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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

Four adult women with histories of rheumatic fever and clinical findings of mitral stenosis and regurgitation had echocardiograms demonstrating moderately severe mitral stenosis (EF slope less than 20 mm/sec, mean left atrial size 3.0 cm/m2, mean anterior mitral leaflet excursion 25 mm) as well as typical mitral valve prolapse. Three patients underwent cardiac catheterization which confirmed the presence of mitral stenosis, as well as systolic prolapse and excessive scalloping of the mitral valve with no visible mitral calcium and no coronary artery disease. One patient had associated mild aortic stenosis and regurgitation. Two patients underwent mitral valve surgery which revealed anterior and posterior commissural fusion consistent with rheumatic disease and intact chordal apparatus. Both leaflets were large and the anterior leaflets were redundant. There were no vegetations. Pathology revealed myxomatous degeneration of the valve leaflets. In the absence of heavy calcification and thickening, the presence of mitral stenosis with commisural fusion does not exclude the possibility of a redundant mitral valve. When these entities coexist, systolic clicks may be absent.
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PMID:Mitral valve prolapse in rheumatic mitral stenosis. 92 8

Of 184 patients with acute rheumatic fever and associated mitral insufficiency encountered during a 15 year period, 34 manifested a mid-late systolic murmur or a nonejection click, or both, during the course of follow-up. The mid-late systolic murmur later disappeared in four patients whose condition is now considered normal. In one of the four, systolic prolapse of the mitral valve was demonstrated on an angiocardiogram obtained when the systolic murmur was present. Since disappearance of the murmur there has been no evidence of systolic prolapse on meticulous echocardiographic study of the mitral valve. In another child with angiographically demonstrated systolic prolapse of the mitral valve the systolic murmur has also disappeared, but systolic prolapse is still evident on echocardiographic study. None of the 34 patients with a mid-late systolic murmur manifested the T wave abnormalities commonly associated with the familial variety of mitral valve prolapse.
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PMID:Late systolic murmur of rheumatic mitral insufficiency. 111 97

The authors describe the results obtained during retrospective examinations of 45 subjects who suffered from acute rheumatic fever 10-14 years before. Of these, 19 subjects were treated with prednisolone in the acute disease period, 16 with indomethacin, and 8 subjects with voltaren. The examinations were mostly randomized (30 subjects); no differences in the anti-inflammatory effect were discovered. Heart disease was found in 9 persons (20%). Of these, 6 were treated with prednisolone, 2 with indomethacin, and 1 with voltaren. The disease relapses were recorded in 4 of them, the signs of valvulitis in the past were shown only by 2 persons (echocardiographically). 12 persons (27%) had mitral valve prolapse which had not been diagnosed on the first admission to the hospital, with any clinical signs of hypermotility lacking. In 18 persons (40%) having no valve lesions (disease, prolapse), an x-ray examination revealed a slight increase of the heart size, estimated as a manifestation of postmyocardial cardiosclerosis. Thus, it has been shown that modern anti-inflammatory therapy does not prevent the development of heart disease. Apparently, its onset is related to specific proneness in some of the patients.
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PMID:[The results of a retrospective examination of patients with acute rheumatic fever]. 145 87

Clinical, radiologic, electrocardiographic and 2-dimensional echocardiographic findings of fifty cases of mitral valve prolapse syndrome attending the Pediatric Cardiology clinic of I.C.H. and Childrens Hospital, Medical College, Kottayam over a period of ten years from 1980-1989 are presented. Mitral valve prolapse syndrome (MVPS) accounted for 2% of cardiac problems attending our pediatric cardiology clinic. Isolated MVPS constituted 64% of the cases. The common causes of secondary MVPS were Marfan Syndrome-18%, Atrial Septal Defect-10% and Rheumatic fever-8%. Associations of MVPS included Pectus excavatum (8%), Isolated arachnodactyly (2%) and Straight back syndrome (2%). 2-D echocardiogram demonstrated prolapse of both leaflets of Mitral valve in 44%, Isolated posterior mitral valve leaflet prolapse in 32% and Isolated anterior mitral valve leaflet prolapse in 24% of cases. No complications were seen during follow up.
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PMID:A clinical profile of mitral valve prolapse syndrome. 213 7

Between March, 1969 and March, 1984, 89 children aged from 2 to 12 years (mean: 8.3 +/- 2.5 years) and presenting with mitral valve regurgitation underwent valvuloplasty by the Carpentier technique. The cause of the regurgitation was rheumatic fever in 84 cases (94 p. 100), bacterial endocarditis in 4 cases and Barlow's disease in 1 case. Mitral valve regurgitation was divided into 3 types, namely: type I, normal valve motion (5 cases), type II, valve prolapse (74 cases) and type III, restricted valve motion due to fibrosis of the leaflets or chordae (20 cases). The hospital mortality rate was 2.3 p. 100 (2 deaths). The cumulative follow-up was 546 patients/years, and the actuarial survival rate at 10 years was 89.96 +/- 8.5 p. 100. At 10 years the actuarial thromboembolic complication rate was 2 p. 100, or 0.3 +/- 0.2 p. 100 per patient year, and the actuarial valvuloplasty deterioration rate was 27 +/- 8.5 p. 100. The risk of re-operation was 2.2 +/- 0.6 p. 100 per patient year. At 10 years 78.4 +/- 7.2 p. 100 of the children were free of all re-operation, and 69 p. 100 had no complication. Thus, whenever possible (i.e. in 90 p. 100 of the cases, according to our experience) and considering the satisfactory long-term results, all children with acquired mitral valve regurgitation should undergo mitral valvuloplasty as first-line treatment.
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PMID:[Valvuloplasties for acquired mitral insufficiency in children (Carpentier's technic). Long-term results in 87 cases]. 312 87

An eight-year-old girl with mitral regurgitation in acute rheumatic fever was examined by echocardiography. The examination showed posterior displacement of the coaptation point of the anterior mitral leaflet, i.e. anterior mitral prolapse, and did not indicate signs of edematous change or verrucous fibrin deposits on the valves. Mitral valve prolapse is thought to be one of the causes of mitral regurgitation in acute rheumatic carditis.
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PMID:A case of acute rheumatic fever: echocardiographic findings for mitral regurgitation in acute rheumatic carditis. 344 93

In this study we reevaluated whether the sole cause of mitral valve prolapse (MVP) and aortic valve prolapse (AVP) is myxomatous degeneration. Forty-two surgical cases of prolapsed valves with mitral and/or aortic regurgitation were reviewed (AVP in nine, MVP in 27, and combined AVP and MVP [CVP] in six). On microscopic examination, myxomatous degeneration was observed in 20 patients, including six with AVP, 13 with MVP, and one with CVP. In the other 22 patients, including three with AVP, 14 with MVP, and five with CVP, microscopic examination revealed fibrosis with vascularization and scattered infiltration of inflammatory round cells caused by postinflammatory changes with or without chronic inflammation. We coined the term "postinflammatory valve prolapse" (PIVP) to describe these valves. Both postinflammatory and myxomatous degeneration were observed in seven patients with floppy mitral valves attributable to PIVP. Rupture of chordae tendineae was present in six patients with myxomatous mitral valve and three with PIVP. Seven patients with PIVP had a history of rheumatic fever. The results suggest that valvular prolapse is produced not only by myxomatous degeneration but also by postinflammatory changes, including those caused by rheumatic fever.
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PMID:Postinflammatory mitral and aortic valve prolapse: a clinical and pathological study. 359 77

A total of 103 patients, age range 2 to 77 years, had some type of Carpentier reconstruction for mitral insufficiency. The mitral insufficiency resulted from ruptured chordae in 52, prolapse in 13, rheumatic fever in 16, coronary disease in eight, congenital disease in nine, and endocarditis in five. Multiple abnormalities were usually present. Four patients had severe calcification of the anulus. A reconstruction was accomplished in almost all patients. A ring annuloplasty was performed in all but two small children, but annuloplasty alone was adequate in only 17 patients. Fifty-eight had resection of 1 to 4 cm of diseased mitral leaflet. In 23 patients, chordal transposition or shortening was employed. Aortic leaflet repair was done in 28. Shortened, fused chordae (one to eight) were divided in 13 patients. Additional procedures performed in 28 patients included coronary bypass in 14. A successful repair was accomplished in all but one patient (moderate residual insufficiency). Two late hospital deaths were unrelated to the mitral repair. Following hospital discharge, ring dehiscence necessitated repeat operation in one patient. Thromboembolism produced a permanent minor neurological deficit in only one patient. There have been no late recurrences of insufficiency. Recurrent endocarditis necessitated valve replacement in three patients. A late Doppler evaluation of 95 patients for mitral insufficiency revealed none in 82, a trace in 12, and moderate insufficiency in one. Late catheterization in 16 patients revealed no insufficiency. The data suggest that reconstruction, rather than prosthetic valve replacement, can be successfully performed in over 90% of patients with nonrheumatic, noncalcified mitral valves. A much wider use of the technique seems strongly indicated.
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PMID:Experiences with the Carpentier techniques of mitral valve reconstruction in 103 patients (1980-1985). 403 72

An association between rheumatic fever/rheumatic heart disease and mitral prolapse has been suggested. Since mitral stenosis in adults is a reliable indicator of rheumatic heart disease, we undertook this study to define the association between rheumatic heart disease and prolapse by estimating the frequency with which mitral stenosis and mitral prolapse coexist in the same patient. A second purpose was to assess the usefulness of two-dimensional and standard M-mode echocardiograms in making the diagnosis of mitral prolapse in the presence of mitral stenosis. Twenty patients with moderate to severe mitral stenosis were studied. Standard M-mode echocardiographic criteria for prolapse were used; in the two-dimensional echocardiograms, we searched for arching of the mitral leaflets cephaloposteriorly above the atrioventricular ring. Left ventricular angiograms were evaluated for prolapse both subjectively and objectively by using the posterior medial scallop length index criteria. We found that the majority of these mitral stenosis patients satisfied the M-mode criteria for prolapse, whereas movement of the mitral leaflets into the left atrium by two-dimensional echocardiography and angiography occurred in fewer patients. Three patients met all echocardiographic and angiographic criteria for prolapse, but none had clinical evidence of prolapse. We conclude that the coexistence of mitral prolapse and mitral stenosis, if it occurs at all, is uncommon. M-mode echocardiography alone is unreliable to diagnose prolapse when mitral stenosis is present, since the M-mode criteria for prolapse are met by the majority of mitral stenosis patients.
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PMID:Does mitral prolapse occur in mitral stenosis? Echocardiographic-angiographic observations. 724 14


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