37 resultados para endocarditis


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Background:The applicability of international risk scores in heart surgery (HS) is not well defined in centers outside of North America and Europe.Objective:To evaluate the capacity of the Parsonnet Bernstein 2000 (BP) and EuroSCORE (ES) in predicting in-hospital mortality (IHM) in patients undergoing HS at a reference hospital in Brazil and to identify risk predictors (RP).Methods:Retrospective cohort study of 1,065 patients, with 60.3% patients underwent coronary artery bypass grafting (CABG), 32.7%, valve surgery and 7.0%, CABG combined with valve surgery. Additive and logistic scores models, the area under the ROC (Receiver Operating Characteristic) curve (AUC) and the standardized mortality ratio (SMR) were calculated. Multivariate logistic regression was performed to identify the RP.Results:Overall mortality was 7.8%. The baseline characteristics of the patients were significantly different in relation to BP and ES. AUCs of the logistic and additive BP were 0.72 (95% CI, from 0.66 to 0.78 p = 0.74), and of ES they were 0.73 (95% CI; 0.67 to 0.79 p = 0.80). The calculation of the SMR in BP was 1.59 (95% CI; 1.27 to 1.99) and in ES, 1.43 (95% CI; 1.14 to 1.79). Seven RP of IHM were identified: age, serum creatinine > 2.26 mg/dL, active endocarditis, systolic pulmonary arterial pressure > 60 mmHg, one or more previous HS, CABG combined with valve surgery and diabetes mellitus.Conclusion:Local scores, based on the real situation of local populations, must be developed for better assessment of risk in cardiac surgery.

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1.-Since the parietal endocarditis represents a chapter generally neglected, owing to the relative lack of cases, and somewhat confused because there various terms have been applied to a very same morbid condition, it justifies the work which previously we tried to accomplish, of nosographic classification. Taking into account the functional disturbances and the anatomical changes, all cases of parietal endocarditis referred to in the litterature were distributed by the following groups: A-Group-Valvulo-parietal endocarditis. 1st . type-Valvulo-parietal endocarditis per continuum. 2nd. type-Metastatic valvulo-parietal endocarditis. 3rd. type-Valvulo-parietal endocarditis of the mitral stenosis. B-Group-Genuine parietal endocarditis. a) with primary lesions in the myocardium. b) with primary lesions in the endocardium. 4th type-Fibrous chronic parietal endocarditis (B A Ü M L E R), « endocarditis parietalis simplex». 5th type-Septic acute parietal endocarditis (LESCHKE), «endocarditis parietalis septica». 6th type-Subacute parietal endocarditis (MAGARINOS TORRES), «endocarditis muralis lenta». 2.-Studying a group of 14 cases of fibrous endomyocarditis with formation of thrombi, and carrying together pathological and bacteriological examinations it has been found that some of such cases represent an infectious parietal endocarditis, sometimes post-puerperal, of subacute or slow course, the endocardic vegetations being contamined by pathogenic microörganisms of which the most frequent is the Diplococcus pneumoniae, in most cases of attenuated virulence. Along with the infectious parietal endocarditis, there occur arterial and venous thromboses (abdominal aorta, common illiac and femural arteries and external jugular veins). The case 5,120 is a typical one of this condition which we name subacute parietal endocarditis (endocarditis parietalis s. muralis lenta). 3.-The endocarditis muralis lenta encloses an affection reputed to be of rare occurrence, the «myocardite subaigüe primitive», of which JOSSERAND and GALLAVARDIN published in 1901 the first cases, and ROQUE and LEVY, another, in 1914. The «myocardite subaigüe primitive» was, wrongly, in our opinion, included by WALZER in the syndrome of myocardia of LAUBRY and WALZER, considering that, in the refered cases of JOSSERAND and GALLAVARDIN and in that of ROQUE and LEVY, there are described rather considerable inflammatory changes in the myocardium and endocardium. The designation «myocardia» was however especially created by LAUBRY and WALZER for the cases of heart failure in which the most careful aetiologic inquiries and the most minucious clinical examination were unable to explain, and in which, yet, the post-mortem examination did not reveal any anatomical change at all, it being forcible to admit, then, a primary functional change of the cardiac muscle fibre. This special cardiac condition is thoroughly exemplified in the observation that WALZER reproduces on pages 1 to 7 of his book. 4.-The clinical picture of the subacute parietal endocarditis is that of heart failure with oedemas, effusion in the serous cavities and passive chronic congestion of the lungs, liver, kideys and spleen associated, to that of an infectious disease of subacute course. The fever is rather transient oscillating around 99.5 F., being intersected with apyretic periods of irregular duration; it is not dependent on any evident extracardiac septic infection. In other cases the fever is slight, particularly in the final stage of the disease, when the heart failure is well established. The rule is to observe then, hypothermy. The cardiac-vascular signs consist of enlargement of the cardiac dullness, smoothing of the cardiac sounds, absence of organic murmurs and accentuated and persistent tachycardia up to a certain point independent of fever. The galloprhythm is present, in most cases. The signs of the pulmonary infarct are rather expressed by the aspect of the sputum, which is foamy and blood-streaked than by the classic signs. Cerebral embolism was a terminal accident on various cases. Yet, in some of them, along with the signs of septicemia and of cardiac insufficiency, occurred vascular, arterial (abdominal aorta, common illiac and femurals arteries) and venous (extern jugular veins) thromboses. 5. The autopsy revealed an inflammatory process located on the parietal endocardium, accompanied by abundant formation of ancient and recent thrombi, being the apex of the left ventricle, the junction of the anterior wall of the same ventricle, with the interventricular septum, and the right auricular appendage, the usual seats of the inflammatory changes. The region of the left branch of HIS’ bundle is spared. The other changes found consist of fibrosis of the myocardium (healed infarcts and circumscribed interstitial myocarditis), of recent visceral infarcts chiefly in lungs, spleen and brain, of recent or old infarcts in the kidneys (embolic nephrocirrhosis) and in the spleen, and of vascular thromboses (abdominal aorta, common illiacs and femurals arteries and external jugular veins), aside from hydrothorax, hydroperitoneum, cutaneous oedema, chronic passive congestion of the liver, lungs, spleen and kidneys and slight ictericia. 6. In the subacute parietal endocarditis the primary lesions sometimes locate themselves at the myocardium, depending on the ischemic necrosis associated to the arteriosclerosis of the coronariae arteries, or on an specific myocarditis. Other times, the absence of these conditions is suggestive of a primary attack to the parietal endocardium which is then the primary seat of the lesions. It matters little whatever may be the initial pathogenic mechanism; once injured the parietal endocardium and there being settled the infectious injury, the endocarditis develops with peculiar clinical and anatomical characters of remarkable uniformity, constituting an anatomo-clinical syndrome. 7.-The histologic sections show that recent lesions…

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1 – A close inquiry into 6700 post mortem examinations reveals amongst them 589 cases of endocarditis which, as causa mortis, thus concur with an 8.82% score. 2 – As to their etiology, the endocarditis cases are classified in: Rheumatic E………………417cases or 6.22% of the necropsies; Syphilitic E……………….106 cases or 1.58% of the necropsies; Malignant E………………….66 cases or 0.98% of the necropsies . 3 – With the exception of the cases of syphilitic endocarditis, or aortic endocarditis connected with syphilitic changes, as well as of malignant (bacterial) endocarditis, 417 cases of rheumatic endocarditis are left which constitute 6.22% of the total amount of the post mortem examinations and 70.79% of the endocarditis cases. 4 – As to their anatomical location, the cases of rheumatic endocarditis are distributed as follows: Valvular E………..396 cases or 94.96% of the endocarditis cases; Mural E………..21 cases or 5.04% of the endocarditis cases; 5 – As to valvular changes, the following location was observed: Mitral E…………….156 cases or 39.39%; Aortic E……………120 cases or 30.30%; Tricuspid E…………10 cases or 2.51%; Pulmonary E…………2 cases or 0.50%; Mitral-aortic E……….88 cases or 22.22%; Mitral-tricuspid E………….10 cases or 2.51%; Mitral-tricuspid-aortic E…………9 cases or 2.27%; Mitral-tricuspid-pulmonary E………….1 cases or 0.25%. 6 – As to sex, 59.21% are males and 40.70% females. As regards mitral endocarditis, the incidence for both sexes is practically one and the same (49.55% of males and 50.47% of females), whilst as regards aortic endocarditis 74.16% of males and 26.84% of females are affected by. 7 – As to colour: White……..50.24% of the cases; Black……………28.50% of the cases; Brown……………21.25% of the cases. 8 – As to nationality: Brazilians…………81.86% of the cases; Aliens…………..18.13% of the cases. 9 – As to age: 0 to 10 years…………7 cases, 51 to 60 years……57 cases; 11 to 20 years……..33 cases, 61 to 70 years……51 cases; 21 to 30 years……..64 cases, 71 to 80 years……..21 cases; 31 to 40 years……..79 cases, 81 to 90 years……1 cases; 41 to 50 years…………58 cases, 91 to 100 years……..2 cases.

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Bartonellae are fastidious Gram-negative bacteria that are widespread in nature with several animal reservoirs (mainly cats, dogs, and rodents) and insect vectors (mainly fleas, sandflies, and human lice). Thirteen species or subspecies of Bartonella have been recognized as agents causing human disease, including B. bacilliformis, B. quintana, B. vinsonii berkhoffii, B. henselae, B. elizabethae, B. grahamii, B. washoensis, B. koehlerae, B. rocha-limaea, and B. tamiae. The clinical spectrum of infection includes lymphadenopathy, fever of unknown origin, endocarditis, neurological and ophthalmological syndromes, Carrion's disease, and others. This review provides updated information on clinical manifestations and seroepidemiological studies with an emphasis on data available from Brazil.

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Coxiella burnetii is the agent of Q fever , an emergent worldwide zoonosis of wide clinical spectrum. Although C. burnetii infection is typically associated with acute infection, atypical pneumonia and flu-like symptoms, endocarditis, osteoarticular manifestations and severe disease are possible, especially when the patient has a suppressed immune system; however, these severe complications are typically neglected. This study reports the sequencing of the repetitive element IS1111 of the transposase gene of C. burnetii from blood and bronchoalveolar lavage (BAL) samples from a patient with severe pneumonia following methotrexate therapy, resulting in the molecular diagnosis of Q fever in a patient who had been diagnosed with active seronegative polyarthritis two years earlier. To the best of our knowledge, this represents the first documented case of the isolation of C. burnetii DNA from a BAL sample.

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We report the complete genome sequence and analysis of an invasive Corynebacterium diphtheriae strain that caused endocarditis in Rio de Janeiro, Brazil. It was selected for sequencing on the basis of the current relevance of nontoxigenic strains for public health. The genomic information was explored in the context of diversity, plasticity and genetic relatedness with other contemporary strains.

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Tissue factor is a transmembrane procoagulant glycoprotein and a member of the cytokine receptor superfamily. It activates the extrinsic coagulation pathway, and induces the formation of a fibrin clot. Tissue factor is important for both normal homeostasis and the development of many thrombotic diseases. A wide variety of cells are able to synthesize and express tissue factor, including monocytes, granulocytes, platelets and endothelial cells. Tissue factor expression can be induced by cell surface components of pathogenic microorganisms, proinflammatory cytokines and membrane microparticles released from activated host cells. Tissue factor plays an important role in initiating thrombosis associated with inflammation during infection, sepsis, and organ transplant rejection. Recent findings suggest that tissue factor can also function as a receptor and thus may be important in cell signaling. The present minireview will focus on the role of tissue factor in the pathogenesis of septic shock, infectious endocarditis and invasive aspergillosis, as determined by both in vivo and in vitro models.