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

Fibrin is the primary constituent of the vegetation in infective endocarditis, and tissue factor expression is a major mechanism of coagulation activation on infected valves. To determine which cells may participate in coagulation activation in this setting, expression of procoagulant activity (PCA; shown to be tissue factor) was studied in cultured endothelial and stromal cells derived from human cardiac valves. Endothelial cells had negligible PCA (99 +/- 50 mU/10(5) cells, mean +/- 1 standard deviation) unless stimulated by lipopolysaccharide or interleukin-1, which increased PCA to 5,592 +/- 1,482 and 5,901 +/- 1,497 mU/10(5) cells, respectively, in 6 h. Incubation of cells with viable enterococci or viridans streptococci or with an enterococcal cell wall preparation did not induce PCA. Cultured valve stromal cells constitutively expressed high levels of PCA (14,276 +/- 8,738 mU/10(5) cells) which was not changed with exposure to interleukin-1. PCAs of stromal or stimulated endothelial cells from valves of both right and left sides of the heart were comparable. The results suggest that endothelial cells may contribute to fibrin deposition during infection if stimulated, but PCA is not directly induced by bacteria. Stromal cells could contribute PCA if exposed to blood in the course of valve injury.
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PMID:Effects of interleukin-1, lipopolysaccharide, and streptococci on procoagulant activity of cultured human cardiac valve endothelial and stromal cells. 249 62

The production of procoagulant activity, tissue factor-like, by human mononuclear phagocytes stimulated by Legionella microorganisms is here hypothesized as a key moment in the pathogenesis of Legionella prosthetic valve endocarditis.
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PMID:Production of procoagulant activity, tissue factor-like, by human mononuclear cells and its role in the pathogenesis of Legionella prosthetic valve endocarditis. 281 16

In vitro infection of cultured human cardiac valve endothelium (HCVE) with Staphylococcus aureus was used as a model to study potential mechanisms of vegetation formation in infective endocarditis. S. aureus was observed to adhere to and be ingested by HCVE. Infection for 8 h resulted in increased levels of procoagulant activity in HCVE, shown to be tissue factor by a specific assay. Mean activity in infected HCVE was 662 +/- 149 (mU/10(5) HCVE +/- 1 SD) versus 221 +/- 78 in control HCVE; surface-expressed activity was 57 +/- 25 in infected monolayers and undetectable (less than or equal to 10) in controls. Bacteria alone had no activity. These results suggest that endothelium may have a functional role in the pathogenesis of S. aureus endocarditis and may provide one potential mechanism for activating coagulation to initiate vegetation formation on a colonized cardiac valve.
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PMID:Staphylococcus aureus induces tissue factor expression in cultured human cardiac valve endothelium. 334 66

The pathophysiology of infective endocarditis comprises at least three critical elements: preparation of the cardiac valve for bacterial adherence, adhesion of circulating bacteria to the prepared valvular surface, and survival of the adherent bacteria on the surface, with propagation of the infected vegetation. It appears that circulating bacteria do not readily adhere to normal endothelial surfaces. Trauma to the valve, however, produces an alteration in the endothelial cells, leading to either disruption of the surface and deposition of platelets and fibrin, or other phenomena that render the surface susceptible to colonization by circulating bacteria. Once the surface is prepared, some bacterial strains appear to adhere to the fibrin-platelet matrix more avidly than others. The bacterial virulence factors that promote adherence are complex, but at least one, an extracellular polysaccharide (dextran), has been identified. Adherence can be blocked by antibodies directed against various surface structures. The survival of bacteria adherent to the surface of the vegetation appears to be complex as well, requiring resistance in situ to the bactericidal properties of complement and phagocytosis by white cells. In addition, vegetation propagation involves activation of the clotting cascade. For at least some streptococci, this occurs partly through perturbation of the valvular cells to produce tissue factor (tissue thromboplastin), which results in the deposition and growth of a fibrin-platelet clot over the rapidly growing bacterial colonies.
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PMID:Pathogenesis of endocarditis. 401 76

We examined the possible mechanisms of local initiation of coagulation in vegetation formation in enterococcal endocarditis by using a rabbit model. Contact activation and tissue factor expression by freshly excised aortic valves were assessed using assays developed for use with cultured cells. Bacteria alone lacked procoagulant activity and contact activation of plasma by excised valves did not occur. 4-d infected but not control valves expressed significant tissue factor activity (231 +/- 17 mU vs. 51 +/- 7 SE), which did not correlate with numbers of bacteria in vegetations. Tissue factor activity was also present in valves from rabbits infected for 1 and 2 d, as well as those from granulocytopenic and monocytopenic animals. Our findings suggest that tissue factor, expressed by host cells in response to infection, is a major stimulus for fibrin deposition in vegetation development.
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PMID:Tissue factor is a major stimulus for vegetation formation in enterococcal endocarditis in rabbits. 642 79

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

In order to produce infection, enterococci must be able to colonize host tissues, resist the host's non-specific and immune defence mechanisms and produce pathological changes. With regard to colonization of host tissues, adherence assays have shown that enterococci can attach to intestinal and urinary tract epithelial cells and heart cells by means of adhesins expressed on the bacterial surface. The expression of these adhesins by enterococci has further been shown to be affected by bacterial growth conditions. In addition, the adherence of Enterococcus faecalis to renal tubular cells in vitro is enhanced if the organisms produce aggregation substance, a proteinaceous surface material that aggregates donor and recipient bacteria to facilitate plasmid transfer. Bacterial growth conditions also affect the interaction of enterococci with polymorphonuclear leucocytes (PMNLs), with serum-grown organisms showing less association with PMNLs than organisms grown in broth. Efficient killing of enterococci by PMNLs in vitro requires the presence of serum complement proteins and is enhanced by anti-enterococcal antibodies. Enterococci produce a number of factors that may be associated with pathological changes in the host. Both sex pheromones and plasmid-encoded pheromone inhibitors produced by E. faecalis are chemotactic for PMNLs in vitro, and may mediate, at least in part, the inflammatory response often associated with enterococcal infection. E. faecalis may also produce a plasmid-encoded haemolysin, which is associated with increased severity of infection. In addition, enterococci are capable of inducing platelet aggregation and tissue factor-dependent fibrin production, which may be relevant to the pathogenesis of enterococcal endocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pathogenicity of enterococci. 792 3

We report 4 cases of Trousseau's syndrome, in which spontaneous recurrent or migratory venous thromboses, arterial emboli caused by nonbacterial thrombotic endocarditis, or both, develop in a patient with a recognized or occult malignant tumor. The clinical course of 3 of the patients emphasizes a key point: The occurrence for no known reason of thromboses preventable by anticoagulation therapy with heparin but not with warfarin sodium should alert a physician to focus diagnostic efforts on uncovering an underlying malignant lesion. Thromboses may occur months to years before the tumor is discovered, and a thorough negative initial examination does not obviate the need for a continuing search. Patients with Trousseau's syndrome have persistent low-grade intravascular coagulation, and therapy with heparin should be continued indefinitely. Stopping heparin therapy for even a day may permit a new thrombosis to develop. Immunostaining a biopsy specimen from 1 patient provided evidence that 2 properties of a neoplastic lesion are required for the syndrome to develop: The malignant cells express surface membrane tissue factor, and structural features of the tumor permit the malignant cells or vesicles it sheds to be exposed to circulating blood.
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PMID:Trousseau's syndrome. 831 22

High-altitude hypoxia causes a hypercoagulable state. In our previous study on the blood coagulation system in rats, nonbacterial thrombotic endocarditis (NBTE) developed after 4-12 weeks' exposure to the equivalent of 5500 m in altitude. We hypothesized that TF (tissue factor)-producing cells in the cardiac valves might be induced by the hypobaric hypoxic environment (HHE) and then trigger NBTE. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m altitude for 1-12 weeks. We measured TF activity in the plasma and studied morphological changes in the mitral valves using immunohistochemical and immunoelectrical methods for TF protein and in situ hybridization for TF mRNA. After 4 weeks or more of exposure to HHE, 28 of the 56 surviving rats had developed NBTE. After 4-8 weeks' exposure to HHE, the plasma TF activity level was significantly higher than in control rats. There was a significant correlation between plasma TF activity and the incidence of NBTE. After 1 weeks' exposure to HHE, immunoreactivity for TF protein was detected in foamy macrophages and stromal cells in the cardiac valves. In rats with NBTE, TF protein was present in foamy macrophages and spindle stromal cells and focally present in the extracellular matrix. TF mRNA was detected in some foamy macrophages within the thrombus, TF protein was localized to the rough endoplasmic reticulum and plasma membrane of many macrophages, some fibroblasts, and a few endocardial cells. TF is associated with the pathogenesis of the NBTE induced by exposure to HHE. The accumulation of TF-producing macrophages during exposure to HHE may be responsible for initiating thrombus formation.
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PMID:Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats. 980 40

Thrombosis is a common complication of malignancy. This is felt to be related to increased activity of the coagulation system as evidenced by markers of accelerated thrombin generation and increased platelet reactivity. Alterations in the hemostatic balance have been documented in patients with malignancy with increased tissue factor (TF) generation and the production of a cysteine protease. These can stimulate the coagulation mechanism via the extrinsic pathway and/or by activating factor X. The thrombotic presentations in malignancy are protean and may be venous or arterial. The underlying clinical pictures may be related to varying degrees of consumptive coagulopathy, microangiopathy, and nonbacterial endocarditis. Prophylaxis and management are, to a significant degree, dependent on the underlying malignancy and the prothrombotic mechanism. Specific agents and drugs must be selected from an expanding menu of options that includes unfractionated heparin, low-molecular-weight heparin (LMWH), warfarin, plasma apheresis, and the newer antithrombin agents.
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PMID:Thrombosis and cancer. 1086 23


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