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)

A case of rhabdomyosarcoma of the left atrium and left ventricle demonstrated by echocardiography was reported. A 31-year-old man was admitted to our hospital for evaluation of recently developed exertional dyspnea. A holosystolic murmur and a protodiastolic sound were audible at the apex. A chest X-ray showed pulmonary congestion without cardiomegaly. The two-dimensional echocardiogram showed a dense stratified mass of echoes occupying the medial half of the left ventricular cavity, and a part of the abnormal mass of echoes was observed to move toward the left ventricular outflow tract during systole. Another small mass attached to the anterior mitral leaflet was also observed to prolapse partly into the left atrium during systole. The interatrial septum showed a thick and hard band of echo in the short-axis view. Right cardiac catheterization revealed pulmonary hypertension and the levogram of the pulmonary angiography showed left atrial and left ventricular filing defects. The repeated echocardiographic study showed the growth of the abnormal mass. The patient underwent operation, but he died of congestive heart failure thereafter. The necropsy diagnosis was rhabdomyosarcoma of the heart, involving the left atrium and left ventricle.
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PMID:[Rhabdomyosarcoma of the heart involving the left ventricle and left atrium]. 664 8

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

Although myasthenia gravis (MG) is frequently mentioned in standard textbooks and journal articles as a rare cause for pulmonary hypertension and right heart failure, no case can actually be found in the literature. The case described in this report is the first documented case of chronically decompensated MG manifesting itself as pulmonary hypertension, severe right heart failure, and functional prolapse of both the mitral and tricuspid valves. Interestingly, no hepatic biochemical abnormalities were present in spite of significant congestive hepatomegaly.
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PMID:Rare cardiopulmonary complications of chronically decompensated myasthenia gravis. 742 Apr 43

Between 1980 and 1993, 20 patients less than 1 year of age underwent operations for congenital mitral valve disease. Ten patients had congenital mitral incompetence and 10 had congenital mitral stenosis. Mean age was 6.6 +/- 3.4 months and mean weight was 5.6 +/- 1.5 kg. Atrioventricular canal defects, univentricular heart, class III/IV hypoplastic left heart syndrome, discordant atrioventricular and ventriculoarterial connections, and acquired mitral valve disease were excluded. Indications for operation were intractable heart failure or severe pulmonary hypertension, or both. Associated lesions, present in 90% of the patients, had been corrected by a previous operation in seven. In congenital mitral incompetence there was normal leaflet motion (n = 3), leaflet prolapse (n = 2), and restricted leaflet motion (n = 5). In congenital mitral stenosis anatomic abnormalities were parachute mitral valve (n = 4), typical mitral stenosis (n = 3), hammock mitral valve (n = 2), and supramitral ring (n = 1). Mitral valve repair was initially performed in 19 patients and valve replacement in one with hammock valve. Concurrent repair of associated lesions was performed in 12 patients. The operative mortality rate was zero. There were six early reoperations in five patients for mitral valve replacement (n = 4), a second repair (n = 1), and prosthetic valve thrombectomy (n = 1). One late death occurred 9 months after valve replacement. Late reoperations for mitral valve replacement (n = 2), aortic valve replacement (n = 1), mitral valve repair (n = 2), subaortic stenosis resection (n = 1), and second mitral valve replacement (n = 1) were performed in five patients. Actuarial freedom from reoperation is 58.0% +/- 11.3% (70% confidence limits 46.9% to 68.9%) at 7 years. After a mean follow-up of 67.6 +/- 42.8 months, 94% of living patients are in New York Heart Association class I. Doppler echocardiographic studies among the 13 patients with a native mitral valve show mitral incompetence of greater than moderate degree in one patient and no significant residual mitral stenosis. Overall, six patients have mitral prosthetic valves with a mean transprosthetic gradient of 6.2 +/- 3.7 mm Hg. These results show that surgical treatment for congenital mitral valve disease in the first year of life can be performed with low mortality. Valve repair is a realistic goal in about 70% of patients and possibly more with increased experience. Reoperation rate is still high and is related to complexity of mitral lesions and associated anomalies, but late functional results are encouraging.
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PMID:Surgery for congenital mitral valve disease in the first year of life. 781 93

The question of whether to repair or replace the mitral valve in the elderly remains unanswered. The purpose of our study is to describe our experience with mitral valve repair (MVR) using Carpentier's technique in patients 70 years and older. Fifty consecutive patients underwent MVR between 1984-1992. There were 30 female patients. All had 2 + or more mitral regurgitation (MR). The valve pathology included ischemic (n = 28), myxomatous (n = 7) and rheumatic (n = 6), leaflet prolapse (n = 11) and healed bacterial endocarditis (n = 3). The clinical findings included: myocardial infarction (n = 17), congestive heart failure (n = 18), atrial fibrillation (n = 14) and pulmonary hypertension (n = 10). The surgical technique involved placement of a Carpentier ring (n = 41) or Duran ring (n = 3), resection of leaflets (n = 9), shortening of the chordae (n = 8) and commissurotomy (n = 6). At surgery, coronary bypass was carried out in 32 patients while the aortic valve was replaced in five and repaired in one. Postoperative complications included atrial fibrillation (n = 14), transient neurologic events (n = 4), heart block requiring pacemaker (n = 3) and prolonged intubation (n = 4). Echocardiogram carried out postoperatively showed 2 + MR in three patients, 1 + in four, and a trace or none in the remaining (n = 39). No patient required re-operation for MR. Three patients (6%) died within 30 days after surgery due to low output (n = 1), malignant ventricular arrhythmia (n = 1) and heart block with cardiac arrest (n = 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitral valve repair in patients over the age of 70 years. 808 76

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

Atrial septal aneurysm is a localized "saccular" deformity, generally at the level of the fossa ovalis, which protrudes to the right or the left atrium or both. For 39 months we prospectively analyzed 205 consecutive patients in whom atrial septal aneurysm was diagnosed echocardiographically. The direction and movement of atrial septal aneurysms were carefully studied in multiple views, and, according to our findings, we now propose a new classification: type 1R if the bulging is in the right atrium only, type 2L if the bulging is in the left atrium only, type 3RL if the major excursion bulges to the right atrium and the lesser excursion bulges toward the left, type 4LR if the maximal excursion of the atrial septal aneurysm is toward the left atrium with a lesser excursion toward the right atrium, type 5 if the atrial septal aneurysm movement is bidirectional and equidistant to both atria during the cardiorespiratory cycle. We found an incidence of 1.9%, a mean age of 63 years (25 to 97 years), a female/male ratio of 2:1, valvular regurgitation 74%, hypertension 64%, left ventricular hypertrophy 38%, coronary heart disease 32%, patent foramen ovale 32%, pulmonary hypertension 31%, stroke 20%, dysrhythmias 16%, valvular prolapse 15%, and atrial septal defect 3%. No differences were found between mobile and motionless types of atrial septal aneurysm. However, differences were found between predominantly left bulging or right bulging atrial septal aneurysm (134 versus 57 patients), as well as other variables. All types of atrial septal aneurysm have particular clinical or echocardiographic characteristics. The new classification is a complete, simple, and practical form. Atrial septal aneurysm is associated with congenital and acquired heart diseases but also can present as an isolated abnormality.
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PMID:Atrial septal aneurysm: a new classification in two hundred five adults. 928 54

Serial changes in patients with isolated VSD during adolescence have not previously been investigated. Hemodynamic status, diameter of the defect, and growth were studied yearly in 106 children with VSD. The mean duration of the follow-up was 13.16 years and ranged in 80% of subjects from 7 to 19 years (1395 patients years). The mean ages at pre- and postpuberty were 8.62 and 16.67, respectively. The presented longitudinal study, in which losses due to death and operation were minimal (4%), ideally reflected the natural history of VSD. Although weight showed retardation during prepuberty, this lag was caught up by the end of adolescence. Stature showed no retardation in pre- and postpuberty. Cardiothoracic ratio decreased significantly from a mean of 0.48 to 0.44 and showed normal variation. Although the mean defect diameter at prepuberty was 5.33 mm, this decreased to 2.7 postpubertally. The individual decrease (1.7 +/- 2.34 mm) was significant (t = 5.349, p < 1/10(5)). The defect closed spontaneously in 24 (22.6%). In the 75 patients without pulmonary hypertension and with mild left-to-right shunting, 52 remained in the same class and spontaneous closure was observed in 23. In the 24 patients with moderate to severe left-to-right shunt, this decreased in 23 and only one remained stable. The 2 patients (1.9%) with Eisenmenger syndrome remained stable and 1 died. Aortic regurgitation developed in 10 patients (9.4%); however, this was of mild degree in most of them. No infective endocarditis was observed. It is concluded that patients with VSD should be followed closely through adolescence, because the diameter of the defect, as well as left-to-right shunting, can decrease, and it is concluded that the spontaneous closure of the defect is to be expected in a considerable 23%, and aortic prolapse or mild regurgitation may develop in approximately 10%.
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PMID:The natural course of isolated ventricular septal defect during adolescence. 956 19

Subarterial ventricular septal defect (VSD) is relatively common in Orientals. We reviewed the outcome of 214 patients (137 males) who were followed for 8.6 +/- 5.2 years (range 0.1 to 24.3) and addressed the issue regarding the necessity and optimum timing of closing subarterial defects before development of aortic valve deformities. Demographic data, transthoracic and transesophageal echocardiographic findings, cardiac catheterization results, and operative findings were reviewed. Kaplan-Meier actuarial analysis was performed to assess the development of aortic valve complications over time. Seventy-five patients with heart failure and pulmonary hypertension underwent surgical closure of VSD at the age of 2.4 +/- 2.9 years. No patient had aortic cusp prolapse before operation and none developed aortic cusp prolapse or aortic regurgitation (AR) on follow-up. In contrast, of the 139 asymptomatic patients managed conservatively, 102 (73%) developed aortic cusp prolapse, 78% of whom (80 of 102) developed AR. The prevalence of aortic cusp prolapse and AR at 1, 5, 10, and 15 years old was 8%, 30%, 64%, and 83%, and 3%, 24%, 45%, and 64%, respectively. Significant prolapse or AR prompted surgical closure of VSD with (n = 22) or without (n = 26) valvoplasty in 48 of 102 patients (47%). The size of the VSD was significantly larger in patients with heart failure (9.6 +/- 3.3 mm) or aortic cusp prolapse (11.7 +/- 4.1 mm) compared with those without heart failure (4.5 +/- 1.4 mm, p <0.001). All patients with aortic cusp prolapse and all but 1 with heart failure had a defect size of > or =5 mm. In conclusion, subarterial VSD of > or =5 mm should be closed as early as possible to prevent development of aortic cusp prolapse and AR. Asymptomatic patients with small defects <5 mm could be managed conservatively.
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PMID:Analysis of indications for surgical closure of subarterial ventricular septal defect without associated aortic cusp prolapse and aortic regurgitation. 1137 52

The timing of surgery in patients with chronic mitral regurgitation is a controversial issue. Left ventricular dysfunction progresses silently and is partly predictable; depressed left ventricular contractility sometimes accompanies a normal ejection fraction. Severe symptoms remain a clear recommendation for surgery. However several factors suggest that surgery should not be delayed until severe symptoms appear: impact on survival of ejection fraction < 60%, preoperative symptoms, and atrial fibrillation. Early surgery is justified in patients with degenerative mitral regurgitation independently of the type of lesion (prolapse of posterior, anterior or both the leaflets), because the addition of new techniques to the surgical armamentarium has neutralized prolapse of the anterior leaflet as an incremental risk factor for reoperation. In conclusion, early surgery is a reasonable treatment for low-risk patients with repairable valves and should be considered in asymptomatic patients with ejection fraction approaching the lower limit of normal, history of paroxysmal atrial fibrillation or pulmonary hypertension during exercise.
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PMID:Mitral regurgitation of degenerative etiology: should the timing of surgery be changed in the mitral valve repair era? 1261 Nov 20


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