Presence of a congenitally bicuspid aortic valve among patients having combined mitral and aortic valve replacement

Although bicuspid aortic valve occurs in an estimated 1% of adults and mitral valve prolapse in an estimated 5% of adults, occurrence of the 2 in the same patient is infrequent. During examination of operatively excised aortic and mitral valves because of dysfunction (stenosis and/or regurgitation), we encountered 16 patients who had congenitally bicuspid aortic valves associated with various types of dysfunctioning mitral valves. Eleven of the 16 patients had aortic stenosis (AS): 5 of them also had mitral stenosis, of rheumatic origin in 4 and secondary to mitral annular calcium in 1; the other 6 with aortic stenosis had pure mitral regurgitation (MR) secondary to mitral valve prolapse in 3, to ischemia in 2, and to unclear origin in 1. Of the 5 patients with pure aortic regurgitation, each also had pure mitral regurgitation: in 1 secondary to mitral valve prolapse and in 4 secondary to infective endocarditis. In conclusion, various types of mitral dysfunction severe enough to warrant mitral valve replacement occur in patients with bicuspid aortic valves. A proper search for mitral valve dysfunction in patients with bicuspid aortic valves appears warranted.     

Morphologic features of the normal and abnormal mitral valve

Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.     

Clinical and necropsy observations early after simultaneous replacement of the mitral and aortic valves

Clinical and necropsy findings are described in 54 patients, aged 25 to 83 years (mean 53), who died within 60 days of simultaneous replacements of both mitral and aortic valves. The patients were separated into 4 groups on the basis of the presence of stenosis (with or without associated regurgitation) or pure regurgitation of each valve: 30 patients (56%) had combined mitral and aortic valve stenosis; 12 patients (22%) had mitral stenosis and pure aortic regurgitation; 8 patients (15%) had pure regurgitation of both valves; and 4 patients (7%) had pure aortic regurgitation and mitral stenosis. Necropsy examination in the 54 patients disclosed a high frequency (48%) of anatomic evidence of interference to poppet or disc movement in either the mitral or aortic valve position or both. Anatomic evidence of interference to movement of a poppet or disc in the aortic valve position was twice as common as anatomic evidence of interference to poppet or disc movement in the mitral position. Interference to poppet movement is attributable to the prosthesis's being too large for the ascending aorta or left ventricular cavity in which it resided. The ascending aorta is infrequently enlarged in patients with combined mitral and aortic valve dysfunction irrespective of whether the aortic valve is stenotic or purely regurgitant. Likewise, the left ventricular cavity is usually not dilated in patients with combined mitral and aortic valve stenosis, the most common indication for replacement of both left-sided cardiac valves. Of the 54 patients, 12 (22%) had 1 mechanical and 1 bioprosthesis inserted. It is recommended that both substitute valves should be mechanical prostheses or both should be bioprostheses.     

Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation

Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.     

Clinical and morphologic observations after simultaneous replacement of the tricuspid, mitral and aortic valves

Clinical and morphologic observations are described in 12 patients who underwent simultaneous replacement of the tricuspid, mitral and aortic valves. All 12 patients had mitral stenosis, 10 aortic valve stenosis and 2 pure aortic valve regurgitation; 5 had tricuspid valve stenosis and 7 pure tricuspid valve regurgitation. Of the 10 patients who died within 60 days of triple valve replacement, 7 had the low cardiac output syndrome, which in 4, and possibly 5, of the 7 was attributed to prosthetic aortic valve stenosis. In none of the 12 patients was the ascending aorta dilated, and in the 4 (possibly 5) patients with low cardiac output, the space between the surface of the caged poppet (4 patients) or margins of the tilting disc (1 patient) in the aortic valve position and the aortic endothelium appeared inadequate to allow unobstructed flow despite small-sized prostheses in all but 1 patient. Thus, aortic valve replacement in the setting of triple valve dysfunction is hazardous or potentially so. The relative small sizes of the hearts in these patients also make valve replacement more difficult (and hazardous) compared to hearts with larger ventricles and aortas.     

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)     

Techniques of modified mitral valve replacement with preservation of the posterior leaflet and chordae tendineae

Modified mitral valve replacement (MVR) was performed mostly with mechanical valves in 117 patients consisting of 53 patients with mitral regurgitation (MR) and 64 patients with mitral stenosis (MS) or combined mitral valve disease (MSR). Concomitantly, aortic valve replacement (AVR) was carried out in 42 patients, tricuspid annuloplasty (TAP) in 26, tricuspid valve replacement (TVR) in 2 and other procedures in 4. There were 3 hospital deaths and 3 late deaths. In this series, 4 types of technique were utilized in order to preserve the posterior leaflet and chordae tendineae. The authors recommend the following techniques. In pure or predominant MS, after removal of the anterior leaflet and chordae, buttress sutures are placed from the valvular annulus to the posterior leaflet near its free margin. In pure or predominant MR, excising part of the posterior leaflet is added prior to the above-described technique. By using these two techniques, modified MVR can be performed for any type of valve lesion and with any kind of prosthetic valve.     

Determinants of long-term prognosis following prosthetic mitral valve replacement

Data of 235 patients with chronic mitral valve disease (NYHA class III or IV) were analyzed retrospectively. Mitral valve replacement was performed in all patients between 1974 and 1983, 46 patients underwent additional tricuspid valve repair during the same operation. Preoperatively, right and left heart catheterization as well as coronary angiography were carried out in all patients. Operative mortality was 8%. For all patients 5 year survival rate was 76% and 10 year survival rate was 72%. Patients with pure mitral insufficiency had a poorer long-term prognosis than patients with mitral stenosis or patients with mixed mitral valve disease (5 year survival rate 54 versus 79%, p less than 0.0014). Patients with previous closed mitral commissurotomy had a poorer long-term prognosis than patients without previous surgery (5 year survival rate 62 versus 81%, p less than 0.0019). Age, NYHA class, associated tricuspid valve repair, pulmonary vascular resistance and mean right atrial pressure had no effect on survival. Conclusion: Long-term survival is generally good after mitral valve replacement, but pure mitral insufficiency and previous closed mitral commissurotomy are risk factors for long-term prognosis.     

Outcome of significant functional tricuspid regurgitation late after mitral valve replacement for predominant rheumatic mitral stenosis

Significant tricuspid regurgitation (TR) can contribute to increased morbidity and mortality in patients undergoing mitral valve surgery for mitral stenosis. The aim of this study was to evaluate the association between the severity of preoperative functional TR and late adverse outcomes in patients undergoing mitral valve replacement (MVR). The study group comprised 68 patients (54 women, 14 men; mean age 45 +/-10 years) with rheumatic mitral stenosis (MS) who had undergone MVR without tricuspid valve surgery between 4 and 13 years (mean 8.1 +/-2.6 years) before their last clinical examination. All patients underwent a complete preoperative and late postoperative color-Doppler echocardiographic examination. The severity of TR was assessed echocardiographically by using color-Doppler flow images and flow direction in the inferior vena cava or hepatic veins. Patients were classified into 2 groups; 42 with mild (62%) and 26 with significant (38%) TR. Patients with significant TR showed longer preoperative symptomatic period and more atrial fibrillation than those with mild TR. All patients had medical treatment. Functional capacity and NYHA class of the patients in both groups improved significantly after MVR. Freedom from symptomatic heart failure (functional class III or IV) was higher (86% vs 54%) and the need for hospitalization was significantly lower for the mild TR group. Significant preoperative functional TR diagnosed by echocardiography was associated with an adverse outcome. Therefore, further studies are needed to evaluate the effect of concomitant tricuspid valve repair on the late outcome of patients undergoing mitral valve surgery in order to prevent significant late morbidity.     

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.     

Tricuspid regurgitation late after mitral valve replacement: clinical and echocardiographic evaluation

BACKGROUND AND AIM OF THE STUDY: Significant tricuspid regurgitation (TR) can contribute to increased morbidity and mortality in patients after mitral valve replacement (MVR), both in the immediate and late postoperative period. The aim of this study was to evaluate the prevalence and the clinical importance of TR late after MVR, as assessed both clinically and echocardiographically. METHODS: The study group comprised 65 patients (39 women, 26 men; mean age 61+/-12 years) with rheumatic heart disease who had undergone MVR without tricuspid valve surgery between one and 30 years (mean 11.3+/-8 years) before their last clinical examination. All patients underwent a complete color-Doppler echocardiographic examination. The predominant presurgical mitral lesion was stenosis in 44 patients and regurgitation in 21. The severity of the tricuspid valve disease was assessed echocardiographically using color-Doppler flow images and flow direction in the inferior vena cava or hepatic veins, and by clinical evaluation. RESULTS: Echocardiography revealed significant late TR in 44 patients (67%), which was moderate in 16 and severe in 28, and evident on physical examination in 24 cases (37%). Age (relative risk (RR) = 1.1; C.I. 1-1.1) and female sex (RR = 1.8; C.I. = 1.0-3.2) were identified as statistically significant predictors for late clinical TR development, but only age was found as a statistically significant predictor for echocardiographic TR development. An elevated RR for organic TR and predominant mitral regurgitation was found. In contrast, pre- and postoperative pulmonary artery pressure, predominant mitral lesion, prosthetic valve gradient and regurgitation were similar in patients with and without late TR. CONCLUSIONS: Significant TR diagnosed by echocardiography late after MVR is common, and clinically evident in more than one-third of patients. Therefore, a lower threshold for tricuspid valve repair should be considered when mitral valve surgery is carried out.     

Combined aortic and mitral valve replacement in an adult with mucopolysaccharidosis (Maroteaux-Lamy syndrome)

Summary A 41-year-old man with aortic stenosis, mitral stenosis, and tricuspid regurgitation due to Maroteaux-Lamy syndrome underwent aortic and mitral valve replacement with tricuspid annuloplasty. The annular diameter of the aortic and mitral valves was extremely small. The valve prostheses were 19 mm in diameter in the aortic position and 25 mm in the mitral position. Histologically, the valves showed thickening and hyalinization of the collagen fibers, and the presence of foamy cells that contained a large quantity of pure acid mucopolysaccharide. On an echocardiographic examination performed 2 years after the surgery, the peak systolic gradient of the trans-aortic valve was 18 mmHg at rest, and 26 mmHg during exercise. Careful observation of the residual pressure gradient will be needed. The patient's present New York Heart Association (NYHA) status is grade I and he has returned to work.     

Mechanisms of severe mitral regurgitation in mitral valve prolapse determined from analysis of operatively excised valves

Certain clinical and mitral valvular morphologic findings are described in 83 patients (age 26 to 79 years [mean, 60]; 26 women [31%] and 57 men [69%]) with mitral valve prolapse (MVP) and mitral regurgitation (MR) severe enough to warrant mitral valve replacement. All 83 operatively excised valves were examined by the same person, and all excised valves had been purely regurgitant (no element of stenosis). No patients had hemodynamic evidence of dysfunction of the aortic valve. In each valve a portion of the posterior mitral leaflet was elongated such that the distance from the distal margin to basal attachment of this leaflet was similar to the distance from the distal margin of the anterior leaflet to its basal attachment to the left atrial wall. Two major mechanisms for the severe MR were found: dilatation of the mitral anulus with or without rupture of chordae tendineae and rupture of chordae tendineae with or without dilatation of the mitral anulus. Of the 83 patients, 48 (58%) had both dilated anuli (greater than 11 cm in circumference) and ruptured chordae tendineae; 16 (19%) had dilated anuli without ruptured chordae, and 16 (19%) had ruptured chordae without significant anular dilatation. In three patients the anulus was not dilated, nor were chordae ruptured, and therefore the mechanism of the MR is uncertain. Mitral chordal rupture was nearly as frequent in the 64 patients with clearly dilated anular circumferences as in the 19 patients with normal or insignificantly dilated anular circumferences (less than or equal to 11 cm).     

Progression of isolated tricuspid regurgitation late after mitral valve surgery for rheumatic mitral valve disease

BACKGROUND AND AIMS OF THE STUDY: Severe tricuspid regurgitation (TR) may develop late after mitral valve surgery without significant mitral stenosis, regurgitation and other causes of left heart failure. The study aim was to investigate severe isolated TR late after mitral valve surgery for rheumatic mitral valve disease. METHODS: A total of 208 patients who underwent mitral valve surgery (valve replacement in 121, commissurotomy in 62, valvuloplasty in 25) was investigated. The mean (+/-SD) follow up was 13+/-6 years. Severe isolated TR was defined clinically by elevated venous pressure, and echocardiographically by grade 4+ TR without significant mitral stenosis, regurgitation, other causes of left heart failure, pulmonary hypertension or rheumatic tricuspid valve. RESULTS: Severe isolated TR was identified in 30 patients (14%) at four to 24 years after mitral valve surgery. All patients had atrial fibrillation. Of these patients, 23 had medical treatment and seven had tricuspid valve surgery. Three of the medically treated patients were in NYHA class IV and died from multiple organ failure at three to seven years after severe TR was diagnosed. Among surgically treated patients, four were in NYHA class IV and had postoperative complications (one early death, one late death), while three NYHA class II/III patients had very few postoperative complications. CONCLUSION: Severe isolated TR was detected in 14% of patients after mitral valve surgery. It is important to detect patients with progressive heart failure and to indicate earlier reoperation in order to prevent significant late mortality.     

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.     

Mitral valve commissurotomy versus replacement. Considerations based on examination of operatively excised stenotic mitral valves.

Among 164 patients who underwent mitral valve replacement because of mitral stenosis (with or without mitral regurgitation) and had radiographs taken of their operatively excised mitral valves, 20 had absent or minimal calcific deposits in the excised valves and absent or minimal mitral regurgitation as determined, except for one patient, by left ventricular angiography preoperatively. This report focuses on these 20 patients to ask if mitral valve replacement was preferable to mitral valve commissurotomy. Although in the pre-valve replacement era, all 20 patients almost surely would have been considered good candidates for mitral commissurotomy, other factors, namely, the need to replace one or more other cardiac valves (13 patients), the utilization of cardiopulmonary bypass allowing visual inspection rather than simple palpation of the diseased mitral valve (all 20 patients), relatively little experience with mitral commissurotomy in four of the five surgeons (17 patients), displeasure with attempted commissurotomy (three patients), previous mitral commissurotomy (11 patients), and incorrect identification of mitral calcific deposits (two patients), each contributed in one or more patients to the final decision of replacement versus commissurotomy. Even though mitral commissurotomy has been in use for 30 years, the mere alternative of valve replacement may have altered somewhat the definition of the stenotic mitral valve previously considered ideal for mitral commissurotomy.     

Mitral valve stenosis and pure tricuspid valve regurgitation: comparison of necropsy patients having simultaneous mitral and tricuspid valve replacements with necropsy patients having simultaneous mitral valve replacement and tricuspid valve anuloplasty

Clinical and morphologic observations are described in 30 patients (23 [77%] of whom were in functional class III or IV) who underwent replacement of the mitral valve for mitral stenosis and either simultaneous replacement (13 patients, group I) or anuloplasty (17 patients, group II) of the tricuspid valve for pure tricuspid valve regurgitation. Comparison of the 13 patients in group I with the 17 patients in group II disclosed similar mean ages (55 vs 58 years), similar average preoperative right ventricular systolic pressures (64 vs 61 mm Hg), similar average right atrial mean pressures (10 vs 9 mm Hg), similar average left ventricular systolic pressures (126 vs 120 mm Hg), similar average pulmonary artery wedge-left ventricular mean diastolic pressures (16 vs 18 mm Hg), similar cardiac indexes (2.1 vs 2.0 liters/min/m2), similar mean heart weights (507 vs 535 g), and similar percents with grossly visible foci of left ventricular necrosis (15% vs 12%) and fibrosis (23% vs 12%). Of the 13 patients in group I, 10 (77%) died early (less than or equal to 60 days of tricuspid valve replacement) and 3 (23%) died late (29, 37 and 120 months); of the 17 patients in group II, 14 (82%) died early and 3 (18%) died late (4, 9 and 98 months). The causes of early death in the 2 groups were different: of the 10 patients in group I who died early, the cause was excessive bleeding in 5, low cardiac output of undetermined etiology in 3, dysfunction of both prostheses in 1 and cerebral insult in 1; of the 14 patients in group II who died early, none died from excessive bleeding, 4 from decreased cardiac output of uncertain cause, 5 from left ventricular inflow obstruction (produced by a Starr-Edwards ball-valve prosthesis in 4 and from a Starr-Edwards disc prosthesis in 1), 1 from left ventricular outflow obstruction (by a porcine bioprosthesis), 2 from technical mishaps (incision into left ventricular free wall with rupture in 1 and ligation of the left circumflex coronary artery with resulting acute myocardial infarction in 1) and 2 died suddenly for reasons not determined. Of the 6 patients dying greater than 60 days after operation, 4 died from chronic congestive cardiac failure, 1 from a cerebral embolus and 1 from prosthetic valve endocarditis.     

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)     

Pathology of mitral valve stenosis and pure mitral regurgitation—Part I

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenitally malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae.