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

Our review of an entire institutional experience with primary repair of congenital and acquired mitral valve (MV) anomalies in children with concordant atrial-ventricular-arterial connections but without atrioventricular septal defects included 48 patients (1962 to September 1986). Mitral stenosis (MS) was the predominate lesion in 24 patients, mitral incompetence in 22, and mixed in two. Most patients with MS had so-called typical congenital MS (Van Praagh) with abnormalities of all valvular components; virtual or complete absence of chordal development was a consistent finding. Other anatomic substrates (not mutually exclusive) producing MS included supramitral ring with Shone's complex (n = 5), parachute mitral valve (n = 2), hypoplastic mitral ring (n = 3), and rheumatic lesions (n = 3). The anatomic substrates producing mitral incompetence included annular dilatation (n = 16; isolated in seven), leaflet prolapse (n = 7), cleft leaflet (n = 6), leaflet deficiency (n = 3), and rheumatic lesions (n = 2). Concurrent repair of associated lesions was performed in 29 (60%) patients for relief of left ventricular outflow tract obstruction (n = 16) and closure of ventricular septal defects (n = 9; double-outlet right ventricle in three). Six (12.5%) patients had previous repair of coarctation of the aorta. The operative mortality rate was 18.7% (70% confidence limits [CL]; 12.8% to 24.6%), with one death in 35 patients since 1975 (2.9%; 70% CL; 0% to 5.8%). The actuarial freedom from early or late death and reoperation (+/- SEM) was 44.0% +/- 14.8% at 8 years postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical experience with reparative techniques in patients with congenital mitral valvular anomalies. 362 34

A 5-year-old boy with deletion of the long arm of chromosome 11 presented with trigonocephaly, bilateral ptosis, epicanthus, antimongoloid lid axes, and bilateral iris coloboma. In order to avoid complication by a torticollis a Guyton-Friedenwald fadenoperation was performed. In 1981 Grosse et al. listed among the pediatric symptoms retarded development, ventricular septum defect, mitral stenosis, and skeletal and urogenital anomalies.
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PMID:[Ophthalmologic findings in 11 q-deletion syndrome]. 362 12

Twenty-five patients (14 males and 11 females aged 11 to 45 years) with rhythm disorders and valvular defects were operated on. Supraventricular paroxysmal tachycardia was the most common of rhythm disorders occurring in 15 cases, with Ebstein's anomaly in 11, mitral valve incompetence in 2, combined mitral defects in 1 and aortic stenosis in 1 of those. Atrial fibrillation was recorded in 7 patients, with Ebstein's anomaly in 2, mitral stenosis in 2, mitral incompetence in 2 and mitral prolapse in 1 of those. Nodal tachycardia was found in 1 patients with Ebstein's anomaly and in 1 patient with mitral valve incompetence. Left-ventricular tachycardia was diagnosed in a female patient with mitral prolapse. The operations were simultaneous and comprised two steps; they were performed under extracorporeal circulation and drug- and cold-induced cardioplegia, with the elimination (surgical interruption) of accessory conduction pathways or removal of arrhythmogenic areas as the first step, and reconstructive surgery on heart valves as the second step.
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PMID:[Surgical treatment of rhythm disorders with simultaneous correction of heart valve defects]. 371 46

Echocardiographic investigation of 65 patients with systemic scleroderma showed that the left ventricular sizes and indices of central hemodynamics were frequently lowered in them; an increase in sizes was observed mainly in the patients with stage II-III of disease. In 3/4 of the same patients pericarditis was revealed; on the whole, it was detected in 26 (40%) examinees. One patient had changes which were typical of asymmetric obstructive cardiopathy. In location of the valvular apparatus signs of mitral stenosis were found in one patient, those of mitral insufficiency in one patient and those of aortic insufficiency in one patient. Signs of mitral prolapse were noted in 7 (10.9%) patients, i.e. twice more frequently than in the entire population. Echocardiography made it possible to specify the nature of cardiac pathology and brought to light some additional features of the involvement of different heart membranes in systemic scleroderma.
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PMID:[Echocardiographic study of heart function in systemic scleroderma]. 382 23

This case report describes a mitral systolic honk originating from the mitral valve and adjacent structures in a 52 year-old woman with mitral stenosis. The patient was hospitalized because of dyspnea. Auscultation of the heart revealed a grade 3/6 apical early systolic honk accompanied by an increased first heart sound, an opening snap and a diastolic rumble. The phonocardiogram demonstrated an early systolic honk at a frequency of 115 Hz. Intensity of the honk varied on beat to beat basis, increasing in the short preceding R-R interval compared to that in the long one. The M-mode echocardiogram showed early systolic fluttering of the mitral valve and chordae tendineae at the same frequency as the honk. The two-dimensional echocardiogram showed bulging of the anterior mitral leaflet toward the left atrium in early systole. After treatment with digitalis and diuretics, the early systolic honk disappeared in beats with preceding long R-R intervals (greater than 1100 msec). In beats without the honk, systolic fluttering of the mitral valve was not observed. The genesis of the early systolic honk is analogous to that of the honk audible in mitral or tricuspid valve prolapse. The bulging of the anterior mitral leaflet into the left atrium may produce vibrations of the mitral valve leaflets and adjacent structures.
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PMID:[Systolic honk in mitral stenosis: a case report]. 384 6

Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.
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PMID:Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation. 395 62

Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.
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PMID:Morphologic features of the normal and abnormal mitral valve. 633 91

Cardiac involvement of mucopolysaccharidosis has not been well characterized by echocardiography. In this paper, we reported a case of Hunter syndrome with special reference to the noninvasive diagnosis of cardiac anomalies. A 21-year-old male of Hunter syndrome was referred to our noninvasive laboratory for the evaluation of his heart murmurs. He was strikingly dwarfed, 115 cm in height and 28 kg in weight, and had apparently Gargoyle-like facial appearance. Physical examination disclosed a mild funnel chest and a loud systolic murmur. Blood pressure was 98/56 mmHg and regular pulse rate was 100/min. The chest X-ray film revealed a shift of the heart to the left with a prominent pulmonary artery segment. There were no signs of pulmonary congestion. The electrocardiogram demonstrated right axis deviation, clockwise rotation and left atrial overload. In phonocardiograms, a basal ejection and an apical scratchy systolic murmurs were recorded. The latter was associated with a presystolic murmur and a loud first heart sound. A loud pulmonary second heart sound was also present. Outstanding findings were observed in the two-dimensional and M-mode echocardiograms, which showed remarkable thickening of both mitral valve leaflets with reduced opening. There was also generalized thickening of tricuspid and aortic valves, and endocardium of the free ventricular wall. Two leaflets of the tricuspid valve were visualized to prolapse, but the aortic valve motion appeared intact. In addition, echocardiograms revealed the dilatation of right-sided cardiac chambers and pulmonary artery, but the size of the left ventricle was rather small. Pulsed Doppler echocardiography demonstrated systolic turbulence in the right atrium in the vicinity of the tricuspid valve orifice. Stenotic turbulence was also recorded in the inflow tract of the left ventricle during diastole. Thus, the final diagnosis of predominant mitral stenosis associated with tricuspid valve prolapse and pulmonary hypertension was obtained. In conclusion, cardiac involvements in Hunter syndrome were precisely evaluated by noninvasive methods. Hunter syndrome may be considered as one of the etiologies producing mitral stenosis.
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PMID:[Echocardiographic manifestations of the heart in the Hunter syndrome: report of a case]. 682 Nov 4

Results of two-dimensional echocardiographic examinations were compared with angiographic, hemodynamic and surgical results in 44 patients with bioprosthetic valves in mitral and aortic positions who were undergoing elective or urgent reinvestigation 24 to 87 months (mean 34) after implantation. In these patients, there were 18 homograft aortic valves in the aortic position, 9 stent-mounted homograft aortic valves in the mitral position, 13 porcine xenograft valves in the mitral position and 12 in the aortic position. Poor cusp support, gross fluttering and prolapse of cusps behind or below the anulus identified aortic insufficiency by two-dimensional echocardiography in six patients with an aortic homograft and four patients were identified with insufficiency of a stent-mounted aortic homograft in the mitral position. Two-dimensional echocardiographic examination revealed mitral stenosis in three patients with a porcine xenograft valve in the mitral position and suggested mitral insufficiency in two others. Bacterial endocarditis on homograft or porcine xenograft valves was associated with easily imaged vegetations by two-dimensional echocardiography in 10 patients. Despite difficulties in imaging valve cusps, and the skill required to obtain good echocardiographic images of bioprosthetic valves, significant valve deterioration or infected prostheses were quite effectively imaged by two-dimensional echocardiography in this study.
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PMID:Detection of deterioration or infection of homograft and porcine xenograft bioprosthetic valves in mitral and aortic positions by two-dimensional echocardiographic examination. 687 8

The etiology and clinical significance of asynchronous relaxation of the left ventricle during isovolumic relaxation period was studied. Fifty patient with angina pectoris, 50 with myocardial infarction, 40 with normal heart, 20 with mitral stenosis and 10 with mitral prolapse syndrome were investigated. Asynchronous relaxation was observed in the following order: 72% in angina pectoris, 46% in myocardial infarction, 30% in mitral valve prolapse and 10% in both pure mitral stenosis and normal heart. In left anterior descending coronary artery disease, asynchronous relaxation was observed in 80%. Asynchronous relaxation seen before aortocoronary bypass graft to the left anterior descending coronary artery either disappeared or decreased after surgery. The contractility of the site, where asynchronous relaxation was seen, was normal in most cases and akinetic in none. The results of this study suggest the possibilities that asynchronous relaxation is at least partially related to localized myocardial ischemia and that it may be an early phenomenon of the effect of myocardial ischemia. With regard to asynchronous relaxation and hemodynamic alterations, force-velocity lissajous was analysed. Distortion of the lissajous in relaxation phase was seen in 73% who showed asynchrony. This distortion can be interpreted as indication of ununiformity of the left ventricular relaxation.
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PMID:Asynchronous relaxation of the ischemic left ventricle. 697 48


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