< or = 50 mm Hg). Between 1993 and June 2001, 88 consecutive patients were operated on for rheumatic mitral valve disease associated with significant tricuspid regurgitation and without severe pulmonary hypertension. The severity of the tricuspid valve disease was assessed by echocardiography. Sixty-three patients had severe (> or = grade 3) tricuspid regurgitation (Group I), and 25 patients had moderate (grade 2) tricuspid regurgitation (Group II). There was no hospital mortality. six patients died during follow-up. The overall actuarial survival rate for 8 years was 92.1% +/- 3.1%. Cox proportional hazard regression analysis showed that age ( p = 0.006) and pulmonary complication ( p = 0.01) were associated with increased late mortality. Freedom from death was similar in both groups at 8 years (93.1% +/- 3.3% versus 88% +/- 8%, p = 0.7). Severe postoperative tricuspid regurgitation (> or = grade 3), caused by the failure of tricuspid repair or leaving the valve untouched, impaired long-term survival after surgery, and actuarial survival was 96.1% +/- 2.7% and 83% +/- 7.8% at 7 years ( p = 0.048), respectively. Severe tricuspid regurgitation, functional or organic, should be corrected at the time of mitral valve surgery, whereas untouched functional moderate tricuspid regurgitation improves after mitral valve surgery.     

Immediate postoperative results following conservative surgery of rheumatic mitral valve insufficiency in children

The immediate post-operative results of conservative surgery were evaluated objectively in 31 children aged under 13 years referred to us for surgical correction of severe rheumatic mitral valve regurgitation. 16 patients had pure mitral regurgitation. In the others, lesions which required additional surgery were aortic regurgitation in 7 cases, tricuspid of the mitral valve and left ventricle was studied by two-dimensional TM-mode echocardiography. This examination was combined with a pulsed doppler study in search of a possible residual mitral regurgitation signal, with special attention to the depth at which it was recorded in the left atrium -- a semi-quantitative indication of the severity of residual leakage. Two mitral valve replacements were performed, and two early reoperations were needed for residual regurgitation developed between the 5th and 8th post-operative days. Three deaths occurred due to supra-systemic pulmonary arterial hypertension. The post-operative evaluation of mitral valvuloplasty results therefore involved 25 patients. In the absence of significant residual mitral regurgitation, two-dimensional echocardiography was inconclusive since the images obtained varied considerably according to the surgical procedures performed. There was a distinct reduction of end-diastolic diameters (43.5 +/- 5.9 versus 62.1 +/- 8.7 mm pre-operatively), reflecting the disappearance or marked decrease of the pre-operative ventricular volume overload consecutive to mitral regurgitation. The reduction of end-systolic diameters was also significant (31.2 +/- 6.7 mm versus 39.2 +/- 7.1 mm pre-operatively), though less pronounced than that of end-diastolic diameters, which explains the diminution observed in the percentage of fibre shortening, although the figures remained within normal limits (28.7 +/- 9.7 p. 100 versus 37.0 +/- 6.8 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)     

Tricuspid and pulmonary valve disease evaluation and management

The clinical detection and quantification of tricuspid valve disease, although important, is not entirely accurate. Diagnostic evaluation is based on echocardiography, and color flow Doppler is useful for quantifying tricuspid regurgitation. Echocardiography provides information on heart chamber dimensions, right ventricular function, and the degree of pulmonary hypertension. In addition, tricuspid stenosis can be accurately assessed using mean and end-diastolic pressure gradient measurements. The treatment options for tricuspid stenosis include balloon valvuloplasty and surgical valve repair. Functional tricuspid regurgitation associated with left heart disease may require surgical attention during an operation to treat the left heart disease. Severe tricuspid regurgitation usually requires surgery to be performed in association with mitral valve surgery. Mild-to-moderate tricuspid regurgitation requires surgery when annular dilatation or severe pulmonary hypertension is present. The surgical options include tricuspid valve repair, with or without an annuloplasty ring. In patients with a primary anatomic deformity of the tricuspid valve, replacement of the valve with a bioprosthesis or mechanical valve may be considered. Intermediate and long-term results favor annuloplasty valve repair over valve replacement. Pulmonary valve disease is predominantly congenital, and generally takes the form of pulmonary stenosis. Pulmonary regurgitation often results from surgical or balloon valvuloplasty and is associated with deleterious long-term sequelae. The recent development of percutaneous valve replacement was a major advance.     

Three-dimensional assessment of left ventricular geometry and annular dilatation provides new mechanistic insights into the surgical correction of ischemic mitral regurgitation

BACKGROUND: The aim of this study was to investigate the relationship between LV geometry, annular shape and the amount of regurgitation in patients with ischemic mitral regurgitation (group 1, n = 30) compared to patients with primary mitral valve lesions (group 2, n = 30). METHODS: LV geometry was assessed by the sphericity index, i.e., LV volume divided by the volume of a sphere with a diameter equal to the longest axis. Annular geometry was evaluated by diameters, areas and their percentual shortening. The degree of mitral regurgitation was assessed as jet volumes by 3D-echocardiography. RESULTS: Group 1 showed significantly larger longitudinal (54.3 +/- 3.1 vs. 40.9 +/- 2.6 mm) and antero-posterior (32.2 +/- 3.3 vs. 27.1 +/- 2.9 mm) annulus diameters and areas (993.3 +/- 66.6 vs. 702.1 +/- 47.9 mm (2)) than group 2. No asymmetric annular enlargement was found in either group. Annular enlargement correlated to the degree of mitral regurgitation in group 1 but not in group 2. Annular area shortening was significantly impaired in group 2 and the sphericity index was larger in group 1 than in group 2. In group 1, the sphericity index was significantly correlated to the degree of mitral regurgitation (r = 0.87; P < 0.001). CONCLUSIONS: These findings suggest that ischemic mitral regurgitation was mostly associated with a global left ventricular enlargement, in which annulus dilatation and its reduced contraction play a significant role.