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

In this paper demographic characteristics, etiology, pathology and clinical features of infective endocarditis are reviewed simultaneous presentation of the data from our series of 50 cases with infective endocarditis. The peak incidence of infective endocarditis is between 11 and 15 years. Both sexes are equally affected. Patients with congenital or acquired heart disease tend to have hemodynamic trauma to the endocardium and vascular endothelium. These sites form the nidus for circulating bacteria of either spontaneous origin or the result of any oro-dental, genitourinary or other surgery or procedures and produce vegetations characteristic of infective endocarditis. The location of the vegetation is dependent upon the predisposing cardiac lesion. Embolic phenomenon is another cardinal feature of endocarditis and may occur in any organ system. Although a large variety of microbes have been known to cause endocarditis, streptococci and staphylococci remain the most frequent offenders. Clinical diagnosis of infective endocarditis is difficult because of the insidious onset and varied clinical features. A high degree of suspicion is essential for early diagnosis. Any patient with known heart disease and unexplained fever should be suspect for endocarditis. Splenomegaly, petechiae and embolic phenomena support this diagnosis. New or changing murmurs, splinter hemorrhages, Osler's nodes. Janeway's lesions and Roth's spots may be present. Elevated sedimentation rate, microscopic hematuria, leukocytosis with a shift-to-the-left and anemia may further support the diagnosis. Congenital or acquired heart disease and fever are all that will be present in many cases. Only isolation of the causative agent from the blood can confirm the diagnosis.
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PMID:Infective endocarditis: a review. I. Incidence, etiology, pathology and clinical features. 72 71

A growing amount of clinical and experimental evidence suggests a link between infection and atherosclerotic diseases including both myocardial and cerebral infarction. A prime example is a greatly increased risk of stroke in septicaemic patients with and without endocarditis. Controlled clinical studies have recently shown, however, that certain other milder bacterial infections are also a risk factor for infarction. A preceding febrile respiratory infection was a major risk factor for stroke in young and middle aged patients. In patients with acute myocardial infarction Chlamydia pneumoniae and dental infections seem to be risk factors according to one controlled clinical study. Several possible mechanisms could explain the observed association of infection and infarction. For instance, infection causes a hypercoagulable state which increases the risk of thrombosis. In addition, infection has profound and harmful effects on prostaglandin and lipid metabolism. Infection may also have some role in the atherosclerotic process itself by inducing damage and inflammation in vascular endothelium in the presence of hypercholesterolemia. So far, however, little clinical evidence is available to suggest that by controlling infection the risk of infarction or development of atherosclerotic lesions might be reduced except in patients with endocarditis, where the risk of thromboembolic complications rapidly diminished when the infection is controlled with antimicrobial therapy.
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PMID:Infection as a risk factor for infarction and atherosclerosis. 175 23

Since infective endocarditis may affect individuals without pre-existing valvar heart disease, and Staphylococcus aureus is the organism most commonly involved, the binding characteristics of S aureus to several components of normal vascular endothelium and subendothelium were studied. S aureus adhered specifically to endothelial monolayers (6.08(1.10)%; p less than 0.005), fibronectin (5.43(0.81)%; p less than 0.001), fibrinogen (7.13(1.43)%; p less than 0.001), and acid soluble calf skin collagen (2.38(0.90)%; p less than 0.001). S aureus also adhered specifically to Von Willebrand factor (1.62(0.28)%, p less than 0.001). Protein A containing (Cowan I) and deficient (Wood) strains of S aureus adhered similarly to all surfaces and substrates (NS). Escherichia coli adhered poorly. Immunofluorescence microscopy of preconfluent endothelial cells identified an extensive pericellular fibronectin network at regions of cell to cell contact. Light microscopy showed S aureus binding solely within these regions. Therefore, the ability of S aureus to infect valvar endothelium may be dependent on the presence of a fibronectin receptor. The existence of specific receptor for S aureus on the endothelial cell surface itself remains undetermined.
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PMID:Bacterial tissue tropism: an in vitro model for infective endocarditis. 328 1

It seems appropriate in a symposium dedicated to the examination of septicemia, that one of the topics for discussion should be the examination of the factors which allow circulating bacteria to adhere to intracardiac or vascular endothelium. In the last 10-12 years our understanding of the pathogenesis of this disease has increased markedly. This can be attributed to a large extent to the development by Dr Freedman and hist colleagues at Yale of reproducible, simple, inexpensive animal model of infective endocarditis. The purpose of this discussion will by to summarize studies aimed at helping to explain why bacteria stick to cardiac valves, what forms the stimulus for vegetation propagation, and some new idea for possible prevention of this event.
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PMID:Factors influencing the pathogenesis and prevention of infective endocarditis. 695 38

Arterial and venous thrombotic occlusions, migrating thrombophlebitis, pulmonary artery branches embolism, abacterial thrombotic endocarditis, paradoxal hemorrhages, thrombotic microangiography arising in patients with various malignant tumours are understood under hemostasiologic paraneoplastic syndrome. The following factors are at the basis of paraneoplasia pathogenesis: 1) procoagulants synthesis by tumour cells, namely tissue factor and activators of blood coagulation factor X; 2) procoagulant activity of tumour-associated macrophages and their activity in the extra- and intravascular conversion of fibrinogen into fibrin; 3) damage of vascular endothelium by tumour cells and cytokines, for example necrotizing factor of tumours; 4) multifactorial enhancement of thrombocyte aggregational properties. According to the current concepts, such neoplastic phenomena as metastasizing, uncontrolled growth, escaping from immunological control, secondary tumour changes are viewed through the disturbances of hemostasiologic balance.
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PMID:[Thrombosis and embolism as paraneoplastic syndrome]. 784 15

Approximately 40% of transforming growth factor-beta 1 null (knockout) mice generated in our laboratory develop normally to term, but 60% die in utero. The animals appear normal during the first 2 weeks of life but develop a rapid wasting syndrome and die by 3 to 4 weeks of age. All of the knockout mice have a multifocal inflammatory disease in many tissues. The heart and lungs are most severely affected. Increased adhesion of leukocytes to the endothelium of pulmonary veins is the initial lesion seen at day 8 postnatally and is soon followed by perivascular cuffing as well as inflammatory infiltrates in lung parenchyma. The lesions in the heart begin as endocarditis and then progress to myocarditis and pericarditis. Within the lung, chronic inflammatory infiltrates consist of T and B lymphocytes, including plasma cells, whereas macrophages are the primary inflammatory cell type in the heart. Increased expression of major histocompatibility complex class I and II proteins is seen in pulmonary vascular endothelium as early as day 8. An immunoblastic response in mediastinal and mandibular lymph nodes and spleen is also seen. In the absence of any pathogens, this massive inflammatory disease, together with overexpression of major histocompatibility complex class I and II proteins and overproduction of immunoglobulins by lymphocytes, offers circumstantial evidence for an autoimmune etiology.
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PMID:Transforming growth factor-beta 1 null mice. An animal model for inflammatory disorders. 785 32

We report two cases of Campylobacter fetus endocarditis. The first case involved a bicuspid native aortic valve in a 60-year-old woman, and the second involved a prosthetic aortic valve in a 76-year-old woman. No source of infection was identified in either case. Despite antibiotic therapy, hemodynamic deterioration necessitated valve replacement; both patients recovered completely. C. fetus is an uncommon cause of human infection but may be responsible for severe illnesses such as endocarditis and thrombophlebitis because of its tendency to attack the vascular endothelium. Review of the literature revealed 21 cases of endocarditis caused by this organism, usually involving the aortic valve. To our knowledge, there are only two reported cases of prosthetic valve endocarditis. Our second patient is the oldest one encountered so far with this condition.
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PMID:Campylobacter fetus endocarditis: two case reports and review. 801 32

Thrombin-induced platelet microbicidal protein (tPMP) exerts potent in vitro microbicidal activity against pathogens commonly found in the bloodstream, including Staphylococcus aureus, Staphylococcus epidermidis, and Candida albicans. Localized platelet release of tPMP may be important in defense against infections involving the vascular endothelium caused by tPMP-susceptible organisms. In contrast, pathogens capable of surviving in the presence of tPMP could then exploit the platelet as an adhesive surface for attachment to damaged endothelium. To examine these hypotheses, we derived a tPMP-resistant (tPMP(r)) C. albicans strain from its tPMP-sensitive (tPMP(s)) parental strains were equivalent in vitro as assessed by genotyping (electrophoretic karyotype and restriction endonuclease analysis of genomic DNA), biotyping, germination, platelet aggregation, adherence to vascular endothelial cells, and growth characteristics. In addition, the tPMP(r) phenotype was stable following multiple in vitro and in vivo passages. We then investigated the in vivo relevance of tPMP susceptibility on endovascular infection using a rabbit model of endocarditis and hematogenous dissemination. Rabbits with transaortic catheters (n = 15 in each group) were challenged with either the tPMP(s) or tPMP(r) C. albicans strain. All rabbits developed C. albicans-induced endocarditis, as determined by the presence of infected vegetations. In rabbits challenged with tPMP(s) strain (P < 0.001). These results were seen in the absence of differences in either initial adherence of strains to cardiac valves or vegetation weights. Furthermore, although these C. albicans strains induced equivalent rates and extent of hematogenous renal infection, only the tPMP(r) strain disseminated hematogenously to the spleen (15 of 15 rabbits) versus 0 of 15 [tpmp(s) strain]; P < 0.0001). Thus, tPMP(r) C. albicans caused more-severe endocarditis and produced greater metastatic sequelae than the tPMP(s) counterpart.
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PMID:Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis. 860 4

Like vascular endothelium, the EE plays a role in transendothelial transport, in coagulant and thrombotic processes, and in interactions with inflammatory cells. In addition, EE is involved in the modulation of cardiac performance of subjacent myocardium. EE dysfunction includes insufficient as well as excessive performance of any of its multiple functions. Dysfunction can progress from a disturbed modulation of myocardial performance and an imbalance in the release of growth factors to changes in EE cytoskeletal organization, with concomitant changes in transendothelial permeability, and in extreme cases, to loss of endothelial integrity and frank denudation. Structural and functional impairment of EE and of endocardial interstitial cells may be primary or secondary to the disease. Mechanical stress, various hormones and cytokines can initiate EE dysfunction. EE dysfunction may influence the development of cardiac failure in endo(myo)cardial fibrosis (Loeffler's endocarditis and carcinoid syndrome) and in dilated cardiomyopathy. Although Bouillaud, in 1836, was referring to endocarditis when stating: (quote: see text) his statement may presently find a much broader field of applicability in cardiology.
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PMID:Endocardial endothelial dysfunction and heart failure. 895 79

Twenty-four adults (average age 28 years) patients with congenital heart disease were examined; infective endocarditis was diagnosed in all of them by Duke criteria and was confirmed in 18 by surgery and/or pathology. Patients were divided into 2 groups. Group A was made up of 13 patients with left ventricular outflow obstruction, including ten with bicuspid aorta. Group B was made up of 11 patients with shunts (PDA or VSD), either isolated or associated with other abnormalities. The principal alterations associated with the infectious processes were trauma to the endocardium or vascular endothelium from accelerated turbulent flow (jet lesion) and valvular deformities. The principally transesophageal echocardiographic recordings showed infective vegetations on the four cardiac valves, mural endocarditis in both ventricles and right atrium, perivalvular abscesses and fistulae. The echocardiographic information aided in selecting the type of treatment in this group of patients with high intrahospital mortality (25%).
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PMID:[Transthoracic and transesophageal echocardiography in the study of adults with congenital cardiopathy and infectious endocarditis]. 981 Mar 66


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