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 frequency and significance of mitral valve prolapse (MVP) were assessed in 35 patients with idiopathic ventricular tachycardia (VT) (12 with sustained VT and 23 with nonsustained VT). They were classified as MVP and non-MVP groups according to their results of two-dimensional echocardiography. The frequency and characteristics of MVP in idiopathic VT, symptoms during VT, QRS configurations on electrocardiogram during VT, and induction of VT in electrophysiologic study were evaluated. MVP was recognized in 12 (34.3%) of 35 patients with idiopathic VT, all of whom had mild prolapse of the anterior leaflet. The frequency of MVP in patients with sustained VT was higher than that in patients with nonsustained VT (58.3% vs 21.7%, p < 0.05). Of all the symptoms during VT, palpitation was most frequently observed in the MVP group (66.7%), while no characteristic symptom was observed in the non-MVP group. This symptomatic difference was considered to be attributable to different patterns of VT duration. QRS configurations during VT showed monomorphism in all patients. The right bundle branch block pattern was dominant in the MVP group (91.7%), while the left bundle branch block pattern was prominent in the non-MVP group (69.6%) (p < 0.01), suggesting that VT mainly originated in the left ventricle in the MVP group and in the right ventricle in the non-MVP group. The induction rate of VT by programmed ventricular stimulation was higher in the MVP group (58.3%) than in the non-MVP group (34.8%) (p < 0.07) and was considerably higher in patients with sustained VT (75.0%) than in patients with nonsustained VT (26.1%) (p < 0.01). However, there was no significant difference in the induction rates between patients with sustained VT in the MVP and non-MVP groups. The difference in the VT induction rates between the 2 groups may be related to other factors besides the duration of VT. In conclusion, the incidence of MVP was relatively high in patients with idiopathic VT, and the difference of the clinical and electrophysiologic characteristics of idiopathic VT may depend on whether MVP is present or not.
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PMID:[Mitral valve prolapse in idiopathic ventricular tachycardia: clinical and electrophysiologic characteristics]. 184 22

Since 1977, six patients (five males and one female), aged 14 to 35 years, resuscitated from ventricular fibrillation, were referred to our department for detailed evaluation, after exclusion of major cardiac pathologic conditions. Four patients had a family history of heart disease. Basic ECGs showed sinus rhythm in all of them. PR interval was prolonged in one. Two patients had complete and one had incomplete right bundle branch block. One patient had inverted t waves in V1-3 and late potentials. Three had an upsloping ST-T segment elevation in V1-2. The cardiothoracic index was less than 0.5 in five and 0.50 in one. In one of the five patients studied, the clinical episode of ventricular fibrillation was reproduced by stimulation of the right ventricular outflow tract during electrophysiologic study. Results of cross-sectional echocardiography and angiography showed predominantly structural and wall motion abnormalities of the right ventricle in five patients and slight wall motion abnormalities of the left ventricle in two. Two patients also had mitral and tricuspid valve prolapse. Coronary arteries were normal in all five patients examined. Results of endomyocardial biopsy showed no abnormalities in one patient, fibrosis in two, and fibrolipomatosis in one. Two patients died during follow-up: autopsy was performed in one and results showed right ventricular cardiomyopathy. Thus in five of these selected patients with apparent idiopathic ventricular fibrillation, some abnormalities, predominantly of the right ventricle, were documented only after detailed investigation; however, clinical history and some nonspecific ECG abnormalities were factors in the diagnostic procedure.
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PMID:Ventricular fibrillation without apparent heart disease: description of six cases. 258 61

Tricuspid regurgitation due to nonpenetrating trauma occurred in a 60-year-old male patient who had received chest trauma in a motorcycle accident. He was admitted because of shortness of breath and palpitation on exertion. On admission physical examinations revealed pulsated and dilated jugular veins, hepatomegaly, and systolic murmur. The chest X-ray film showed an enlarged heart and electrocardiograms revealed complete right bundle branch block. Echocardiography demonstrated systolic prolapse of the tricuspid anterior leaflet into the right atrium. Right atrial v wave pressure was 20 mmHg. Tricuspid valve replacement with a Carpentier-Edwards 33 mm using super interpose method was performed successfully 13 years after the trauma. At operation, it was found that the chordae tendineae of the anterior leaflet was ruptured.
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PMID:[A case of traumatic tricuspid regurgitation]. 259 6

A 40-year-old man was admitted to our hospital in May 1982 for evaluation of a heart murmur. A standard 12-lead electrocardiogram (ECG) showed an abnormal Q wave in lead III. Echocardiography revealed prolapse of the anterior mitral valve leaflet (MVP), but neither dilatation nor wall motion abnormalities of the left ventricle (LV) were observed. Thallium-201 scintigraphy revealed an abnormal thallium uptake at the apex and inferior wall. He had no episode of acute myocardial infarction or myocarditis, but complete right bundle branch block suddenly appeared, and he was hospitalized in October 1984. He had no coronary artery lesions, and only mild mitral regurgitation on left ventriculography. The motion of the interventricular septum and apex was reduced on echocardiography and a persistent perfusion defect was observed at the inferior wall and the interventricular septum on T1-201 scintigraphy. In December 1985, he experienced an Adams-Stokes attack due to complete atrioventricular block. Echocardiographically, the left ventricle became enlarged and the wall motion abnormality and a perfusion defect on T1-201 scintigrams were of relatively severe degree. Thus, left ventricular dilatation and wall motion abnormality may progress in some cases of MVP as it did in this one. We consider this case a very interesting one in speculating on the relationship between MVP and DCM.
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PMID:[Regression of mitral valve prolapse to a state masquerading as dilated cardiomyopathy: a case report]. 350 16

Idiopathic congestive (dilated) cardiomyopathy with an autosomal dominant inheritance pattern affected eight individuals (four males) in three of four generations of a 63-member kindred of non-consanguineous ancestry. Average age at presentation was 39.5 years (range 32-54). A malignant course with relentless cardiac failure occurred in six cases; one member who died suddenly had been asymptomatic and the eighth is alive but in cardiac failure 44 months after initial presentation. Average time course to death from onset of symptoms suggestive of cardiomyopathy in six affected members was 16 months (range three to 55 months). In three cases, sudden death occurred and was the mode of presentation in one. Myocardial histological examination, available from three cases, showed variation in muscle fibre size with interstitial fibrosis. Forty-two family members in two generations including the propositus (19 males), age range three to 46 years (mean 17.9) when first assessed were prospectively evaluated. Two had basal systolic murmurs and two had right bundle branch block. Excluding the propositus, three members showed Doppler echocardiographic evidence of regurgitation without associated structural anomalies and three had valve prolapse with Doppler echocardiographic evidence of regurgitation. Cardiac chamber dimensions were within normal limits in all members and no cardiac arrhythmias were seen. Among the various therapeutic approaches now available cardiac transplantation, especially in younger patients with unremitting disease, is a potential option which should be considered.
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PMID:Familial idiopathic congestive cardiomyopathy in three generations: a family study with eight affected members. 368 46

Double-chambered right ventricle is an uncommon congenital anomaly consisting of obstruction of the trabecular zone of the ventricle by an elevated, hypertrophied moderator band, with or without additional muscle bundles(s). During an 18 month period (August 1984 to February 1986) 12 patients underwent repair of double-chambered right ventricle. Their ages ranged from 13 months to 12 years (mean 4.4 years). Associated lesions were ventricular septal defect in 11 patients (three closed spontaneously), atrial septal defect in two, left superior vena cava in three, aortic valve prolapse in one, and mild subaortic stenosis in two. Right ventricular outflow tract gradients were from 30 to 165 mm Hg (mean 77.2 +/- 37.3 mm Hg). The initial six patients (Group 1) were treated in the "classical" manner with a right ventriculotomy for muscle resection and ventricular septal defect closure (4/6). All patients survived. Five of the six required pharmacologic support for signs of mild to moderate right ventricular failure. The right ventricular outflow tract gradient postoperatively was 0 mm Hg in five patients and 25 mm Hg in one patient. Oxygen saturations were checked in the right atrium and pulmonary artery in all six patients, and one patient had a step-up of more than 10%. In the next six patients (Group 2) a previously unreported right atrial-pulmonary artery approach was used to avoid a ventriculotomy. The right ventricular outflow tract gradient was 0 mm Hg in five patients and 5 mm Hg in the sixth. A ventricular septal defect was closed in four of the six patients. There were no deaths, and no patient required inotropic support. Follow-up has been from 2 to 20 months. There have been no late deaths, and all patients are asymptomatic. One patient in Group 1 still has signs of a residual ventricular septal defect at 1 year. No patient has echocardiographic evidence of right ventricular outflow tract obstruction. All patients have remained in sinus rhythm with right bundle branch block. No patient has been recatheterized. Repair of double-chambered right ventricle is easily performed without a ventriculotomy. The atrial exposure of the ventricular septal defect is excellent. The muscle bundle(s) can be visualized easily through an initial transverse pulmonary arteriotomy with completion of resection through the tricuspid valve.
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PMID:Surgical repair of double-chambered right ventricle with or without ventriculotomy. 382 Nov 48

The authors report 2 cases of myocardial infarction with normal coronary arteries occurring at an interval of 2 months in 2 brothers aged 32 and 34. Following an episode of angina, the younger brother, a sportsman, but a smoker, developed an antero-septal infarct at rest, which was complicated by complete persistent right bundle branch block. Ventriculography and coronary angiography were normal. Induced spasm tests were not performed. The elder brother presented an infero-apico-lateral infarct on effort, without any prodromal syndrome, which was complicated by apical akinesia. Ventriculography revealed mitral prolapse. Coronary angiography was normal and the methylergometrine test was negative. In relation to this example of familial infarction with normal coronary vessels, the authors review the features of this type of infarction reported in the literature which predominantly occurs in young people. They discuss the principal points of interest, including the incidence, the criteria of definition based on the coronary angiography, the elements of the prognosis, the pathophysiological mechanisms and the possibility of a genetic predisposition.
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PMID:[Myocardial infarction with normal coronary vessels in young subjects. Apropos of 2 cases with an interval of 2 months in 2 brothers aged 32 and 34]. 400 92

35 patients with mitral valve prolapse (MVP) underwent investigation by Holter monitoring with computerised analysis. Ventricular arrhythmias were observed in 70% patients with MVP. There does not seem to be a close correlation between the severity of the arrhythmia and the degree of prolapse. The mechanisms of the ventricular arrhythmia are variable: two patients had the necessary criteria for ventricular reentry, at least six had parasystolic foci, protected or not from the sinus rhythm. The most severe ventricular arrhythmias are characterised by their variable morphology (but usually showing right bundle branch block), a clear diurnal rhythm, the inducing role of exercise or emotion and a greater diurnal variation of the sinus rhythm suggesting increased sympathetic tone. The results of beta blockade are better in the patients with the most marked diurnal rhythms.
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PMID:[Ventricular arrhythmias and mitral valve prolapse. A study of 35 cases]. 677 43

A case of severe tricuspid insufficiency with ruptured chordae tendineae due to nonpenetrating major chest trauma caused by a car accident is described. Electrocardiographic signs of complete right bundle branch block and olosystolic murmur were present and not observed before. Transthoracic echocardiography showed a significant prolapse of the septal tricuspid leaflet with severe tricuspid regurgitation and severe right heart overload, which progressively worsened. Transesophageal echocardiography confirmed the transthoracic echocardiographic findings. It also demonstrated the presence of ruptured chordae tendineae and the coexistence of a severe prolapse of the tricuspid anterior leaflet with flail movement. Although the patient remained asymptomatic, these findings prompted us to refer the case to the surgeon. The patient underwent valvuloplasty with excellent late result. In presence of traumatic tricuspid insufficiency the use of transesophageal echocardiography can be helpful to optimize the anatomic evaluation of the valvular apparatus allowing adequate therapeutic decision.
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PMID:[Tricuspid insufficiency with rupture of the chordae tendineae caused by closed thoracic trauma: evaluation by transesophageal echocardiography. Description of a case]. 808 75

A 32-year-old woman developed chronic progressive hearing impairment, trunkal ataxia, bilateral ptosis and external ophthalmoplegia. She also showed slowly progressive mild to moderate proximal dominant muscle weakness and atrophy. ECG showed incomplete right bundle branch block. An aerobic exercise test showed abnormal blood lactate elevation and muscle biopsy revealed ragged-red fibers in addition to the myopathic change. Analysis of mitochondrial DNA extracted from biopsied muscle and fibroblast samples revealed a 1,758bp deletion from the cytochrome b to ND6 coding regions. Common mutations in tRNALeu(UUR) coding region to the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) were not present. She was diagnosed as having incomplete Kearns-Sayre syndrome (KSS). Since the age of 35, she developed complex partial seizure attacks with secondary generalization frequently and at the age of 42, she had a severe generalized seizure with delayed consciousness loss followed by left hemiplegia. MRI showed wide T2-high signal lesions in the right temporo-parieto-occipital area. The proton MR-spectroscopy showed prominent increase of lactate beyond the lesions detected by MRI, indicating diffuse aerobic metabolic dysfunction in the central nervous system. We reviewed two other KSS cases with a stroke like episode, who also had epilepsy and large deletion but no tRNALeu(UUR) mutation, in mitochondrial DNA. Patients with KSS who have seizure may develop the stroke-like episode as seen in MELAS patients.
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PMID:[A case of incomplete Kearns-Sayre syndrome with a stroke like episode]. 940 43


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