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

We studied 27 Duchenne muscular dystrophy patients having spinal fusion for scoliosis. One patient died intraoperatively of cardiac arrest; all others have done well with no instances of malignant hyperthermia, postoperative ventilatory system dependence, pneumothorax, persisting infection, neurologic damage, nonunion, or pain. The anesthetic management included primarily intravenous general anesthetics with minimal myocardial depressant effects, avoiding succinylcholine and inhalation agents. Preoperative cardiac studies aided anesthetic management intra-operatively. There was an almost universal sinus tachycardia. Holter monitoring defined 4 of 16 with ventricular premature beats, 4 of 16 with atrial premature beats, and no ventricular tachycardia or atrial flutter or fibrillation. Echocardiogram demonstrated mitral prolapse in 2 of 22, frequent abnormal systolic performance with abnormal shortening fraction less than 28% in 7 of 16, and reduced rate-corrected velocity of fiber shortening in 9 of 15. Afterload was elevated in 7 of 15. The mean forced vital capacity (FVC) preoperatively was 45.3 +/- 15.9% with continuing diminution to 28.7 +/- 14.9% at 3.3 +/- 2.2 years after surgery. The main benefit of surgical stabilization is the relative ease and comfort of wheelchair seating compared with those nonoperated patients who develop progressive deformity. We have not seen lasting improvement or stabilization in FVC following surgery as decreasing function is related primarily to muscle weakness.
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PMID:Spinal fusion in Duchenne muscular dystrophy: a multidisciplinary approach. 158 53

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

A 23-year-old woman developed 3 degrees AV block with syncope. Insertion of a permanent pacemaker lead was followed by the onset of a persistent murmur in late systole preceded by single or multiple clicks. The murmur was best heard at the left sternal edge, grade 3-4/6 with two major frequencies (60-250 Hz), increased with inspiration and on assuming the erect posture. It was considered to be tricuspid in origin and related to interference of the tricuspid valve apparatus by the pacemaker lead resulting in tricuspid regurgitation. No tricuspid valve prolapse or flutter was seen on echocardiography. Withdrawal of the pacemaker lead resulted in immediate disappearance of the new auscultatory findings. Review of the literature suggests that the appearance of such a murmur following pacemaker insertion could be associated with later complications in relation to tricuspid valve dysfunction. It is therefore recommended that, under these circumstances, permanent pacemaker leads should be appropriately repositioned.
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PMID:Presumptive tricuspid valve malfunction induced by a pacemaker lead: a case report and review of the literature. 616 Apr 99

Among 160 patients with mitral-valve prolapse but no other illness there were 118 with cardiac arrhythmias. 30 had frequent or multifocal ventricular premature systoles, 21 had coupled ventricular extrasystoles, and seven had ventricular tachycardia. In six patients the prematurity index was under 1. Supraventricular premature systoles were registered in 56 patients, with seven each having paroxysmal atrial tachycardia and paroxysmal atrial flutter or fibrillation. Ventricular arrhythmias were significantly more frequent in late-systolic prolapse and with positive auscultation findings (systolic click or systolic murmur). Long-term ECG monitoring was more valuable than an exercise ECG. About half the patients with frequent arrhythmias had palpitations and rapid heart action. Coupled ventricular premature systoles and ventricular tachycardias, as well as R-on-T were relatively rare; our findings thus tend to suggest a relatively favourable prognosis for these arrhythmias.
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PMID:[Cardiac arrhythmias and their clinical significance in mitral valve prolapse]. 620 30

Various pathological changes of the mitral valve (MV) apparatus have been reported to be associated with ruptured chordae tendineae (RCT). We studied the clinical importance of echocardiographic examination to detect the etiology of RCT in 15 cases with patho-anatomical findings obtained. The commonly observed echocardiographic abnormalities were diastolic MV flutter (80%), systolic MV vibration (73%), flicky (or exaggerated) MV motion (73%), MV prolapse (47%), and abnormal systolic echoes in the left atrium (53%). Diastolic flicky motion of the MV was observed exclusively in the patients of bacterial endocarditis accompanied with MV vegetations. The main ruptured chordae of the MV were recognized as floating chordal echoes. MV prolapse was associated with myxomatous changes of the valve or multiple echoes chordae tendineae. These results show that M-mode and two-dimensional echocardiography may be predictive to evaluate the etiology of RCT.
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PMID:[Echocardiographic recognition of ruptured chordae tendineae: patho-anatomical evaluation of the diagnostic criteria]. 667 72

An echocardiographic finding presenting itself as a ruptured noncoronary aortic cusp is described. The basic finding included a constant diastolic echo separation of the right coronary and noncoronary cusps, noncoronary cusp prolapse in the direction of the posterior aortic wall and its high-frequency diastolic flutter. The diagnosis was confirmed at autopsy. The case study reaffirmed the clinical value of echocardiography which was the only technique, including the invasive ones, permitting to make an accurate morphological diagnosis.
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PMID:Echocardiography of ruptured aortic valvular leaflet. 742 81

Two cases of severe aortic regurgitation due to non-traumatic rupture of the aortic valve commissures are reported. The cause of rupture was hypertension in one patient, but it could not be identified in the other, where microscopic examinations of the aortic wall and the aortic cusps showed no particular pathologic changes. M-mode echocardiography revealed enlargement of the left ventricle, diastolic flutter of the anterior mitral leaflet and diastolic separation of the closure line of the aortic cusps in both patients. Two-dimensional echocardiography showed a downward displacement of the prolapsing motion of the aortic valve cusp during diastole toward the left ventricular outflow tract in one patient, and eccentricity of the coaptation point of the aortic valve without thickening of the cusps in the other. In addition to clinical features of progressive heart failure and characteristic cardiac murmur, echocardiographic studies provided correct diagnosis of aortic valve prolapse resulting from rupture of the aortic valve commissures. Both patients underwent aortic valve replacement successfully.
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PMID:Aortic regurgitation due to non-traumatic rupture of the aortic valve commissures: report of two cases. 774 98

The purpose of this study was to determine the most discriminating clinical and echocardiographic features that are most helpful in correctly identifying Ebstein's anomaly of the tricuspid valve from other causes of tricuspid regurgitation. Ebstein's anomaly is an uncommon malformation of the tricuspid valve with diagnostic echocardiographic features. Other cardiac disorders associated with tricuspid valve regurgitation and predominate right-sided heart chamber enlargement can be misdiagnosed as Ebstein's anomaly. All patients who were referred to our institution between 1982 and 1995 with the diagnosis of Ebstein's anomaly but were found to have other abnormalities of the tricuspid value or right ventricle were identified. Their clinical, echocardiographic, and surgical records were reviewed retrospectively. Twenty-two patients (12 males and 10 females), aged 7 to 68 years (mean 33 years), were referred to our institution with the diagnosis of Ebstein's anomaly but were found to have another abnormality that mimicked clinical and diagnostic features of Ebstein's anomaly. The most common initial symptom was exercise intolerance (13 [59%] patients) followed by atrial arrhythmia (seven [32%] patients). Two patients had cyanosis. Three patients had paroxysmal and six had chronic atrial fibrillation/flutter. Cardiomegaly on chest x-ray film was noted in 18 (82%) patients. Referral diagnosis of Ebstein's anomaly had been made by echocardiography (12 patients), cardiac catheterization (four patients), both techniques (five patients), and echocardiography and magnetic resonance imaging (one patient). All 22 patients had predominate right atrial and right ventricular enlargement, and 18 (82%) of 22 patients also had right ventricular dysfunction. However, Ebstein's anomaly was confidently ruled out with repeat comprehensive echocardiography at our institution by establishing (1) absence of significant apical displacement of the septal tricuspid valve leaflet (> or = 8 mm/m2) and (2) lack of a redundant, elongated, anterior tricuspid valve leaflet in all 22 patients (100%). All had significant tricuspid regurgitation caused by tricuspid valve dysplasia (nine patients), tricuspid valve prolapse (four patients), trauma (four patients), right ventricular dysplasia (three patients), endocarditis (one patient), and annular dilation caused by free pulmonary regurgitation (one patient). In all 15 patients who subsequently underwent surgery (tricuspid valve repair [seven patients] or replacement [eight patients]), the absence of Ebstein's anomaly was confirmed. Echocardiographic absence of the characteristic degree of displacement of the septal leaflet of the tricuspid valve (> or = 8 mm/m2) and the presence of a nonelongated, nonredundant anterior tricuspid valve leaflet consistently excluded the diagnosis of Ebstein's anomaly. Under such circumstances, other anomalies of the tricuspid valve or right ventricle were consistently identified. Recognition of the mimics of Ebstein's anomaly had important surgical implications.
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PMID:Mimics of Ebstein's anomaly. 932 9