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 occurrence of concealed infection or "natural remission" in infective endocarditis was investigated microscopically in 35 consecutive patients (36 valves) with infective endocarditis (between April 1987 and May 1995). Four patients were considered as having concealed or silent infective endocarditis. Preoperative diagnosis of these patients was mitral valve prolapse, rheumatic aortic valve stenosis with insufficiency, aortic valve prolapse and hypertrophic cardiomyopathy, respectively. These patients did not present with any clinical signs of infective endocarditis such as cardiac murmur and ventricular dysfunction. Histological examination of the excised valves revealed valvular perforation, small round cell infiltration, neovascularization, remnants of vascular smooth muscle cells, and organizing vegetations. These findings are consistent with the histological findings of infective endocarditis. Latent infective endocarditis may be present without inflammatory manifestation.
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PMID:[Concealed infective endocarditis]. 921 Nov 11

The patient was 22-year-old female. She had undergone aortic valve replacement and Manouguian's anulus enlargement with low porosity woven Dacron patch for congenital aortic stenosis 13 years ago, and developed mitral regurgitation 9 years after that operation. Two regurgitant flow were observed. One was originated from the orifice due to mitral prolapse. The other was from a tear in the anterior leaflet. It was around the tip of the prosthetic patch, approximately 7 mm in size, and was repaired easily. But the mitral valve itself was found to be malformed and prolapsed, requiring mitral valve replacement. Her postoperative course was uneventful.
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PMID:[Reoperation for mitral regurgitation 13 years after aortic valve replacement and manouguian's anulus enlargement: report of a case]. 940 9

Isolated mitral regurgitation without supravalvular aortic stenosis is rarely identified in Williams syndrome. We describe the case of a 24-year-old man with isolated mitral regurgitation in Williams syndrome. Severe regurgitation due to prolapse of the anterior leaflet was noted in an echocardiogram and color Doppler, and a left ventriculogram showed grade IV regurgitation. No pressure gradient between the left ventricle and the ascending aorta was found. Mitral regurgitation had been noted since his birth, and pediatricians suspected Williams syndrome because of postnatal growth deficiency, mental deficiency, unusual personality, and unusual facial features in his childhood. The diagnosis was confirmed by demonstration of the hemizygous deletion of 7q11.23 in the karyotype by the fluorescent in situ hybridization technique after his admission to our department. The patient underwent mitral valve replacement, and microscopic examination of the excised valve revealed myxomatous degeneration.
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PMID:Mitral regurgitation without supravalvular aortic stenosis in Williams syndrome. 1238 35

Noonan's syndrome is characterized by craniofacial anomalies, i. e. ptosis, webbing of the neck and a deep nuchal hairline, as well as skeletal deformities such as short stature, clinodactyly, pectus carinatum and funnel chest and other organ anomalies, mainly cardiac valve disease, less often testicular retention or kidney malformations. Noonan syndrome presents with aspects similar to Ullrich-Turner syndrome, but can be found in both male and female patients. In about one half of the patients with Noonan's syndrome cardiovascular anomalies occur, mostly anomalies of the right heart (mainly valvular pulmonary stenosis). Aortic stenosis and coarctation of the aorta are rarely seen. We report on a patient with four sequential potentially stenosing and stenosed parts of the proximal systemic circulation: hypertrophic cardiomyopathy, bicuspid aortic valve, coarctation of the aorta and a hypoplastic aortic arch as a part of Noonan's syndrome. This patient presents with a unique combination of anomalies, as he also shows a Madelung like deformity of the wrist.
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PMID:[Noonan's syndrome with an unusual combination of hypertrophic cardiomyopathy, congenital bicuspid aortic valve, coarctation of the aorta and hypoplastic aortic arch]. 1508 76

We report the case of a 76-year-old woman found on preoperative evaluation for vaginal prolapse to have coronary artery disease, aortic stenosis, and a large recurrent anterior diaphragmatic hernia. The clinical presentation and surgical management of this case, and the review of the literature are discussed.
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PMID:Massive recurrent anterior diaphragmatic hernia, coronary artery disease, and valvular heart disease. 1579

Valvular dystrophies due to myxoid degeneration are common and potentially serious cardiac pathologies. They constitute a heterogeneous group of which the most usual is idiopathic mitral valvular prolapse (Barlow's disease). The majority of mitral valvular prolapses are sporadic, but there are several familial forms. Transmission is usually autosomal dominant with incomplete penetrance and variable expression. The first chromosomal location to be identified was on the 16p11-13 chromosome. Since then, two other loci have been identified on the 11p15.4 and 13q31-32 chromosomes. Our team has recently identified the first gene responsible for myxoid valvulopathy linked to the X chromosome, from a large family of 318 members. This is the gene that codes for filamin A, which is a cytoskeleton protein. The frequency of mutations in this gene is still unknown, but out of 7 families in which transmission was compatible with X-linked transmission, mutations were discovered in 4 of the families. Thanks to a genetic epidemiological approach, we have also demonstrated that there are familial forms of aortic stenosis, which are probably common. Identification of the genes implicated in these common forms of valvular pathology is important, as it will allow a better understanding of the pathophysiology of these valvular disorders and could lead to better therapeutic management in the future.
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PMID:[Genetic aspects of valvulopathies]. 1822 15

We report the case of a severe prosthetic aortic stenosis in a 61-year-old male patient with an aortic Mitroflow LF bioprosthesis (Sorin Group) at early (6 months) postoperative echocardiographic follow-up. At reintervention, we found significant stent deformation, asymmetric orientation of the posts, and subsequent central kinking and prolapse of one leaflet. Maldistribution of pledgeted mattress sutures over the flexible stent was found to be the origin of its permanent deformation. Simple technical preventive strategies of this previously unreported complication are suggested.
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PMID:Mitroflow bioprosthesis stent deformation: a rare cause of early prosthetic stenosis. 1938 88

Similar to mitral repair, newer methods of aortic valve reconstruction are achieving excellent outcomes with an 85% to 90% freedom from valve-related complications at 10 years. The goal of this review is to illustrate these newer and more stable techniques of aortic valve repair. Most patients with aortic insufficiency from either trileaflet or bicuspid aortic valves are candidates for repair, in addition to selected patients with mixed aortic stenosis/insufficiency and aortic root aneurysms. Initially, aggressive commissural annuloplasty is performed to reduce measured valve diameter to 19 to 21 mm. Leaflet prolapse is corrected with plication stitches placed in the free edge of each leaflet adjacent to the Nodulus Arantius. In this regard, the leaflet free edge functions as the chorda tendinea of the aortic valve, and shortening with plication stitches raises the leaflet to a proper "effective height." Leaflet defects are augmented with gluteraldehyde-fixed autologous pericardium, and mild-to-moderate strategically placed spicules of calcium are removed with the cavitron ultrasonic surgical aspirator. Using these methods, most insufficient aortic valves, and many with mixed lesions, can be satisfactorily repaired. Six cases are illustrated in this review, spanning the spectrum of pathologies from annular dilatation without leaflet defects, to standard congenital bicuspid valve with prolapse, to trileaflet prolapse, to unusual bicuspid pathology with calcification, to a moderately calcified trileaflet valve with mixed lesions, and to aortic root aneurysms with severe aortic insufficiency. All valves were repaired using the techniques described above with trivial residual leak and minimal gradients. All repairs have been followed with yearly echocardiography, and valve reconstruction with these methods is now quite stable with excellent late outcomes. Most insufficient aortic valves now can undergo stable repair with minimal late valve-related complications. Greater application of aortic valve repair seems indicated.
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PMID:Techniques of aortic valve repair. 2243 68

An 86-year-old man with severe symptomatic aortic stenosis underwent an aortic valve replacement. A transesophageal echocardiogram (TEE) was performed during the surgery and demonstrated mild mitral regurgitation (MR). The patient's symptoms persisted despite surgery, and subsequent TEE demonstrated prolapse of the posteromedial commissural leaflet, with evidence of a severe, very eccentric MR jet which was directed laterally and superiorly. The jet was almost missed in most imaging planes and could finally be exposed by withdrawing the probe to the level of the aortic valve and left atrial appendage.
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PMID:Commissural mitral regurgitation detected by abnormal blood flow pattern in the left atrial appendage. 2296 99

The histopathological characteristics of congenital aortic valve malformations in children were investigated. All the native surgically excised aortic valves from 32 pediatric patients suffering from symptomatic aortic valve dysfunction due to congenital aortic valve malformations between January 2003 and December 2005 were studied macroscopically and microscopically. The patients' medical records were reviewed and the clinical information was extracted. The diagnosis was made by the clinical presentation, preoperative echocardiography, intraoperative examination, and postoperative histopathological study, excluding rheumatic or degenerative aortic valve diseases, infective endocarditis and primary connective tissue disorders, e.g. Marfan syndrome. Among 32 children with congenital aortic valve malformations, the age was ranged from six to 18 years, with a mean of 14.9 years, and there were 27 boys and five girls (male: female = 5.4:1). There were five cases of aortic stenosis (AS, 15.62%), 25 cases of aortic insufficiency (AI, 78.13%) and two cases of AS-AI (6.25%), without other valve diseases. Twenty cases still had other congenital heart diseases: ventricular septal defect (19 cases), patent ductus arteriosus (two cases), double-chambered right ventricle (one case), aneurysm of the right anterior aortic sinus of valsalva (three cases). Histopathological examination indicated that the cusps became thickening with unequal size, irregular shape (coiling and prolapse edge), enhanced hardness, and partly calcification. Microscopic investigation revealed the unsharp structure of valve tissue, fibrosis, myxomatous, reduced collagen fiber, rupture of elastic fibers, different degrees of infiltration of inflammatory cells, secondary calcareous and lipid deposit, and secondary fibrosis. Congenital aortic valve malformations in children involve males more than females, mostly associated with other congenital heart diseases. Aortic insufficiency is more common in children with congenital aortic valve malformations. Histopathologically, the leaflets of aortic valve are mainly myxomatous, thickening with unequal size, irregular shape (coiling and prolapse edge), reduced collagen fiber, rupture of elastic fibers, without small vessel proliferation and inflammatory cell infiltration, fibrosis and calcification rarely seen.
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PMID:Histopathological study of congenital aortic valve malformations in 32 children. 2455 22


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