Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of and the Doppler color-flow echocardiographic characteristics of aortic valve prolapse with nonrheumatic aortic regurgitation were examined. Aortic valve prolapse was observed in 21 of 243 patients (15 men and 6 women) with aortic regurgitation as detected by Doppler color-flow echocardiography (rheumatic, 112; nonrheumatic, 131) in 1247 consecutive patients. Patients with aortic valve prolapse included three patients with essential hypertension and one with annuloaortic ectasia. The remaining 17 patients (7% of those with aortic regurgitation) had no other associated cardiovascular disease (idiopathic aortic valve prolapse). Prolapse of the mitral or the tricuspid valve or both was associated with aortic valve prolapse in seven patients. Aortic regurgitation jet was markedly deviated from the axis of left ventricular outflow tract toward the anterior mitral leaflet or the interventricular septum in 17 of 21 (81%) patients with aortic valve prolapse, whereas 28 of 110 (25%) patients with nonrheumatic aortic regurgitation without prolapse and 17 of 112 (15%) patients with rheumatic aortic regurgitation without prolapse showed the deviation of regurgitant jet (p < 0.001). In conclusion, idiopathic aortic valve prolapse is one of the significant causes of aortic regurgitation, and a marked deviation of regurgitant jet is a characteristic Doppler color-flow echocardiographic finding of aortic regurgitation that results from aortic valve prolapse.
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PMID:Aortic valve prolapse with aortic regurgitation assessed by Doppler color-flow echocardiography. 144 99

The prevalence and clinical significance of aortic valve prolapse were determined prospectively in 2000 consecutive patients undergoing routine clinical cross sectional echocardiography. Two hundred and twelve patients were excluded because the aortic cusps were not adequately visualised. Aortic valve prolapse was defined as downward displacement of cuspal material below a line joining the points of attachment of the aortic valve leaflets. Twenty four cases of aortic valve prolapse (1.2%) were identified. The patients were aged 12-64 years and nine were women. All had underlying valvar heart disease and the commonest lesion (in 11 cases) was prolapse of the larger cusp in bicuspid valves. Aortic valve prolapse was seen in four patients with mitral valve prolapse (two with severe regurgitation), one of whom had marfanoid aortic root dilatation. The remaining examples of aortic prolapse were seen in patients with various disorders including one with pulmonary atresia, two with aortic root disease (one with dissection and one with idiopathic dilatation), and one case of severe mitral regurgitation. Valves destroyed by infective endocarditis were seen in two cases. Aortic valve prolapse may be detected in various cardiac disorders and does not imply the presence of aortic regurgitation, but when bicuspid aortic valves are present it may well be important in producing such regurgitation. Although aortic valve prolapse may be associated with severe forms of mitral valve prolapse, these patients rarely have aortic regurgitation.
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PMID:Prevalence and clinical significance of aortic valve prolapse. 401 27

Historically, indications for ventricular septal defect closure have included congestive heart failure, pulmonary hypertension, aortic insufficiency with or without aortic valve prolapse, and prior bacterial endocarditis. However, controversy exists as to how the lifetime risk of an isolated, nonoperated restrictive ventricular septal defect compares with the risk of surgical closure in an asymptomatic child. Between 1980 and 1991, cardiac catheterization and elective ventricular septal defect closure (age > 1 year, pulmonary to systemic flow ratio < 2.0) were performed in 141 patients aged 1 to 23 years (mean age, 6.1 +/- 4.7 years). Mean systolic pulmonary artery pressure was 26.9 +/- 13.0 mm Hg, and mean pulmonary to systemic flow ratio was 1.6 +/- 0.3. Aortic valve prolapse was present in 63 patients (45%), aortic insufficiency was present in 25 (18%), and 5 (3.5%) had prior bacterial endocarditis. There were no early or late deaths or major morbidity. No patient required a ventriculotomy to accomplish ventricular septal defect closure. Mean postoperative intensive care unit stay was 1.3 +/- 0.9 days, and mean hospital stay was 5.5 +/- 1.9 days. There were no instances of permanent complete atrioventricular dissociation, reoperations for bleeding, postoperative wound infections, or reoperations for residual or recurrent ventricular septal defect. These improved results justify a reevaluation of historic indications for ventricular septal defect closure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restrictive ventricular septal defect: how small is too small to close? 823 92

Laubry-Pezzi syndrome is a clinical entity in which prolapse of an aortic valve cusp into a subjacent ventricular septal defect (VSD) due to Venturi effect results in progressive aortic valve insufficiency. Aortic valve prolapse is found in over 5% of children with VSDs, most commonly in association with supracristal VSDs, and the risk of development of aortic regurgitation increases during childhood, peaking at 5 to 10 years of age. The VSD closure eliminates the low-pressure zone that is the cause of ongoing aortic valve cusp deformity and, if performed early, prevents the development of aortic regurgitation. However, the management of this rare pathology is still a matter of some debate with respect to indications, operative techniques, and timing. We report the case of a patient with Laubry-Pezzi syndrome, originally operated on at six years of age for VSD closure and plasty between the left and the right aortic cusps. However, in the follow-up the patient developed severe aortic regurgitation and aortic root dilatation. Eventually, a Bentall and De Bono procedure was performed.
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PMID:Laubry-Pezzi syndrome with aortic root dilatation treated with a bentall and De Bono procedure. 2432 1