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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For half a century the systolic click and late systolic murmur lay dormant as innocent auscultatory curiosities. The thirteen years since Barlow related these phenomena to mitral leaflet prolapse have witnessed an astonishing information explosion. We have sought to bring together the accumulated data in this review. An Historical Perspective traces the evolution from the now abandoned "pericardial" or "extracardiac" phases, through the leafletchordal phase (redundancy), the myocardial phase (segmental left ventricular contraction abnormalities), to the anular phase (dilatation and faulty systolic contraction). Functional Anatomy is dealt with in terms of pathology, pathophysiology, hemodynamics, angiocardiography, echocardiography, and physical and pharmacological interventions. Clinical Manifestations are concerned with prevalence, natural history, symptoms, physical signs, electrocardiographic abnormalities and roentgen fingings. The four Major Complications- sudden death, infective endocarditis, spontaneous rupture of chordae tendineae, and progressive mitral regurgitation- are examined. Associated Cardiac Diseases, i.e., Marfan's syndrome, ostium secundum atrial septal defect and atherosclerotic coronary artery disease, are discussed, and a section on Treatment deals chiefly with prophylaxis for infective endocarditis and the management of arrhythmias and chest pain. A final section on Evolving Information considers etiologic concepts, the nature of left ventricular contration abnormalities, the cause of chest pain, the relationship to Marfan's syndrome and ostium secundum atrial septal defect, and the effect of aging and sex differences on leaflet chordal redundancy.
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PMID:Mitral valve prolapse. 77 40

Mitral valve prolapse syndrome (MVPS) is the name given to the heart valve abnormality described by Barlow over two decades ago. This condition is of particular importance to the dentist as these patients are thought to be at risk of developing infective endocarditis with routine dental procedures which may cause gingival bleeding. This paper is an updated version of an article that originally appeared in the University of Toronto Dental Journal in 1990. In 1984, guidelines for antibiotic prophylaxis were provided by the American Heart Association (AHA). More current prophylactic regimens are also presented, with emphasis on the current recommendations of the AHA, recently published in December of 1990.
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PMID:Mitral valve prolapse: a review of the syndrome with emphasis on current antibiotic prophylaxis. 182 88

From 1969 to 1985, mitral valve repairs using Carpentier's technique were performed for acquired mitral valve incompetence. 72 patients required a reoperation 3 days to 13 years later (mean 5 +/- 3.5 years). The reoperation rate risk was dependent upon the etiology: Barlow 0.6 +/- 0.2% patient year, fibro-elastic deficiency 0.7 +/- 0.3, endocarditis 1.7% Rheumatic disease 4.6 +/- 1.4%. The risk of reoperation in Rheumatic disease is significantly higher (p less than 0.05) than in degenerative disease. The causes of failures could be categorized into two groups according to whether they are surgeon related or valve related: Group I, Prosthetic ring dehiscence or malposition 15%, anulus dilatation (when no ring was implanted) 4%, triangular resection of the anterior leaflet 4% residual prolapse 8.3%. Group II, Recurrent prolapse 16.6% valve stenosis 17%, leaflet retraction 35%. Failures in Group I can be reduced with "increased" experience as opposed to group II. At reoperation valve repair was possible in 15.3% of the cases whereas valve replacement was necessary in 84.7% with an overall operative mortality of 1.4%. We conclude that mitral valve repair in acquired mitral incompetence carries out a small risk of reoperation. Most of the repair failures are surgeon related in degenerative disease and valve related in rheumatic disease.
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PMID:Failures in reconstructive mitral valve surgery. 194 82

Since its original description by Barlow over a quarter of a century ago, mitral valve prolapse has become one of the commonest heart diseases around the world. It is commoner in women than men, in thinner than heavier subjects, and in younger than older persons. A unifying concept of a valvular-ventricular disproportion serves to explain the various conditions in which mitral valve prolapse occurs. The etiology of chest pain which is the most frequent symptom that brings the patient with mitral valve prolapse to a physician is multifactorial. Diagnosis of mitral valve prolapse is based on clinical grounds chiefly by careful auscultation. Echocardiography, angiocardiography, and radionuclide ventriculography are valuable adjuncts. Prognosis in the majority is excellent except when complications occur, such as progressive mitral regurgitation, infective endocarditis, cerebral ischemic episodes, and sudden death. For mitral valve surgery repair is preferred to replacement.
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PMID:Mitral valve prolapse: an overview. 267 3

Idiopathic mitral valve prolapse, also called Barlow's disease, has been estimated to affect 5 p. 100 of the general population. Normally a benign disease, it becomes life-threatening in only a very small number of cases. High risk subjects could be detected by simple TM-mode echocardiography, provided this examination is of good quality and reproducible, for it shows a 5 mm or more thickening of mitral leaflets. Should this be the case, according to the Mayo Clinic authors, serious complications, such as sudden death, infective endocarditis or ischaemic cerebral vascular accidents, would be expected to occur in 10 p. 100 of the patients. Sudden death, of which only 60 cases have been published, is exceptional; it mainly concerns young subjects (mean age 40 years), predominantly women, with a family history of sudden death, who have experienced one or several syncopes and present with severe per- or intercritical dysrhythmias. Such subjects must be regularly supervised clinically as well as by basal or ambulatory electrocardiography and, if necessary, by electrophysiological or even haemodynamic exploration. Treatment with appropriate beta-blockers or antiarrhythmic agents is often required as is, in refractory cases, implantation of an automatic defibrillator. Infective endocarditis is a cause of death in 10 to 20 p. 100 of the patients. It mainly threatens subjects whose mitral valve regurgitation is suspected on the presence of a holo- or end-systolic murmur and confirmed by Doppler echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Barlow's disease and risk for life]. 313 Aug 21

It is not easy to evaluate the prognosis of mitral valve prolapse. First of all, a positive diagnosis is difficult: the clinical insufficiencies are ill-compensated by sonocardiography as it is less reliable than expected; the very existence of the "mitral valve prolapse" described by Barlow is being challenged. Secondly, the most severe complications of mitral prolapse are rare, with respect to its frequency. Some complications are currently well defined. Thus, severe mitral insufficiency, leading to valve replacement, affects elderly men more than young women, although the pathological lesions correspond to the same disease. Endocarditis is rare and only occurs when there is an audible murmur. Rhythm disorders are varied, with however, frequent junction tachycardias and a marked influence of catecholamines, which may explain the clinical effectiveness of beta-blockers. Unfortunately, severe complications are not as well known. Thus, the risk of sudden death and cerebral vascular accident cannot be figured out from large statistical studies. Only studies of some so called "risk" sub-groups, should allow a better knowledge of these two complications and a more effective prevention.
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PMID:[Evaluation of the prognosis of mitral valve prolapse]. 332 56

Extensive calcification of the mitral valve anulus is a pathologic entity frequently associated with degenerative valvular disease. The calcification process remains localized to the anulus in 77% of the cases. It may extend, however, to the underlying myocardium. Whenever an operation is necessary for an associated valve insufficiency, the question arises whether it is preferable to repair or to replace the valve and how to manage the calcification. In the first part of this paper the pathology of this disease is studied, and in the discussion a mechanism is proposed to explain the development of the process of calcification. In the second part, a new operation is described, which comprises the temporary detachment of the leaflets, en bloc resection of the calcium deposit, annular reconstruction, and valve repair. For patients in whom the calcification extends to the myocardium a "sliding atrioplasty" of the left atrium is described, which allows the area of exposed muscular fibers to be covered. Between 1986 and 1994, among 68 patients with extensive calcification of the anulus and severe mitral valve insufficiency, 67 benefited from these repair techniques. Ages ranged from 18 to 82 years (mean 62 years). Thirty-two patients had a billowing mitral valve (Barlow), 27 a fibroelastic deficiency, and two Marfan's disease. The calcification involved more than one third of the anulus in 88% of the patients, the posterior anulus in 10.5%, and the whole anulus in 1.5%. The calcification process extended to the myocardial wall in 12% of the patients and to the papillary muscles in 4.5%. In the group of 67 valve repairs, there were two hospital deaths (2.9%), no instances of anulus dehiscence, and no early reoperations. The follow-up period extended from 4 months to 8 years (mean 3 years 8 months). There were two late deaths, 2 and 17 months after the operations, for an actuarial survival of 93% at 7 years. Late reoperation (6 to 62 months) was necessary in four patients (6.4%) for residual mitral valve incompetence (n=2), hemolysis (n=1), or endocarditis (n=1). In one of these patients a new repair was possible, whereas the three other patients required a valve replacement. All patients but one survived the reoperation. Actuarial freedom from reoperation was 87% at 7 years. All 60 patients with valve repair were reviewed for this study by clinical examination and echocardiography. All but one were in functional class I or II. There was no incompetence or trivial residual mitral valve incompetence in 55 patients and moderate incompetence in five. Two thromboembolic events have been recorded for a linearized rate of 1%/pt-yr. This study shows that complete anulus decalcification and valve repair can be done safely in patients with mitral valve insufficiency and extensive calcification of the anulus, even when the calcification process deeply involves the myocardium. It also demonstrates that an initially good result remained stable up to 7 years.
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PMID:Extensive calcification of the mitral valve anulus: pathology and surgical management. 861 32

Diagnosis of Whipple's disease is difficult, and thus its frequency is probably underestimated, particularly in culture-negative infective endocarditis. However, it must be systematically searched for in such a situation, first because it is associated with a poor natural outcome, and second because Tropheryma whipplei is not covered by the conventional empirical therapy recommended for culture-negative infective endocarditis. Whipple's disease endocarditis is usually associated with weight loss, intestinal and joint involvement. Nevertheless, it is sometimes the only manifestation of the disease, which makes the diagnosis much more difficult. We report the case of a 66-year-old patient with Barlow's disease, who underwent mitral valve replacement for severe mitral regurgitation. Vegetations were observed on the resected valve, both macroscopically and histologically. No microorganism was found at first. The diagnosis of Whipple's disease endocarditis was finally obtained by Polymerase Chain Reaction on valve tissue, and later confirmed by Periodic Acid Schiff staining. The outcome was favorable after a prolonged antibiotic therapy including doxycycline and hydroxychloroquine.
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PMID:[Infective endocarditis as the only manifestation of Whipple's disease: an atypical presentation]. 2127 53

Introduction: Mitral valve prolapse (MVP) is a common valve pathology with a spectrum of disease from isolated prolapse to myxomatous, multi-scallop Barlow's disease. The main complications relate to progression of mitral regurgitation, endocarditis, sudden death, and stroke. The timing of intervention in patients with asymptomatic severe mitral regurgitation is controversial. Areas covered: This article reviews the pathophysiology, genetics, clinical features, diagnostic imaging, complications, long-term outcomes, and indications for intervention in MVP. Expert commentary: Several key dilemmas in the management of MVP remain. Factors which influence progression of mitral regurgitation are unclear and therefore, we have no therapeutic targets to prevent progression. Evidence-based methods to reduce the risk of sudden death, stroke, and endocarditis have not been identified. In symptomatic patients with severe mitral regurgitation valve surgery is recommended. In asymptomatic patients, careful risk stratification incorporating markers of left ventricular dysfunction, atrial fibrillation, pulmonary hypertension, and valve reparability is required to identify the optimal timing of intervention.
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PMID:Mitral valve prolapse. 3048 38

We present a case of infective endocarditis caused by Streptococcus gordonii in an 11-year-old girl with Barlow's mitral valve disease. The differential diagnosis of rheumatic carditis and infective endocarditis was difficult as the patient fulfilled the Jones criteria. Vegetation on the mitral valve which became evident later in course of the disease and positive blood culture allowed diagnosing "definite" infective endocarditis.
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PMID:Streptococcus gordonii-associated infective endocarditis in a girl with Barlow's mitral valve disease. 3128 Jul 38


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