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Query: UMLS:C0014118 (endocarditis)
 15,629 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

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Heart diseases as a cause of cerebral symptoms and syndromes]. 222 59

The patient was a 45-year-old female, who was emergently hospitalized with presyncope. Brain magnetic resonance imaging (MRI) confirmed an infarct in the left middle cerebral artery area. Echocardiography revealed mobile vegetations on the mitral valve and aortic valve, and the patient was diagnosed as having infective endocarditis. She was treated conservatively by appropriate antibiotic therapy. Four days after hospitalization, the patient developed brain hemorrhage due to ruptured mycotic cerebral aneurysm, and craniotomy for removal of the hematoma and brain aneurysm clipping were performed on the same day. As 3-dimensional computed tomography (3D-CT) obtained 2 weeks after the surgery suggested the existence of other brain aneurysms, it was determined that continued conservative management of the infection might not be feasible, and mitral valve and aortic valve replacements were performed 3 weeks after the craniotomy. The postoperative clinical course was satisfactory, without the complications of bleeding, aggravation of the cranial nerve disorders or recurrence of the infection. Ruptured mycotic cerebral aneurysms are usually associated with a poor prognosis. There are no specific guidelines for the treatment of infective endocarditis with brain complications like in this case, and it is important to select therapies tailored to individual cases.
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PMID:[Infective endocarditis complicated by ruptured mycotic cerebral aneurysm that necessitated open heart surgery after craniotomy;report of a case]. 2400 47