Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed anticoagulant related hemorrhage (ACRH) and thromboembolism (TE) in 84 patients after valvular surgery. There were 45 females and 39 males with a mean age of 51.8 years (range 30.5-71.2 years), who underwent valvuloplasty in 14, bioprosthetic valve replacements in 17, mechanical valve replacements in 13. A mean period from the operation to the event were 2.7 years (range 0.01-12.3 years). There were 25 ACRH events after one valvuloplasty, 4 bioprosthetic valve replacements, 20 mechanical valve replacements. About half of them, the prothrombin time were less than 25%, which was considered the effect of warfarin is high, and 8% of them had infective endocarditis (IE) previously. There were 59 TE events after 13 valvuloplasties, 13 bioprosthetic valve replacements, 33 mechanical valve replacements. In the patients with atrial fibrillation, TE occurred irrespective of operative procedures. And in the patients with mechanical valve, severely impaired left ventricular function and past history of IE, thrombi of left ventricule were caused of TE. It was suggested that past history of IE was a risk factor ACRH and TE, and severely depressed left ventricular function and atrial fibrillation were for TE.
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PMID:[Anticoagulant related hemorrhage and thromboembolism after valvular surgery]. 870 22

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

High-altitude hypoxia causes polycythaemia and a hypercoagulable state in humans and animals. This study examines the effects of a hypobaric, hypoxic environment (HHE) on the blood coagulation system in rats. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m in altitude for 1-12 weeks. After 2 weeks of exposure to HHE, platelet counts decreased significantly; after 4 weeks, the prothrombin and activated partial thromboplastin times were significantly prolonged, compared with those of control rats. In addition, individual coagulation factors (VII, IX, X, XI, and XII) were significantly decreased at 8 weeks (P < 0.05). Levels of anti-thrombin III and alpha 2-plasmin inhibitor also decreased (between 4 and 8 weeks). After 4-12 weeks of exposure to HHE, 30 of 56 rats (54 per cent) developed (i) non-bacterial thrombotic endocarditis (NBTE) or (ii) infarction of the myocardium or kidney, or both (i) and (ii). The incidence of NBTE increased from 33 per cent (5/15 rats) at 4 weeks to 100 per cent (7/7 rats) at 12 weeks. Electron microscopy showed detached endothelial cells in the mitral valves at 1 week; platelets adhered to the subendocardial matrix and platelet aggregation with thrombus formation was seen at 2 weeks of exposure. The results suggest that exposure to HHE induces a hypercoagulable state and causes an NBTE in rats that may result in consumption coagulopathy.
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PMID:Hypercoagulable state in a hypobaric, hypoxic environment causes non-bacterial thrombotic endocarditis in rats. 915 22

We recently performed a laparoscopic cholecystectomy on three patients receiving preoperative oral anticoagulant therapy. The patients requiring anticoagulants for pre-existing cardiac conditions have the following risks at surgery: thromboembolism, hemorrhage, endocarditis, and cardiopulmonary dysfunction. In patients receiving anticoagulant therapy, one must thus maintain a balanced international normalized ratio of the prothrombin time to prevent thromboembolism or hemorrhage. Warfarin sodium was discontinued preoperatively in all patients. Heparin sodium was individualized according to each patient's risk of thromboembolism. As a result, these patients all underwent a laparoscopic cholecystectomy without complications. Attention was paid to achieve hemostasis in the operative field and the trocar inserted sites during the procedure. The administration of warfarin sodium was resumed on the first postoperative day in all patients. Restarting warfarin sodium early also helps to simplify postoperative management. A broad spectrum of antibiotic therapy was also used to reduce the risk of endocarditis. Each patient's cardiopulmonary function was carefully monitored. The minimal invasion experienced during a laparoscopic cholecystectomy may thus facilitate the management of gallstones in patients receiving systemic anticoagulation treatment based on the findings of this limited series.
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PMID:Laparoscopic cholecystectomy in patients undergoing anticoagulant therapy. 954 16

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

Cigarette smoking, hypertension, hypercholesterolemia, and periodontal disease have been established as major risk factors for cardiovascular disease. Dentists and physicians should work aggressively to educate periodontitis patients about this relationship in an effort to improve the quality of health and contribute to their long-term survival. Blood pressure should be checked at the initial dental visit and at each subsequent visit in patients whose blood pressure is found to be high and/or has a history of hypertension. Dental and medical assistants should receive in-service training to assure competency in measuring blood pressures. All staff should be certified in basic cardiopulmonary resuscitation. Emergency protocol procedures should be in writing and rehearsed regularly. Patients should take their blood pressure medication as usual on the day of the dental procedure. It is helpful for the patients to bring all medications to the office for review at the time of the dental procedure. Good communication should be established between the dentist and physician to maximize good dental and physical health. Because the patient with periodontal disease is at an increased risk for cardiovascular disease, a standardized form should be developed for the convenient exchange of vital information, including but not limited to: blood pressure, medications, allergies, medical conditions and pertinent highlights of dental procedures. Minimize stress in patients with coronary artery disease. This includes providing solid local anesthesia, avoidance of intravascular medication injections, and encouraging relaxation techniques. Antibiotic prophylaxis is indicated in patients with valvular heart disease but does not guarantee the prevention of endocarditis. These patients should be alerted to monitor any symptoms such as fever, chills or shortness of breath. It has also been documented that toothbrushing, flossing and home plaque removers can cause transient bacteremia in periodontal patients. Epinephrine use should be avoided or utilized cautiously in patients with pacemakers or automatic defibrillator devices because of the possibility of refractory arrhythmia. Consultation with patient's cardiologist is advised. Anticoagulation with coumadin is not a contraindication to dental procedures. The prothrombin time or international normalized ratio laboratory values should be checked on the day of the procedure to assure that it is in an acceptable range. Aspirin therapy is not a problem unless the patient is on very high doses for severe arthritis. Continuing medical and dental education credits should emphasize cross-training in both areas to insure comprehensive treatment of the patient with periodontal disease. Smoking cessation, regular exercise, a low-fat diet and good dental hygiene contribute to a healthy cardiovascular system. Patients should understand as best we know the relationship between periodontal and cardiovascular disease to afford them an opportunity to improve their overall dental and physical health.
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PMID:Medical management of the patient with cardiovascular disease. 1127 61

Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.
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PMID:Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events. 1263 99

Many bacterial pathogens secrete proteins that activate host trypsinogen-like enzyme precursors, most notably the proenzymes of the blood coagulation and fibrinolysis systems. Staphylococcus aureus, an important human pathogen implicated in sepsis and endocarditis, secretes the cofactor staphylocoagulase, which activates prothrombin, without the usual proteolytic cleavages, to directly initiate blood clotting. Here we present the 2.2 A crystal structures of human alpha-thrombin and prethrombin-2 bound to a fully active staphylocoagulase variant. The cofactor consists of two domains, each with three-helix bundles; this is a novel fold that is distinct from known serine proteinase activators, particularly the streptococcal plasminogen activator streptokinase. The staphylocoagulase fold is conserved in other bacterial plasma-protein-binding factors and extracellular-matrix-binding factors. Kinetic studies confirm the importance of isoleucine 1 and valine 2 at the amino terminus of staphylocoagulase for zymogen activation. In addition to making contacts with the 148 loop and (pro)exosite I of prethrombin-2, staphylocoagulase inserts its N-terminal peptide into the activation pocket of bound prethrombin-2, allosterically inducing functional catalytic machinery. These investigations demonstrate unambiguously the validity of the zymogen-activation mechanism known as 'molecular sexuality'.
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PMID:Staphylocoagulase is a prototype for the mechanism of cofactor-induced zymogen activation. 1452 51

Necrosis of the digits is a rare complication of warfarin therapy of obscure pathogenesis. We report a 61-year-old woman with a 12-month history of Raynaud's phenomenon who developed multiple digital necrosis following aortic valve replacement with mechanical prosthesis for aortic insufficiency caused by nonbacterial thrombotic endocarditis. Exacerbation of Raynaud's phenomenon occurred during the postoperative period, with daily episodes of ischemia of the fingers and toes that improved with local warming. However, coincident with the occurrence of immune heparin-induced thrombocytopenia, and while undergoing routine warfarin anticoagulation because of the mechanical valve prosthesis, the patient abruptly developed progression of digital ischemia to multiple digital necrosis on postoperative day 8, at the time the international normalized ratio reached its peak value of 4.3. All limb pulses were readily palpable, and vascular imaging studies showed thrombosis only in the superficial femoral and popliteal veins of the right leg. Coagulation studies showed greatly elevated levels of thrombin-antithrombin complexes and prothrombin fragment F1.2 levels, consistent with uncontrolled thrombin generation. After vitamin K administration, no abnormalities of the protein C anticoagulant pathway were identified, consistent with previous studies of other patients with warfarin-induced necrosis complicating heparin-induced thrombocytopenia. Subsequently, the patient was shown to have metastatic breast adenocarcinoma, which explained the patient's initial presentation with nonbacterial thrombotic endocarditis. This patient case suggests that multiple digital gangrene can result from the interaction of various localizing and systemic factors, including compromised microvascular blood flow (Raynaud's phenomenon), increased thrombin generation (heparin-induced thrombocytopenia, adenocarcinoma), and warfarin-induced failure of the protein C natural anticoagulant pathway.
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PMID:Warfarin-associated multiple digital necrosis complicating heparin-induced thrombocytopenia and Raynaud's phenomenon after aortic valve replacement for adenocarcinoma-associated thrombotic endocarditis. 1469 34

Severe, life-threatening acute upper gastrointestinal bleeding may occasionally occur in patients receiving coumarol prophylaxis for prosthetic heart valves. These patients are exposed to two potential, serious risks: bleeding due to the severe blood loss induced by excessive anticoagulant effect or as a consequence of the cessation of anticoagulation subsequent thrombotic occlusion of the valve and loss of patency. Herein a short case report is presented. The elderly male patient had a prosthetic valve in the aortic position and also suffered from two malignant diseases: chronic lymphocytic leukaemia and a more recently developed lung cancer with metastatic spread into both lungs. The patient had a major gastrointestinal bleed, leading to a sudden fall of haematocrit (0.09), and to a collapse of peripheral circulation due to too excessive a coumarol effect (International Normalized Ratio > 8). An acute left ventricular failure developed during the early period of the emergency blood transfusion, so the correction of prothrombin time by fresh-frozen plasma (due to the large volume requirement) was not feasible. The patient received 50 microg/kg intravenous bolus of NovoSeven (recombinant active factor VII) in an almost desperate situation. The International Normalized Ratio changed to 2.1 in 30 min; bleeding had stopped immediately. There was neither evidence of disseminated intravascular coagulation (in spite of the age and underlying diseases) nor loss of valve patency or infective endocarditis during follow-up. This modest report may call attention to the potential use of recombinant active factor VII in the coumarol-induced severe bleeding episodes of prosthetic heart valve patients.
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PMID:Successful control of massive coumarol-induced acute upper gastrointestinal bleeding and correction of prothrombin time by recombinant active factor VII (Eptacog-alpha, NovoSeven) in a patient with a prosthetic aortic valve and two malignancies (chronic lymphoid leukaemia and lung cancer). 1506 Apr 25


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