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)

Twenty-six patients with Wolff-Parkinson-White (WPW) syndrome were studied by echocardiography. They were classified into the following WPW types: anterior right ventricular pre-excitation (Type I) - six patients; posterior right ventricular pre-excitation (Type II) - six patients; posterior left ventricular pre-excitation (Type III) - fourteen patients. Twenty-three patients were in WPW at the time of study. Four patients with Type I WPW had abnormal systolic motion of the interventricular septum: three paradoxical and one flat. Patients with Type II and Type III WPW had no septal motion abnormalities related to pre-excitation. Three patients had intermittent WPW, Type III; in all three only minor changes in normal septal motion were apparent on WPW beats. Associated cardiac abnormalities were evident in six patients: two mitral prolapse (one Type II WPS and one Tpe III); one idiopathic hypertrophic subaortic stenosis (Type III); one congestive cardiomyopathy (Type III); one hypertrophic nonobstructive cardiomyopathy (Type I); and one atrial septal defect (Type II). We conclude that abnormal interventricular septal motion may occur with Type I WPW abnormality. Other abnormalities are detectable by echocardiography in a high proportion of WPW patients, but do not appear to be associated with any single Wolff-Parkinson-White type.
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PMID:Echocardiography in Wolff-Parkinson-White syndrome. 13 57

To estimate frequency of the posterior mitral valve leaflet prolapse in routinely performed left ventriculography, 1000 consecutive ventriculograms of the right anterior oblique projection were analyzed. A group of patients consisted of 511 women and 489 men at mean age 46,5 years. Clinical diagnosis of heart lesions, myocardial disease, pulmonary hypertension or arrhythmias were indications for hemodynamic studies. In the investigated group of patients, there were no patients with clinical diagnosis of the coronary artery disease. Prolapse of the posterior mitral valve leaflet was diagnosed in 59 patients. Idiopathic mitral valve prolapse was diagnosed in 10 patients. Prolapse of the posterior mitral valve leaflet was most frequent in atrial septal defect (16.6%), myocardial lesion (12.5%), and after mitral commissurotomy (8.9%). Posterior mitral valve leaflet prolapse is not a frequent anomaly in routinely performed left ventriculography. Relatively often occurrence of the mitral valve prolapse in atrial septal defect and only occasional in the aortic lesions and dilated cardiomyopathy seems to point out at a role of the left ventricle size in pathogenesis of this syndrome.
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PMID:[Mitral valve prolapse detected during hemodynamic studies]. 210 30

Heart disease is the most important nonobstetric cause of maternal death; however, most young women with heart disease do well during pregnancy. If the physician is uncertain of the effects of pregnancy on a particular heart condition, needless restrictions may be imposed. The main hazards are: pulmonary edema when it occurs suddenly in mitral stenosis; pulmonary hypertension (because pulmonary vascular disease tends to be exacerbated by pregnancy); infective endocarditis (this is rare); and fulminating peripartum cardiomyopathy. The practical management of the pregnant patient with various concomitant heart conditions (congenital heart disease, pulmonary hypertension, rheumatic heart disease, anticoagulants and artificial valves, constrictive pericarditis, kyphoscoliosis, Marfan's syndrome, mitral prolapse, hypertrophic cardiomyopathy, dilated cardiomyopathy, infective endocarditis, and arrhythmias) is discussed. An absolute indication for therapeutic abortion is severe pulmonary vascular disease; discretionary indications include 'chronic thromboembolic pulmonary hypertension,' cardiomyopathies (depending on the hemodynamic disturbance), and Marfan's syndrome.
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PMID:Cardiovascular disease in pregnancy. 218 16

We have used cross-sectional real time color-coded Doppler echocardiography to characterize the patterns of the regurgitant jet seen in mitral valvar disease of different etiologies. We studied 118 patients with mitral regurgitation due to rheumatic valve disease (n = 26), hypertrophic obstructive cardiomyopathy (n = 22), dilated cardiomyopathy (n = 35) and prolapse of the leaflets of the mitral valve (n = 35). We analyzed the origin, spatial distribution, extent and duration of the regurgitant jet. A semiquantitative grading system was used to evaluate the extent of the jet by measuring its maximal area and the duration of regurgitant flow. Typical flow patterns could be observed in hypertrophic obstructive cardiomyopathy, (in which the crescent shaped jet was elongated in midsystole and directed posteriorly) in dilated cardiomyopathy (in which oval shaped jets were observed throughout systole) and in prolapse of the leaflets (in which early or late systolic regurgitant jets occurred with an eccentric "drop-like" pattern, being directed posteriorly in patients with a prolapse of the aortic leaflet and anteriorly in those with a prolapse of the mural leaflet of the valve). A large variety of patterns was found in rheumatic disease due to the individual deformation of the leaflets. A comparison of the measured area of the jet revealed no significant differences between regurgitation caused by rheumatic valve disease and dilated cardiomyopathy. The regurgitation in 80% of these patients was of moderate to severe degree. In contrast, regurgitation due to prolapse of the leaflets or hypertrophic obstructive cardiomyopathy appeared to be of mild to moderate degree in 90% of cases.
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PMID:Flow patterns of mitral regurgitation due to different etiologies: analysis by color-coded Doppler echocardiography. 272 90

The clinical and echocardiographic features of right atrial thrombi were examined in 9 patients, 5 men and 4 women aged 16 to 86 years. The 2D echocardiographic diagnosis was confirmed at autopsy (4 cases) or by the association of severe recurrent pulmonary embolism (5 cases). Three patients had associated ischaemic heart disease and on patient had dilated cardiomyopathy. The clinical presentation was: acute cor pulmonale (5 cases including 2 patients which biventricular myocardial infarction), chronic post-embolic cor pulmonale (1 case), tricuspid valve obstruction (1 case), general ill health with pyrexia (1 case) and heparin-induced thrombocytopenia (1 case). Predisposing factors included: absence of anticoagulent therapy (7 cases), previous supraventricular arrhythmias (2 cases) and right ventricular failure (6 cases, including 2 of right ventricular infarction). In 2 patients the thrombi were relatively immobile and had a wide base of implantation on the interatrial septum; in 1 patient, multiple thrombi were observed lining the right heart cavities from the inferior vena cava to the pulmonary infundibulum. In the other 6 patients, the thrombi were very mobile with a visible pedicule of implantation (2 cases) or totally free (4 cases). The variable polylobulated appearances, completely irregular whirling motion and intermittent prolapse into the tricuspid valve were characteristic features of the latter 4 cases. They disappeared spontaneously (2 cases) or after fibrinolytic therapy (2 cases) in under 36 hours. Three patients were operated with one postoperative death. The global hospital mortality was 22%. The present occasional detection of right atrial thrombosis will certainly become more common if patients with pulmonary embolism, right ventricular infarction or deep venous thrombosis are systematically examined by 2D echocardiography in the acute phase of their illness.
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PMID:[Clinical, echocardiographic and evolutive aspects of right atrial thrombosis]. 308 12

Fifty-three patients (34 who had diffuse scleroderma, and 19 who had CREST syndrome [calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias]) were studied by noninvasive procedures, including resting electrocardiogram (ECG), continuous 24-hour Holter ECG monitoring, M-mode echocardiography, and 2-dimensional echocardiography. Only 22 patients (42%) had abnormalities such as conduction defects, supraventricular or ventricular arrhythmias, or ST-T changes detected on resting ECG. In contrast, using Holter monitoring, the number of conduction abnormalities seen increased from 10 to 16 patients and transient ST-T changes increased from 2 to 18 patients. Forty-eight patients had ventricular arrhythmias, with multiform ventricular premature beats in 21 (40%), pairs of runs of ventricular tachycardia in 15 patients (28%), and 1 or more runs of ventricular tachycardia in 7 (13%). Echocardiography detected asymmetric septal hypertrophy in 10 patients, impaired ventricular function in 9 patients, congestive cardiomyopathy in 2, mitral prolapse in 4, and pericardial effusion in 3 patients. Multiform and/or repetitive ventricular premature beats occurred more frequently in patients with echocardiographic abnormalities, but were also present in patients who had normal findings on echocardiographic examination. Cardiac involvement was not correlated with clinical variants of scleroderma (CREST syndrome or diffuse scleroderma), nor with other signs and symptoms of the disease. Thus, cardiac involvement is found much more frequently than would be expected from clinical symptoms or from results of resting ECG alone; therefore, Holter monitoring and echocardiography should be included in the routine workup of patients who have scleroderma.
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PMID:Noninvasive evaluation of cardiac dysrhythmias, and their relationship with multisystemic symptoms, in progressive systemic sclerosis patients. 406

In six patients with clinically unsuspected right atrial thromboemboli the diagnosis was made with two-dimensional echocardiography. Five patients had pulmonary emboli, and one had systemic embolization. Three patients had congestive cardiomyopathy, two with tricuspid regurgitation; of the remaining three, one had cor pulmonale complicated by tricuspid regurgitation, one had thrombophlebitis and one had no discernible cardiac illness. Four patients had dizziness or syncope, four had dyspnea, three had chest pain, three had hypotension and tow had cyanosis. Five patients were treated with thrombolytic or anticoagulant therapy, or a combination of the two. In three patients, surgical removal of the thrombus was undertaken because of recurrent pulmonary emboli or tricuspid regurgitation, or both, and progressive right heart failure. The thromboemboli were removed in all three, but one patient died. On two-dimensional echocardiography, four of the six patients' thromboemboli were snake-like, unattached to the right atrium and prolapsed freely across the tricuspid valve into the right ventricle in diastole and back into the right atrium in systole. The other two patients' thromboemboli were attached to the right atrium and did not prolapse across the tricuspid valve. Our cases, together with a review of other reports, suggest that right atrial thromboemboli: 1) can be accurately diagnosed by two-dimensional echocardiography; and 2) result from two different pathophysiologic mechanisms developing a) in situ, either on a foreign body or secondary to reduced cardiac output, or b) as a result of an embolus from systemic vein thromboses.
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PMID:Right atrial thromboemboli: clinical, echocardiographic and pathophysiologic manifestations. 649 Oct 71

In a 46-member kindred with consanguineous ancestry, eight progeny in two generations had congestive cardiomyopathy and markedly elevated urinary taurine levels (range, 411 to 536 mg per gram of creatinine [normal +/- S.D., 89 +/- 32]). Ten other family members had late or holosystolic mitral-valve prolapse, and elevated urinary taurine values (range, 215 to 265 mg). In two with mitral-valve prolapse, congestive cardiomyopathy eventually developed while the amounts of urinary taurine doubled. One member with mitral-valve prolapse died suddenly; histologic examination revealed myocardial fibrosis in the papillary muscles and myocardial taurine values of 16.9 +/- 3.0 mumol per gram of protein (normal +/- S.E., 33.2 +/- 3.6). Four other family members with congestive cardiomyopathy had myocardial fibrosis at autopsy or biopsy and mean myocardial taurine levels of 9.2 +/- 2.2 mumol. We conclude that hypertaurinuria and depressed levels of taurine in the myocardium may be associated with one type of mitral-valve-prolapse syndrome and a rapidly progressive form of congestive cardiomyopathy.
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PMID:Decreased myocardial taurine levels and hypertaurinuria in a kindred with mitral-valve prolapse and congestive cardiomyopathy. 634 48

Two-dimensional echocardiographic examination was performed to investigate pathophysiological mechanism of mitral regurgitation due to papillary muscle dysfunction in 6 patients with myocardial infarction (anterior : 3, inferior: 2 and subendocardial: 1) and 13 patients with dilated cardiomyopathy. The patients were divided into 2 groups; Group I was 9 with mitral valve prolapse and Group II was 10 without mitral valve prolapse (MVP). In Group I MVP was observed in the posterior leaflet in 6 and in both leaflets in the remainder. The apical four-chamber view of all patients in Group II showed that the point of mitral valve coaptation displaced toward the apex of the left ventricle during systole and the both mitral leaflets were convexed toward the left ventricle. Follow-up observation in a patient with dilated cardiomyopathy revealed that the heart was not enlarged (CTR 50%), no murmur was heard and mild anterior mitral leaflet prolapse was observed in 1979, but, in 1981, CTR became 63%, and a grade IV systolic murmur suggesting mitral regurgitation was noted. Two-dimensional echocardiography revealed that mitral leaflets became convex toward the left ventricle and coaptation point of the mitral closure shifted to the apex of the left ventricle below the level of mitral annulus. Thus, the transition to Group II from Group I was suggested. Echocardiographic measurements revealed that left ventricular end-diastolic dimension was 71 +/- 11 mm in Group I and 74 +/- 10 mm in Group II, left ventricular end-systolic dimension was 61 +/- 11 mm in Group I and 62 +/- 11 mm in Group II, and anterio-posterior mitral ring dimension was 31 +/- 3 mm in Group I and 35 +/- 3 mm in Group II (p less than 0.05). In conclusion, it was suggested that two mechanisms of mitral regurgitation are present in papillary muscle dysfunction; 1) mitral valve prolapse and 2) shift of mitral coaptation point toward the apex of the left ventricle associated with marked dilatation of the mitral annulus.
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PMID:[Two-dimensional echocardiographic findings of patients with papillary muscle dysfunction]. 711 89

In light of the nonspecificity of left ventricular angiography and physical examination, and the limitations of M-mode echocardiography to define the presence of mitral valve prolapse syndrome, we evaluated left ventricular longitudinal and apical four-chamber tomographic views of cross sectional echocardiography in 19 subjects with normal left ventricular cineangiography and in 5 patients with congestive cardiomyopathy. None had auscultatory findings suggestive of mitral valve prolapse syndrome. In all 24 control subjects, the apical view demonstrated the coaptation point and the leaflets of the mitral valve to lie inside the left ventricular cavity. A retrospective analysis of 900 consecutive cross sectional echocardiographic studies revealed 105 subjects with no evidence of structural heart disease other than the presence of the mitral valve leaflets in the left atrium in systole defining the existence of idiopathic mitral valve prolapse syndrome. Both mitral leaflets were prolapsed in 90 percent of the involved populations, and the apical tomographic cross sectional echocardiographic view was superior to the left ventricular longitudinal view for the detection of anterior leaflet prolapse. These data suggest that the apical cross sectional view may be the single best technique to define the presence of idiopathic mitral valve prolapse syndrome.
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PMID:Apical cross-sectional echocardiography. Standard for the diagnosis of idiopathic mitral valve prolapse syndrome. 744 1


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