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Query: UMLS:C0014118 (endocarditis)
15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of mitral valve prolapse (MVP) in 80 patients with various thoracic skeletal abnormalities (TSA) was examined prospectively using compete history and physical examination, chest x-rays, electrocardiography, phonocardiography, and echocardiography. There were 76 males and four females, ranging in age from 18 to 80 years. Thirty-four patients had narrow anteroposterior diameter of the chest (asthenic habitus) (Group 1), 13 had straight back (Group 2), and 33 had pectus excavatum (Group 3). Twenty-five of the 80 patients (31 per cent) had evidence of MVP, 22 by echocardiographic criteria and three by phonocardiographic criteria. The incidence of MVP in this predominantly male population was substantially higher than that reported in the general adult population. Thoracic skeletal abnormality is an important nonauscultatory feature of mitral valve prolapse syndrome. The association between TSA and MVP may be a manifestation of a single connective tissue defect during embryonic development of the bony thoracic cage and the atrioventricular valves. All patients with TSA, even when asymptomatic, should be screened for MVP by noninvasive investigations. The recognition of MVP in patients with TSA may be of potential value in prevention of life-threatening endocarditis and cardiac arrhythmia.
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PMID:Incidence of mitral valve prolapse in subjects with thoracic skeletal abnormalities--a prospective study. 42 69

This study included 40 patients over 60 years of age with echocardiographic findings of mitral valve prolapse (MVP). Most of these patients were unaware of any cardiac disorder until the time of echocardiography. In the majority, the clinical manifestations were benign, and the duration of symptoms variable. Congestive heart failure (CHF) was noted in 10 patients (25 percent) who were unaware of having any cardiac disorders until the onset of their symptoms. In 5 patients (4 with CHF and 1 with endocarditis), surgical replacement of the prolapsed mitral valve was necessary. Endocarditis was present in 4 patients (10 percent), none of whom had been instructed in the prophylactic use of antibiotics. The physician's awareness of mitral valve prolapse in the elderly patient is important, since the disorder may not be as benign in aged patients as in younger ones, and life-threatening complications may occur.
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PMID:Mitral valve prolapse in the elderly. 46 55

Systolic flutter of the mitral valve was observed in 11 cases during the past 3-1/2 years. All patients had mitral regurgitation due to mitral valve prolapse or flail leaflets, and nine of the 11 (82%) had prior or concurrent bacterial endocarditis. Systolic flutter is uncommon in the absence of endocarditis and was observed in only two of 15 patients (13%) with proven chordae tendinae or papillary muscle rupture without historical and pathological evidence of infection involving the mitral valve. Systolic flutter was also not seen in a large number of patients with mitral regurgitation due to other causes. It is postulated that the regurgitation jet of blood across the edge of a structurally abnormal but flexible mitral leaflet is important for the development of flutter.
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PMID:Systolic flutter of the mitral valve. 67 75

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

In order to assess the reliability of the echocardiogram in detecting valvular vegetations in patients with mitral valve prolapse (MVP), echocardiograms from 85 consecutive patients with mitral valve prolapse were reviewed. Eleven patients had thick shaggy echoes confined to the anterior mitral leaflet; eighteen patients had shaggy echoes on the posterior leaflet; and five had abnormal echoes on both the anterior and posterior leaflets. Only one patient had clinical evidence of infective endocarditis. Redundant leaflets which present multiple surfaces for the production of echoes may explain the abnormal echoes that were observed. Patients with echographic features suggesting mild prolapse less commonly exhibited shaggy leaflet echoes than those with more severe prolapse. Because a significant proportion (40%) of patients with MVP had shaggy echoes which closely resembled those seen in valvular vegetations, we feel that the echocardiogram is of limited value in diagnosing infective endocarditis in patients with mitral valve prolapse.
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PMID:Limitations of the echocardiogram in diagnosing valvular vegetations in patients with mitral valve prolapse. 88 98

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

Mitral valvuloplasty has become an increasingly accepted alternative to valve replacement, although the strong learning curve attached to the procedure has deterred many surgeons from adopting it. Since it was developed in the late 1960s by Carpentier, comprehensive valvuloplasty has undergone modifications and additions dictated by the experiences thus acquired, which have contributed to make it a more reproducible and predictable procedure. Mitral valve disease, especially that of rheumatic origin, has a multifactorial pathogenesis, as all the components of the valve apparatus are usually involved. Consequently, valvuloplasty requires a combination of multiple techniques, each one directed at correcting each affected component. The excellent median-term results observed by some of the more experienced groups have contributed to change the indications for surgery, and patients are being referred earlier and in a lower functional class. Hence, in mitral valve prolapse surgery is currently offered to asymptomatic patients with significant regurgitation, before dysfunction of the myocardium and dilatation of the cardiac chambers occur. Valve repair has been possible and successful in virtually all patients with this pathological condition. On the other hand, surgeons are becoming more aggressive towards ischaemic mitral regurgitation of mild or moderate severity. More recently, valvuloplasty has also been performed in some patients with infective endocarditis, with good results. By contrast, the long-term results in rheumatic disease appear favourable, especially in children and young patients with acute carditis. Nevertheless, they have still been proven better than those of valve replacement in these population groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitral valve repair into the 1990s. 138 72

We encountered a 65-year-old female with hypertrophic obstructive cardiomyopathy and mitral valve prolapse who had infective endocarditis and hemolytic anemia. The infecting organism of endocarditis was group A streptococci. With regard to the etiology of the hemolytic anemia, fragmentation hemolysis was considered because fragmented red cells and elevated lactic dehydrogenase were observed. Haptoglobin was markedly decreased. Coombs' test, Ham's test and abnormal hemoglobin were negative. She had not had a hemolytic attack in the past. Ultrasonic cardiography showed asymmetrical septal hypertrophy, mitral valve prolapse and 285 mmHg of calculated pressure gradient in the left ventricle. Cardiac catheterization showed 115 mmHg of left intraventricular pressure gradient and mitral regurgitation (grade 2). Hemolysis was slightly improved after treatment with propranolol. Thus, fragmentation of the normal red cells seemed to be due to shear stress.
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PMID:Fragmentation hemolysis in a patient with hypertrophic obstructive cardiomyopathy and mitral valve prolapse. 140 52

A consecutive series of 1288 mitral valves surgically excised from 1981 through 1989 were studied macroscopically and histologically. The explanted valves were affected by: chronic rheumatic disease (1179, 91.5%), floppy mitral valve (84, 6.5%), bacterial endocarditis (19, 1.5%), and post-ischemic mitral incompetence (6, 0.5%). Among 1179 post-rheumatic cases, mixed mitral stenosis and incompetence was the most frequent malfunction (747, 58%). Isolated mitral incompetence was diagnosed in 72 (6.11%) cases only, and isolated stenosis in 360 cases. In 52 valves, excised because of chronic rheumatic disease, the histology showed unexpected signs of acute rheumatism of the leaflets and the papillary muscles. In these patients clinical symptoms and blood tests were negative for rheumatic disease. Mitral incompetence, possibly due to papillary muscle dysfunction, was the prevalent lesion (61.5%). A total of 181 patients (14.05%) with pure mitral incompetence underwent surgery. In 84 patients (46.4%), the floppy mitral valve was the most frequent cause of valve dysfunction, 72 (39.8%) had rheumatic disease, 19 (10.5%) infective endocarditis, and 6 (3.4%) ischemic heart disease. In the group with floppy mitral valve, males were more prevalent than females (51:33). The mean age of the 4 patients with Marfan's syndrome and non-Marfan patients was noticeably different (17 vs 49 yr). Moreover leaflet deformation, tendinous cord elongation and annulus dilatation were the most common causes of valve incompetence. Floppy mitral valve and infective endocarditis were the cause of cordal rupture in 43.5% of the cases. This was a severe complication which always required emergency surgery.
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PMID:Surgical pathology of the mitral valve: gross and histological study of 1288 surgically excised valves. 142 93

The clinical features of an infective embolic choroidopathy are described, from its early onset to late complications in a 45-year-old man with acute Staphylococcus aureus endocarditis of the aortic valve. Initial fundus examination revealed, in addition to fresh choroidal lesions, stigmata of a previous embolic episode secondary to endocarditis from Actinobacillus actinomycetemcomitans. The choroidal lesions were extremely asymmetrical, with a clear preference for localization in the left eye. Similar ocular findings were seen in a 78-year-old female with mitral valve prolapse and acute S. aureus endocarditis. In this case, however, choroidal involvement from septic emboli spread was bilateral and roughly symmetrical. Choroidal neovascular membranes arising in scars from choroidal septic emboli occurred in the macular area of the left eye of both patients, 10 months and 5 years after embolization, respectively.
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PMID:Subretinal neovascularization secondary to choroidal septic metastasis from acute bacterial endocarditis. 143 40


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