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

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

This study describes seven patients with the mitral valve prolapse or click-murmur syndrome who have survived one or more episodes of life-threatening ventricular arrhythmias. These arrhythmias include cardiac arrest due to ventricular fibrillation, recurrent ventricular tachycardia causing syncope or sustained ventricular tachycardia requiring electroversion. These patients were seen over a two-year period in a single medical center. Five of the seven had repolarization abnormalities in the resting electrocardiogram. Premature ventricular contractions were present in the routine resting electrocardiograms of six of the seven patients and were frequent during treadmill testing and ambulatory electrocardiographic monitoring in all six tested. There were electrolyte abnormalities or changes in medications known to affect myocardial repolarization during the week before the episode in three of the four patients with cardiac arrest. The diagnosis of mitral valve prolapse click-murmur syndrome was made prior to the episode of life-threatening arrhythmia in only two of the seven patients. Varying forms of antiarrhythmic therapy were given to these patients during follow-up periods of five to 26 months. Although the incidence of fatal arrhythmias in the mitral prolapse syndrome is probably small, we suggest that such arrhythmias may not be extremely rare, particularly among those patients who have repolarization abnormalities in the resting electrocardiogram and frequent premature beats. Patients with unexplained ventricular arrhythmias should be screened for mitral valve prolapse.
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PMID:Life-threatening arrhythmias in the mitral valve prolapse syndrome. 93 57

In a 14-month period mitral leaflet prolapse was diagnosed in 85 patients by echocardiography or cineangiography. Chest pain alone was the presenting complaint in 30 patients and linked with palpitation, dyspnoea, or syncope in 9. Eleven presented with major neurological disturbances (9 had transient ischaemic attacks), 10 with palpitation, 4 with undue and persistent fatigue, 2 with dyspnoea, and 2 with dizziness. Seventeen were referred not because of symptoms but because of clicks and murmurs. Overall, chest pain affected 61 patients and unless associated with coronary artery disease was not anginal. Palpitation was admitted by 42 patients; dizziness, lightheadedness, or paraesthesiae by 15, and syncope by 12. Systolic auscultatory abnormalities were noted in 69: 25 had single clicks, 3 had multiple clicks, 19 had both click(s) and murmur, and 22 had a murmur alone. Electrocardiography revealed ST segments flat for greater than 0-10 s in 21, prolonged QTc in 18, and T wave flattening or inversion in inferior limb and lateral chest leads in 14. The exercise stress test was abnormal in 13 of 27 patients. Mitral valve echograms showed definite mitral leaflet prolapse in 61, 'possible' prolapse in 14, and were normal in 8 patients with angiographic proof of mitral leaflet prolapse. Cardiac catheterization with left ventriculography showed prolapse of posterior mitral leaflet in 36, of both leaflets in 2, and left ventricular wall motion abnormalities in 16 cases. Selective coronary arteriography in 31 cases showed major vessel narrowing of larger than or equal to 80 per cent lumen diameter in 4, all with angina. This consecutive series indicates that the physical event of mitral leaflet prolapse is more common than hitherto appreciated, is priminently associated with non-anginal chest pain, palpitation, and neurological disturbances, and in 90 per cent of cases could be shown echocardiographically.
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PMID:Clinical features and investigative findings in presence of mitral leaflet prolapse. Study of 85 consecutive patients. 125 39

Systemic injection of monoclonal antibodies to neural acetylcholinesterase in rats causes permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensue. In sympathetic ganglia, cholinergic synapses disappear, but postganglionic adrenergic neurones remain structurally and functionally normal. Somatic motor and parasympathetic systems are also spared. This model of selective cholinergic autoimmunity is a new tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.
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PMID:Selective destruction of preganglionic sympathetic nerves by antibodies to acetylcholinesterase. 181 57

Systemic injection of monoclonal antibodies to neural acetylcholinesterase in adult rats caused a syndrome with permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensued. In sympathetic ganglia, acetylcholinesterase activity disappeared from neuropil but not from nerve cell bodies. Choline acetyltransferase activity and ultrastructurally defined synapses were also lost. Electrical stimulation of presynaptic fibers to the superior cervical ganglion ceased to evoke end-organ responses. On the other hand, direct ganglionic stimulation remained effective, and the postganglionic adrenergic system appeared intact. Motor performance and the choline acetyltransferase content of skeletal muscle were preserved, as was parasympathetic (vagal) function. This model of selective cholinergic autoimmunity represents another tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.
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PMID:Autoimmune preganglionic sympathectomy induced by acetylcholinesterase antibodies. 217 9

The usefulness of pacemaker treatment appears doubtful in patients suffering from syncope of unknown origin after a complete diagnostic evaluation, which includes electrophysiological study. To better assess the effectiveness of this therapy, 24 patients with syncope of unknown origin and negative electrophysiological study were prospectively and alternatively assigned to treatment with pacemaker (group A) vs treatment without pacemaker (group B). Group A included 12 patients (7 males, 5 females) with a mean age of 64 +/- 10 years. No heart disease was present in 7 cases (58%); 3 cases had chronic ischaemic heart disease (25%) and 2 had hypertensive heart disease (17%). The standard ECG was normal in 7 patients, while various conduction abnormalities were observed in the other 5. The mean number of syncopal episodes was 4.8 +/- 3.9 per patient, and the mean between the onset of symptoms and the beginning of this study was 32 +/- 42 months. In these 12 cases a VVI-M pacemaker was implanted, at a programmed rate of 50 or 60 bpm; in three subjects, the pacemaker was of the diagnostic type ("bradycardia event counter"). Group B included 12 patients (8 females, 4 males) with a mean age of 56 +/- 11 years. Organic heart disease was absent in 7 cases (58%); 4 patients showed hypertensive heart disease (33%) and 1 had mitral prolapse (9%). The ECG was normal in 9 subjects. The mean number of syncopes was 3.2 +/- 1.5 per patient; the mean interval since the onset of symptoms was 18 +/- 19 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Syncope of unknown origin after electrophysiologic study: is the treatment with pacemaker useful?]. 218 56

From 1978 to 1983, 111 patients with symptomatic internal hemorrhoids were treated as outpatients by a modification of the Barron ligation technique. Each ligated hemorrhoid was injected with a sclerosant. Follow-up, available for 94 of the patients, ranged from 2 to 60 months (mean 18 months). Presenting symptoms were bleeding in 75 (80%) of the 94 patients, pain in 46 (49%), pruritus in 22 (23%) and prolapse in 24 (26%). Results were excellent in 51 (54%) patients, good in 20 (21%) and fair in 9 (10%). Fourteen (15%) patients had unsatisfactory results; only 4 of these required hemorrhoidectomy. The other 10 had residual symptoms but did not require further treatment. Nine patients had minor complications, which included pain lasting 24 to 72 hours in seven, bleeding in one and syncope in one. The addition of sclerotherapy to traditional band ligation for the management of internal hemorrhoids has the advantages of exciting a greater inflammatory reaction between the mucosa and submucosa and preventing premature slipping of the band. The authors conclude that this method of therapy is effective for symptomatic hemorrhoids and that surgical hemorrhoidectomy is seldom indicated.
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PMID:Long-term follow-up of concomitant band ligation and sclerotherapy for internal hemorrhoids. 406 92

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

Ventricular beats are abnormal rhythms which are frequently detected by modern recording techniques in healthy subjects as well as in patients with heart disease. In the first case, analysis of the literature enables us to exclude any pejorative prognostic implication associated with V.E.B., in the absence of any major risk factor for coronary artery disease. However, when there is an underlying heart disease, a number of subgroups can be distinguished with a high risk of sudden death: coronary insufficiency associated with ischaemic cardiomyopathy, especially in the early post-hospital phase after a myocardial infarction; hypertrophic cardiomyopathy with ventricular tachycardia on the Holter monitor, family history of sudden death, personal past history of syncope; mitral prolapse with clinical symptoms and auscultatory signs; idiopathic long QT syndrome. In contrast, V.E.B.s do not appear to have prognostic significance in idiopathic hypokinetic cardiomyopathies and aortic valvular disease. In general, it is more the clinical setting than the actual morphology which determines the prognostic implications of ventricular extrasystoles. The sub-groups at high risk should be treated with anti-arrhythmics, but the evaluation of the effectiveness of such treatment remains uncertain and the authors believe that the development of studies of ventricular stimulation prior to and during treatment are justified.
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PMID:[Ventricular extrasystole: prognostic value and therapeutic indication]. 620 Nov 23

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


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