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

It has been hypothesized that mitral valve prolapse may account for a substantial number of patients who have symptoms of chronic anxiety neurosis. In a previous investigation, this hypothesis was confirmed in eight of 21 patients who had anxiety neurosis. In the present investigation, we reevaluated the hypothesis that persons with anxiety neurosis have impaired exercise ability by exercising 20 of the anxiety neurotics according to a standard treadmill exercise protocol. Compared with the control group, the anxiety neurotics required less exercise to achieve an equivalent heart rate and therefore their estimated maximum oxygen consumption was less, thus confirming the hypothesis. However, this difference was due entirely to the anxiety neurotics with mitral valve prolapse, and those without prolapse did not differ significantly from the controls. This suggests that impaired exercise tolerance in anxiety neurotics may be attributable to a subgroup of these patients with mitral valve prolapse.
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PMID:Exercise and anxiety neurosis: comparison of patients with and without mitral valve prolapse. 44 18

The conditions associated with prolapse of the posterior leaflet of the mitral valve are multiple. The mechanisms of mitral valve prolapse as well as the pathogenesis of pain and ectopic impulse formation are reviewed. Propranolol appears to be the drug of choice for the symptomatic treatment of patients with this syndrome since it decreases myocardial oxygen demand and wall tension thus reducing or abolishing the discrepancy between myocardial oxygen demand and supply within the mitral apparatus. It has also been reported to modify the auscultatory findings associated with this condition. The frequency of this mitral valve abnormality in patients with obstructive coronary artery disease is reviewed. It appears that prolapse of the posterior leaflet scallops in patients with significant obstructive coronary artery disease represents an intermediate stage before mitral insufficiency occurs. This group of patients with papillary muscle dysfunction includes those with prolapsed leaflets without mitral insufficiency, those with systolic murmurs and compensated heart failure and others with progressive cardiac decompensation and severe mitral regurgitation.
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PMID:Mitral valve prolapse. Recent concepts and observations. 93 60

Four patients with ptosis, external ophthalmoplegia, and ragged-red fibers on muscle biopsy were found to have decreased ventilatory responses to hypoxia and hypercapnia. Respiratory muscle weakness was not responsible for these findings since these responses were normal in muscle disease control patients. An altered metabolic state also can cause diminished ventilatory response, but overall oxygen consumption data in the ragged-red fiber patients were normal. The decreased ventilatory responses may be clinically significant because two of the ragged-red fiber patients had episodes suspicious of hypoventilation with poor response to hypoxia.
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PMID:Depressed ventilatory response in oculocraniosomatic neuromuscular disease. 94 69

Lung function and clinical evidence of muscle weakness were assessed in 12 ASA I patients who received vecuronium 0.01 mg kg-1 pretreatment as a part of their anaesthetic management, before and 3 min after pretreatment. Most patients demonstrated ptosis and diplopia, while five of the 12 were unable to raise the head for > 4 s and had difficulty in swallowing. Significant reductions occurred in forced vital capacity, forced expiratory volume in 1 s, and maximum mid-expiratory flow rate. Among static lung volumes, functional residual capacity and expiratory reserve volume decreased significantly. However, these changes were not serious enough to cause clinically significant impairment of coughing or a decrease in oxygen saturation in any patient.
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PMID:Lung function after vecuronium pretreatment in young, healthy patients. 135

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70

The fuel preference of human muscle mitochondria has been given. Substrates which are oxidized with low velocity cannot be used to detect defects in oxidative phosphorylation. After general anaesthesia, the oxygen uptake with the different substrates is much lower than after local analgesia. The latter was therefore used in the subsequent study. In 15 out of 18 patients with ocular myopathy, defects in oxidative phosphorylation could be detected in isolated muscle mitochondria prepared from freshly biopsied tissue. Measurement of the activity of segments of the respiratory chain in homogenate from frozen muscle showed no, or minor defects. In two of these patients showing exercise intolerance, decreased oxidation of NAD(+)-linked substrates and apparently normal mitochondrial DNA, further study revealed deficiency of pyruvate dehydrogenase in a girl with ptosis and a high Km of complex I for NADH in a man. Both patients responded to vitamin therapy.
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PMID:Oxidative phosphorylation in human muscle in patients with ocular myopathy and after general anaesthesia. 211 84

A case of hemihypertrophy associated with multiple anomalies of the skin, bone and visceral organs is presented. A 31-year-old female was admitted for evaluation of her skin conditions. Her family history is noncontributory, while her past history discloses operations for syndactyly of the right foot, tonsillar hypertrophy, anal prolapse and ovarial cyst. Erythemas of the face and the left upper extremity were noticed during the neonatal period and hypertrophy of the right side of the body started at age 2 months. On admission, hemihypertrophy was observed in the face, trunk and extremities. Multiple faint nevi flammei were seen on the right half of the face and on the left side of the trunk and extremities. Telangiectasis and nevus anemicus were seen in the upper chest. The left upper extremity showed diffuse brown patches that was histologically basal pigmentation with some giant melanosomes. Visceral anomalies consisted of fibromatous tumors of the tip of the tongue and mitral prolapse. Angiography and computed tomography revealed a possible arteriovenous malformation of the right occipital region, small hemangiomas around the patella, dilation of the lateral ventricle, and calcification of the choroid plexus. Tortuous superficial veins were noted in the right leg. She had no seizure, but her IQ was 68. The bone disorders consisted of scoliosis, short forth metacarpus, hypoplastic mandible and peroneal exostosis. Examination revealed a slight diminution of urinary corticosteroid, but no other endocrinological disorders were found. The hemihypertrophy in this case is at least partially due to an arteriovenous shunt, suggested by elevated oxygen saturation of the blood obtained from the internal saphenous vein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congenital hemihypertrophy associated with cutaneous pigmento-vascular, cerebral, visceral and bone abnormalities]. 282 Feb 92

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

Thirty-three patients with prolonged fetal bradycardia (fetal heart rate baseline less than 100 bpm for a minimum of 3 minutes or less than 80 bpm for at least 2 minutes) in labor were studied. They were treated with a bolus injection of terbutaline if the bradycardia persisted at less than 80 bpm for 2 minutes and other efforts to improve the fetal heart rate (oxygen, positional changes) had failed. After the bolus injection a scalp blood pH (or a cord arterial pH in abdominal deliveries) was obtained within 30 minutes. Fetal acidosis was common if the bradycardia lasted 10 minutes or more, particularly if the rate was less than 80 bpm with a flat baseline for 4 minutes or more. The fetal heart rate improved after injection in 30 cases; 23 patients had vaginal delivery of infants in good condition. Ten underwent cesarean section: three for no improvement in fetal heart rate, two for cord prolapse, four for later ominous fetal heart rate, and one for failure to progress. These results suggest that tocolysis in selected cases can be of benefit for the fetus with prolonged bradycardia. In cases with an ominous fetal heart rate pattern preceding the bradycardia and in abruptio placentae immediate operative intervention without delay is probably better. Administration of terbutaline should be regarded as a temporary measure until it is apparent that the fetal heart rate has recovered. Preparation for emergency delivery should be made while a recovery is awaited.
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PMID:Single injection of terbutaline in term labor. I. Effect on fetal pH in cases with prolonged bradycardia. 407 56

Continuous monitoring of fetal scalp tissue pH (tpH), acid base and oxygenation measurements of the blood of the umbilical artery and vein, and APGAR scoring was performed in 152 deliveries. The effect of cord complication on tpH (120, 90, 60, 30, 15, 10, 5, and 0 minutes before delivery), the status of the umbilical artery and vein (pH, pCO2, base excess, standard bicarbonate, pO2, and oxygen saturation), and the APGAR scores (one and five minutes after delivery) were investigated. Thirty-two per cent of the deliveries were associated with on or more cord complication(s). Cord complications in general did not influence the APGAR scores, the acid base state, or the oxygenation of the fetus and newborn. In the very few cases of tight cord complication(s) tpH showed a marked decrease during the last 30 minutes of labour, the umbilical blood was slightly acidotic, but the APGAR scores were normal (8-10 one and five minutes after delivery). No cases of prolapse of the cord were found. Cord complications are very common but in most cases completely harmless.
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PMID:The influence of cord complications on fetal pH, neonatal Apgar score, and the acid base state and oxygenation of the umbilical artery and vein. 725 49


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