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

In a prospective study 31 cases of proved and 10 of highly suspected bacterial endocarditis were analysed. Valve incompetence was the usual consequence but stenosis occurred in 3 cases, all fatal. Congestive heart failure developed in two-thirds. Secondary manifestations were common and as often caused by alpha-streptococci as by other bacteria. Initial antibiotic treatment was mainly applied according to a fixed schedule, generally with continuous intravenous infusion, followed by oral therapy. In 10 patients, the infection was still active after 6 weeks of therapy. Therefore, we now use intermittent injections or infusions for at least 4--6 weeks. Within a year, 9 patients died from uncontrolled infection together with congestive heart failure, and 1 from heart failure and active chronic endocarditis. In 4, myocardial abscesses or inflammations were found. All 10 had underlying factors or advanced stages of the disease. Of 18 patients with alpha-streptococci or enterococci none died from endocarditis, as against 10 of 23 with other or unknown bacteria. Follow-up yielded valuable information on one-third of the patients. The mortality during the initial hospital stay was 22%, after 1 year 24% and after 5 years 39%.
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PMID:Bacterial endocarditis. II. A prospective study with clinical, laboratory and therapeutic observations. 41 66

Coxiella burnetii is the etiological agent of human Q fever and chronic endocarditis. Different plasmids have been found in C. burnetii isolates and a correlation between disease state and plasmid type has been established. The plasmid QpRS was found in all but four of the endocarditis-causing isolates examined. These four isolates did not contain a detectable plasmid. However, when DNA from the plasmidless isolates is hybridized with 32P-labeled QpRS, homologous sequences are detected. It was hypothesized that plasmid sequences had inserted into the chromosomal DNA of the plasmidless isolate. A cosmid chromosomal gene bank was constructed from one of the plasmidless isolates and a number of clones were obtained. One clone, pEAS137, contained all of the EcoR I fragments with homology to the C. burnetii plasmids plus several non-homologous fragments. The EcoR I fragments in pEAS137 were in the same linear order as present in the chromosome of the plasmidless isolate and were shown to exist as a single contiguous sequence. This information supports the hypothesis that plasmid sequences have inserted into the chromosomal DNA and makes pEAS137 a good candidate for studying the relationships between the plasmids. Initial studies comparing pEAS137 to QpRS and QpH1 suggest that pEAS137 is more closely related to QpRS than to QpH1.
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PMID:Comparison of Coxiella burnetii plasmids to homologous chromosomal sequences present in a plasmidless endocarditis-causing isolate. 237 75

Human infection with the rickettsia Coxiella burnetii presents as an acute flulike primary Q fever, as a subacute granulomatous hepatitis, or, rarely, as chronic endocarditis. We have previously described lymphocyte unresponsiveness to Coxiella antigen in patients with Q fever endocarditis. This unresponsiveness was antigen specific and was mediated in part by adherent suppressor cells. In this report we show that the adherent suppressor cells work via prostaglandin E2 (PGE2)4 production. Addition of the cyclooxygenase inhibitor indomethacin to cultures of PBMC from patients with endocarditis or chronic laboratory exposure resulted in consistent increases in Coxiella-specific lymphocyte proliferation. The degree of increase in proliferation induced by indomethacin correlated strongly with the amount of PGE2 produced in a 4-hr culture stimulated by Coxiella antigen, but it also correlated with the sensitivity to inhibition of mitogenesis by PGE2. The suppressor mechanism was antigen nonspecific, because induction of suppression in vitro by Coxiella antigen also suppressed Candida-induced proliferation when both antigens were present in the same culture. Addition of indomethacin to these antigen cocultures totally reversed the Coxiella-induced suppression, confirming the evidence above that the nonspecific effector mechanism of suppression was prostaglandin (PG)-mediated. Elicitation of suppression, however, was antigen specific and involved a T cell-monocyte suppressor circuit. Supernatants from Coxiella-stimulated immune T cells and from the suppressor subset (OKT8+-enriched) of those T cells, but not unstimulated immune cells, induced augmented PGE2 production by unrelated nonimmune PBMC. We conclude that the lymphocyte unresponsiveness characterizing patients with Q fever endocarditis is modulated in part by an antigen-specific T suppressor cell which secretes a lymphokine to stimulate PGE2 production by adherent cells.
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PMID:Cellular immunity in Q fever: modulation of responsiveness by a suppressor T cell-monocyte circuit. 240 35

Human infection with the rickettsia Coxiella burnetii presents as acute influenza-like primary Q fever, subacute granulomatous hepatitis, or chronic endocarditis with hepatitis. To investigate whether persistent infection is associated with a possible immunologic defect, we tested lymphocyte proliferation specific for Coxiella in vitro in peripheral blood mononuclear cells from patients and controls. All four patients with endocarditis had profound lymphocyte unresponsiveness to Coxiella antigens with normal proliferation to control antigens. Hepatitis and primary Q fever were associated with vigorous responses in vitro to Coxiella antigens. Suppression of lymphocyte unresponsiveness was in part mediated by an antigen-nonspecific, glass-adherent cell. We hypothesize that specific T cell unresponsiveness is an important factor in persistent infection with C. burnetii and offer in vitro lymphocyte stimulation as a more specific diagnostic test to distinguish cases of endocarditis among those with chronic hepatitis due to Q fever.
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PMID:Cellular immunity in Q fever: specific lymphocyte unresponsiveness in Q fever endocarditis. 241 42

From 1972 to 1984, 104 cases of aortic valve infectious endocarditis were treated surgically. The average age of the patients was 40 years and the majority were men (69/104). Forty patients had no previous cardiac disease; 44 patients had documented valvular heart disease, which was unlikely in the remaining 20 patients. There were 16 mitral valve, 55 aortic valve, 1 tricuspid, 30 mitro-aortic, 1 mitro-tricuspid and 1 mitro-aorto-tricuspid valve infections. Aerococcus viridans was isolated in only 4 out of 71 positive cultures: the prevalence of the infecting organisms was otherwise normal (30 staphylococcus, 30 streptococcus, 7 rare organisms). Forty one patients were operated because of haemodynamic deterioration, 13 for resistant infection and 13 for an association of both indications; 37 patients were operated for embolism or threatening vegetations. Eight patients were in functional Class I, 26 in Class II, 52 in Class III and 17 in Class IV. The patients were divided into 4 groups according to the degree of surgical emergency (26 extremely urgent, 26 semi urgent, 32 controlled endocarditis and 20 chronic endocarditis). The actuarial survival rate was 70% at 5 years. Poor prognostic factors were the presence of previous valve disease, the isolation of a staphylococcus and an aortic valve localisation. The degree of emergency and the precise surgical indication did not seem to be important. Most patients at long term were in functional Classes I or II. There was no preferential indication for bioprosthetic or mechanical valve replacement in endocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Indications and results of surgery in native valve infectious endocarditis. Apropos of 104 surgically-treated cases]. 308 9

The obligate intracellular bacterium Coxiella burnetii is the etiological agent of acute Q-fever and chronic endocarditis in humans and of several zoonotic infections. The DNA from a variety of these disease isolates was compared for homology to the plasmid QpH1, found in the Nine Mile strain. Three patterns of homology were found in these isolates, i.e., one pattern identical to that of QpH1, one common to several endocarditis isolates and goat abortion isolates, and one common to the remaining group of endocarditis isolates. Plasmid DNA from the endocarditis-abortion isolate group, designated QpRS, was mapped by restriction enzyme analysis and compared with QpH1. These data show that QpRS was 2 to 3 kilobase pairs larger, contained DNA not found in QpH1, but was not generated from QpH1 by a single insertional event. Isolation of plasmid DNA from the second endocarditis group of isolates was not successful and may indicate that the plasmid has integrated into the chromosome. This analysis provides the first clear evidence that differences exist between C. burnetii isolates which cause various diseases, indicating that different C. burnetii strains may have unique virulence characteristics.
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PMID:Correlation of plasmid type and disease caused by Coxiella burnetii. 403 Jan 4

Six cases of chronic endocarditis (more than 1 year duration) have been extracted from a series of 72 cases of endocarditis (delayed in 49) associated with intracardiac prosthesis observed over a 15-year period. In these 6 cases endocarditis developed 6 months to 2 years after valve replacement. The prosthetic material included 3 Starr-Edward's valves, 2 Hancock's valves and 1 intracardiac patch. The micro-organism isolated were Streptococcus in 3 cases, Serratia and Corynebacterium in 1 case each. The 18-month to 5-year course of the disease was marked by 2 to 5 relapses separated by long periods of apyrexia. The most significant complications were dysimmune syndrome (5 cases), embolic accidents (2 cases) and prosthesis disinsertion (4 cases). Five patients benefited from antibiotic therapy; 4 were operated upon with recurrent disinsertion in 2 cases. Two patients died, one of repeated disinsertion, the other of myocardial dysfunction. Bacteriostatic antibiotics were administered continuously to 3 patients whose endocarditis persisted or relapsed, with satisfactory results in two cases followed-up for more than 2 years.
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PMID:[Chronic endocarditis on valve prosthesis. 6 cases]. 622 57

Clinical data from 72 patients with infective endocarditis (41 with defined pathogen, 31 with no pathogen isolated) were analyzed with respect to the diagnostic relevance of immunologic parameters. In our patients from a rural area, no significant changes in the epidemiology and pathogenesis of infective endocarditis were observed. Antiendocardial and antisarcolemmal (ASA) antibodies were demonstrated in 60% to 100% of cases. Their frequency depended on the endocarditic pathogen and on the clinical course: in subacute or chronic endocarditis these antibodies were found regularly, in acute lethal cases their occurrence was diminished. Whereas antiendocardial antibodies are diagnostic markers of endocarditis, ASA and antimyolemmal antibodies in particular most likely indicate myocardial involvement in endocarditis. Only complement fixing antimyolemmal antibodies induced cytolysis of vital, adult, heterologous cardiac cells. Our data suggest that antibody-mediated cytolysis in vitro may also play a pathogenetic role in vivo.
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PMID:Immune reactions in infective endocarditis. I. Clinical data and diagnostic relevance of antimyocardial antibodies. 686 14

The prognostic factors of 122 patients suffering from prosthetic valve endocarditis between 1978 and 1992 were studied by univariate and multivariate analysis. The principal causative organisms were Staphylococcus aureus (33%), streptococci (20%), coagular-negative staphylococci (12%), enterococci (10%) and gram-negative bacilli (9%). The 4 month survival rate was 66% (42 deaths). The main predictive factor for death was infection with S. aureus (75% vs 15% with other organisms). In S. aureus infection, multivariate analysis identified the following predictive factors for death: a prothrombin ratio less than 30% (RR = 8.3), mediastinitis (RR = 4.9), cardiac failure (RR = 4.4) and septic shock (RR = 2.6). In cases of infection with other organisms, the following factors were predictive of death: a prothrombin ratio of less than 30% (RR = 32.26), renal failure (RR = 7.31) and cardiac failure (RR = 6.07). In patients with S. aureus infection, survival was better after than without surgery: 9/20 (45%) versus 0/20 (p < 0.001). In infection with other organisms, there was no difference in a survival after surgical (89%) or medical therapy (81%). Chronic endocarditis relapses over 1 to 5 years was observed in 9 cases. All patients were reoperated a total number of 18 times with 5 deaths. Very prolonged antibiotic therapy is recommended in these patients. The authors conclude that endocarditis not due to S. aureus and without complications may be treated medically. Rapid reoperation is necessary in all other cases.
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PMID:[Prognostic factors of prosthetic valve endocarditis. Apropos of 122 cases]. 876 Jun 51

A right thoracotomy is a well-known alternative for midsternotomy to have access to the left atrium. The Port-Access (Heartport, Inc, Redwood City, CA) approach is an invaluable option to avoid cracking of ribs and cartilage. EndoCPB (Heartport, Inc) and Endo-Aortic Clamp (Heartport, Inc) allows installation of the extracorporeal circulation and cardiac arrest from the groin. Videoassistance and shafted instruments help the surgeon to perform the surgery through a 5 x 2-cm port and fulfill the main goals of minimally invasive cardiac surgery, comfort, cosmesis, and fast rehabilitation. From February 1997 to November 1998, 75 patients (40 men/35 women) had either Port-Access mitral valve repair (n = 41) or replacement (n = 33) for a variety of reasons: myxoid degeneration (n = 45), rheumatic disease (n = 21), chronic endocarditis (n = 4), annular dilatation (n = 2), and sclerotic disease (n = 2). One valve was replaced because of an ingrowing myxoma. There was one closure of a paravalvular leak. The mean age was 59.3 years of age (range, 32 to 83 years). Most patients had normal ejection fractions but different grades of mitral valve insufficiency and were in NYHA class II. One 71-year-old patient died after reoperation on postoperative day 1 for failed repair. Two patients had conversion to sternotomy and conventional ECC for repair of a dissected aorta. One patient died, one patient suffered a minor cerebrovascular deficit. Three patients had prolonged intensive care unit (ICU) stays for respiratory insufficiency, 5 patients underwent revision for bleeding. Mean ICU stay was 2.5 days; and mean hospital stay, 9 days (range, 4 to 36). A significant difference between the first 30 and last 38 patients in terms of length of stay in the ICU and the hospital was noticed. Two late mitral valve replacements for chronic endocarditis after repair occurred. One patient had medical therapy for endocarditis after mitral valve replacement. The debut of Port-Access mitral valve surgery may be nerve-racking; the routine is a smooth and sure surgery with maximum comfort, a very discrete scar, and a fast rehabilitation. There were no paravalvular leakages nor myocardial infarctions. Cerebrovascular accidents owing to thromboembolic phenomena, vascular lower limb or wound complications were not seen. Port-Access mitral valve surgery is a very important investment in the future of cardiac surgery. Some learning curve pitfalls were associated with the process of starting this revolutionary technique.
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PMID:Video-assisted Port-Access mitral valve surgery: from debut to routine surgery. Will Trocar-Port-Access cardiac surgery ultimately lead to robotic cardiac surgery? 1045 Dec 53


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