Myxomatous transformation of the mitral valve producing mitral insufficiency. Floppy valve syndrome.
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With the advent of echocardiography, diagnosis of papillary fibroelastoma in living patients has been made possible, yet papillary fibroelastoma found in the living remains a very rare cardiac tumor. We report a case of papillary fibroelastoma of the mitral valve with rheumatic mitral valve stenosis. A 68-year-old woman was referred to our hospital with a mitral valve tumor and rheumatic mitral valve stenosis. She underwent anticoagulation therapy with Warfarin for 8 years since having a cerebral embolization. Echocardiography revealed a mass attached to the mitral valve, with severe mitral valve stenosis. Electrocardiography demonstrated a chronic atrial fibrillation. Tumor excision with mitral valve replacement and maze procedure were performed. Both the surgical and histological findings depicted papillary fibroelastoma. The postoperative course was uneventful and the patient has remained symptom-free one year after surgery.
Limitations in the long-term results of medical treatment for mitral regurgitation are well recognized, but the advances in its surgical repair have produced good results. Therefore, early surgical intervention has been the focus of treatment in Europe and America. Increased surgical intervention depends on the development of technical skills in mitral reconstruction. This study investigated presurgical factors making surgical reconstruction difficult in 103 patients who underwent mitral operations performed from April 1994 to September 1997 in our hospital. Records were reviewed retrospectively for etiology, type of operation, and the immediate result of operation. The etiology of mitral regurgitation was prolapse in 65 patients (63%), restriction in 14, normal in 11, infectious endocarditis in 10, and others in 3. The type of prolapse involved the anterior leaflet in 22 patients (34%), posterior in 28 (43%), and both leaflets in 15 (23%). Valve repair was attempted in 74 patients, of which 16 were switched to valve replacement during operation. These included anterior leaflet prolapse in 9 patients, posterior leaflet in 1, both leaflets in 3, restriction in 2 and infectious endocarditis in 1. The success rate for reconstruction of anterior leaflet prolapse was not high. The cause of mitral regurgitation was mostly prolapse of the mitral valve, in our country as well as in Europe and America. Prolapsed posterior leaflet is much more common in Europe and America, and there is a high success rate reported for its valve reconstruction. In contrast, this study cannot recommend earlier surgical intervention because of difficult repair for anterior leaflet prolapse.
OBJECTIVES: To understand papillary muscle malformations, such as in parachute mitral valves or parachute-like asymmetric mitral valves, we studied the development of papillary muscles. METHODS: Normal human hearts at between 5 and 19 weeks of development were studied with immunohistochemistry, three-dimensional reconstructions, and gross inspection. Scanning electron microscopy was used to study human and rat hearts. RESULTS: In embryonic hearts a prominent horseshoe-shaped myocardial ridge runs from the anterior wall through the apex to the posterior wall of the left ventricle. In the atrioventricular region this ridge is continuous with atrial myocardium and covered with cushion tissue. The anterior and posterior parts of the trabecular ridge enlarge and loosen their connections with the atrial myocardium. Their lateral sides gradually delaminate from the left ventricular wall, and the continuity between the two parts is incorporated in the apical trabecular network. In this way the anterior and posterior parts of the ridge transform into the anterolateral and the posteromedial papillary muscles, respectively. Simultaneously, the cushions remodel into valve leaflets and chordae. Only the chordal part of the cushions remains attached to the developing papillary muscles. CONCLUSIONS: Disturbed delamination of the anterior or posterior part of the trabecular ridge from the ventricular wall, combined with underdevelopment of chordae, seems to be the cause of asymmetric mitral valves. Parachute valves, however, develop when the connection between the posterior and anterior part of the ridge condenses to form one single papillary muscle. Thus parachute valves and parachute-like asymmetric mitral valves originate in different ways.
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BACKGROUND: In clinical settings, information on morphology of mitral valve leaflet after mitral valve reconstruction is limited. METHODS: Between January 1996 and June 2000, 36 underwent mitral valve repair for mitral regurgitation (MR). The etiology of mitral insufficiency was prolapse, dilated annulus, and ischemic. Ring annuloplasty was performed in all cases. Mitral valve short-axis dimension (MVd), vertical distance between annular line and closing point (Vd), coaptation length (CL), coaptation length index (CL/MVd) were measured by the two-dimensional transesophageal echocardiography for the present 11 cases. RESULTS: In 11 cases, residual MR, using a scale from 0 to 4, was 0 in 5 patients, 1 in 4 patients, 2 in 2 patients whose etiology of regurgitation was cardiomyopathy. MVd and Vd decreased significantly (38.7 +/- 6.2 to 27.0 +/- 5.6 mm, 10.1 +/- 7.7 to 6.5 +/- 4.6 mm, respectively). CL and CLI increased significantly (6.4 +/- 2.4 to 11.6 +/- 4.6 mm, 0.16 +/- 0.06 to 0.44 +/- 0.21, respectively). Among those index, only CLI have a statistically significant negative correlation with the degree of residual MR. CONCLUSION: The mitral valve ring annuloplasty produce the morphologic change of mitral apparatus, especially the increase of CLI, which may be one of the main factors in regulation of regurgitation.
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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.
OBJECTIVE: The aim of this study is to detect the risk factors for hospital mortality in patients who underwent reoperative mitral valve replacement. METHODS: Rheumatic mitral valve patients who underwent primary mitral valve replacement (386 cases) and repeat mitral valve replacement (94 cases) were analysed retrospectively. The incremental effects of the reoperative procedure on hospital mortality were studied by comparing primary and reoperative procedures and analyzing a series of possible predisposing factors. RESULTS: Operative mortality for repeat procedures was found significantly higher than the first operations (respectively 12.8% versus 4.3%, p=0.022). Risc factors affecting the hospital mortality in reoperation group were determined as advanced age, diameter of left atrium, prolonged bypass time and development of postoperative low output state. The indication for surgery also had a significant role in patients' outcome. Mortality found significantly higher in cases operated due to endocarditis or mitral mechanical valve thrombosis compared to other reoperation groups. CONCLUSION: Patients over age of 70 years, with a left atrial diameter over 60 mm, reoperated due to endocarditis and mechanical valve thrombosis, should be reevaluated for risk assessment while giving the decision of optimal operation timing. Especially patients with left ventricular hypertrophy and decreased myocardial reservoirs, efficient myocardial protection during the operation had an important role.
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Thirty-six patients who underwent mitral valve repair were analyzed to evaluate the effect of mitral valve reconstructive technique. The final aim of this technique is to true up the coaptation line of both leaflets. Resection and reconstruction of the leaflet was performed on anterior leaflet in 11, on posterior leaflet in 12, and on both leaflets in 5. The newly contrived wrapping and shortening chordoplasty was performed on anterior leaflet in 6, on posterior leaflet in 3, and on both leaflets in 2. Two patients had replacement of artificial chordae tendinae with EPTFE suture. Commissuroplasty was performed at anterolateral commissure in 5, at posteromedian commissure in 15, and at both commissures in 5. Thirty patients with dilated annulus underwent ring annuloplasty with Carpentier ring. LVEDVI and LVESVI significantly decreased after mitral valve repair, and left ventricular volume overload was markedly reduced. Mitral valve orifice area was 3.23 +/- 1.14 cm2 and did not show the sign of mitral stenosis after repair. Left ventricular pressure volume area, which reflects the oxygen consumption of the myocardium, was markedly reduced after successful mitral repair.
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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.
Since it was demonstrated in experimental studies that preservation of the subvalvular mitral apparatus is of significance for left ventricular function, it was concluded that in mitral valve replacement complete excision of the mitral valve is disadvantageous for the patient. Clinical experience showed that in patients with mitral regurgitation and large mitral annulus, most of the valvular apparatus can be preserved. In stenotic mitral valve disease, it may be possible to decalcify and mobilize the mitral apparatus and to preserve it. If it is necessary to excise the mitral valve completely, one should think of replacing the chordae tendineae and thus improving postoperative left ventricular function.
OBJECTIVES: This prospective, blinded transesophageal echocardiographic study was performed to determine the relative contributions of leaflet redundancy and overlap versus intrinsic tissue thickening as mechanisms for the apparent increase in diastolic thickness of the mitral valve. BACKGROUND: Increased diastolic thickness of the mitral valve has been identified as an echocardiographic feature that predicts subsequent adverse sequelae in patients with mitral valve prolapse (MVP). METHODS: Eleven patients with clinical and transthoracic echocardiographic evidence of MVP and 11 age-matched control subjects underwent protocol transesophageal echocardiography to image the mitral valve in two orthogonal planes and to measure its thickness in systole and diastole. RESULTS: Maximal diastolic width of the slack, unloaded anterior leaflet was significantly greater in patients with MVP than in control subjects (mean +/- SD: 0.64 +/- 0.20 cm vs. 0.30 +/- 0.04 cm, p < 0.001). Similarly, diastolic posterior leaflet width was greater in patients with MVP (0.67 +/- 0.39 cm vs. 0.31 +/- 0.06 cm, p < 0.01). In contrast, minimal systolic width of the distended pressure-loaded mitral valve was not significantly different between patients with MVP and control subjects for either the anterior (0.22 +/- 0.05 cm vs. 0.20 +/- 0.04 cm, p = NS) or the posterior (0.25 +/- 0.07 cm vs. 0.24 +/- 0.05 cm, p = NS) leaflets. The percent change in leaflet width from diastole to systole (% delta W), an index of the contribution of dynamic factors (e.g., leaflet redundancy and overlap) to the apparent increase in diastolic leaflet thickness, was significantly greater in patients with MVP than in control subjects for both the anterior (% delta W 62 +/- 13% vs. 34 +/- 16%, p < 0.001) and the posterior (% delta W 54 +/- 19% vs. 22 +/- 21%, p < 0.005) leaflets. CONCLUSIONS: The apparent increase in diastolic mitral leaflet thickness in patients with MVP versus control subjects is largely attributable to dynamic factors such as leaflet redundancy, overlap and deformation. During diastole, when the mitral leaflets are slack and unstressed, the leaflets appear markedly thickened in patients with MVP. In contrast, during systole, when developed intraventricular pressure distends the leaflets, causing them to stretch and balloon into the left atrium, the intrinsic tissue thickness is much less than that measured in diastole. These findings have important implications for the morphologic criteria used to diagnose MVP and the potential pathophysiologic mechanisms for adverse sequelae in this syndrome.