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

The authors describe two cases with venous thromboembolism and neoplasia (ovary and stomach), which also showed evidence of arterial thromboembolic phenomena--cerebrovascular disease in the 1st case and acute myocardial infarction in the 2nd case--favouring the existence of nonbacterial thrombotic endocarditis. This presentation of neoplastic hypercoagulability is frequently underrated in clinical practice. Pathogenesis, clinical manifestations, etiology, and therapeutics of these syndromes are discussed in relation to the presented cases.
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PMID:[Neoplastic hypercoagulability. Apropos of 2 cases with Trousseau syndrome]. 222 Apr 29

Thrombosis in hemophilia is very rare and is usually associated with the administration of prothrombin complex concentrates. We describe a severe hemophiliac with P. carinii pneumonia who had clinical and laboratory evidence of acute myocardial infarction and disseminated intravascular coagulation, and at autopsy, nonbacterial thrombotic endocarditis as well. We suggest that prothrombin complex concentrates should be used cautiously in the setting of acute infection, and perhaps be given with appropriate doses of anticoagulants such as heparin.
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PMID:Acute myocardial infarction, non-bacterial thrombotic endocarditis, and disseminated intravascular coagulation in a severe hemophiliac. 222 Jul 67

A sensitive and highly specific ELISA assay was developed to determine the anti-myosin humoral immune response (AMA) in various heart diseases: acute viral myocarditis, infective endocarditis, acute myocardial infarction, and valve and coronary bypass surgery. The mean study entry AMA titer of each patient group was already significantly increased compared with age matched controls. During further follow-up (90 d) all the groups except for endocarditis showed a significant increase of AMA titer compared with their entry titer. Anti-myosin antibody titer were higher after cardiac surgery than after myocardial infarction or inflammatory heart disease. These results suggest that anti-myosin immune response is not limited to infectious processes in which the pathogen induces antibodies which cross-react with heart constituents but is merely caused by direct cardiac injury. Myosin as a major compound of heart cellular proteins turned out to be a good candidate to trigger immune response after cardiac injury.
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PMID:Anti-myosin humoral immune response following cardiac injury. 249 42

In a number of cardiac conditions (acute myocardial infarction, chronic left ventricular aneurysm, dilated cardiomyopathy, infective endocarditis and atrial fibrillation in the absence of valvular disease), the risk of embolism gives cause for concern. Although anticoagulation with warfarin (Coumadin)-derivatives has been shown to be effective in some of these situations, there is no evidence regarding the role of antiplatelet agents. The common factor in the thromboembolic potential of acute myocardial infarction, chronic left ventricular aneurysm and dilated cardiomyopathy is mural thrombus. This can be detected by two-dimensional echocardiography and indium-111 platelet scintigraphy. Although of value in elucidating the natural history of mural thrombus, in most cases, management is not substantially aided by these investigations. In patients with extensive myocardial infarction, particularly anterior infarction, moderate intensity anticoagulation started soon after hospital admission reduces the rate of embolism. After 8 to 12 weeks, embolic risk is low so that anticoagulants can usually be discontinued. Patients with chronic left ventricular aneurysm have a low incidence of embolism; anticoagulation is, therefore, inappropriate. Dilated cardiomyopathy is associated with a high risk of embolism; moderate intensity anticoagulation may be advisable in many such cases. Little information is available regarding the incidence of thromboembolism or the role of antithrombotic therapy in the patient with a diffusely dilated left ventricle due to ischemic heart disease. In native valve infective endocarditis, the risk of hemorrhage is high, and the efficacy of conventional anticoagulants unclear; thus, anticoagulation should not be instituted for the cardiac condition as such. However, in prosthetic valve endocarditis, the risk of embolism seems to be very high, and anticoagulant therapy should be continued, but with great care because there is a substantial risk of cerebral hemorrhage. Atrial fibrillation in patients with valvular heart disease is dealt with in a previous review. Patients with nonvalvular atrial fibrillation are at varying risk of embolism, depending on the etiology of the arrhythmia; trials of antithrombotic therapy are needed for the various subsets of patients. In most elderly patients, the etiology is not known, and their stroke risk is high. The risk of embolism in younger patients with idiopathic atrial fibrillation is so low as to make any antithrombotic therapy unnecessary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis and embolism from cardiac chambers and infected valves. 353 72

Four cases of purulent complications in the heart following acute myocardial infarction are described. Fever occurred during the first week after coronary occlusion. In one case thrombophlebitis at an infusion site was followed by purulent pericarditis. One patient had an infected mural thrombus with peripheral septic embolic, and two suffered from streptococcal endocarditis. The association between these infections and recent acute myocardial infarction could be related to tissue necrosis and local thrombosis, but the increasing risk of bacteremia following invasive monitoring procedures in these patients is a risk factor that should not be ignored.
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PMID:Infectious complications of acute myocardial infarction. 363 60

Autologous pericardium was used to reconstruct different parts of the left ventricle in 25 desperately ill patients. Fourteen patients had intractable sepsis resulting from infective endocarditis and myocardial abscess and 10 patients had noninfectious disorders. Of the patients with infections, 12 had valvular endocarditis with periannular abscess and three had interventricular septal abscess. The noninfected patients had acute rupture of the ventricular wall after mitral valve replacement (one patient) heavily calcified or surgically absent mitral anulus (three patients), or rupture of the interventricular septum after acute myocardial infarction (six patients). The interventricular septum, the posterior wall of the left ventricle, and the periannular areas were reconstructed by suturing appropriately tailored pericardial patches directly to the endocardium. In patients who also required valve replacement, the prosthetic valve was partially or completely secured to the pericardial patch. There were three operative deaths. All three patients were in either septic or cardiogenic shock before operation and in none of them was the death related to the pericardial patch. All 22 survivors have been observed from 3 to 34 months, an average of 14 months. There has been no case of patch dehiscence, patch aneurysm, prosthetic valve dehiscence, or recurrent endocarditis. Autologous pericardium appears to be safe for reconstruction of the left ventricle. It is easy to handle and problems with suture line bleeding are practically nonexistent.
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PMID:Reconstruction of the left ventricle with autologous pericardium. 366 99

This is the first reported case of an acute myocardial infarction probably secondary to DF-2 bacterial septicemia and presumed endocarditis. Selective coronary arteriography revealed a long filling defect causing 95% stenosis of the second diagonal branch of the left anterior descending coronary artery. Multiple blood cultures revealed Decarboxylase Fermentor-2 (DF-2) septicemia that responded to penicillin therapy. Two months status after myocardial infarction recatheterization revealed complete recanalization with slight irregularity of the vessel lumen at the site of previous obstruction.
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PMID:Acute myocardial infarction associated with DF-2 bacteremia after a dog bite. 370 97

Clinical and morphologic observations are described in 30 patients (23 [77%] of whom were in functional class III or IV) who underwent replacement of the mitral valve for mitral stenosis and either simultaneous replacement (13 patients, group I) or anuloplasty (17 patients, group II) of the tricuspid valve for pure tricuspid valve regurgitation. Comparison of the 13 patients in group I with the 17 patients in group II disclosed similar mean ages (55 vs 58 years), similar average preoperative right ventricular systolic pressures (64 vs 61 mm Hg), similar average right atrial mean pressures (10 vs 9 mm Hg), similar average left ventricular systolic pressures (126 vs 120 mm Hg), similar average pulmonary artery wedge-left ventricular mean diastolic pressures (16 vs 18 mm Hg), similar cardiac indexes (2.1 vs 2.0 liters/min/m2), similar mean heart weights (507 vs 535 g), and similar percents with grossly visible foci of left ventricular necrosis (15% vs 12%) and fibrosis (23% vs 12%). Of the 13 patients in group I, 10 (77%) died early (less than or equal to 60 days of tricuspid valve replacement) and 3 (23%) died late (29, 37 and 120 months); of the 17 patients in group II, 14 (82%) died early and 3 (18%) died late (4, 9 and 98 months). The causes of early death in the 2 groups were different: of the 10 patients in group I who died early, the cause was excessive bleeding in 5, low cardiac output of undetermined etiology in 3, dysfunction of both prostheses in 1 and cerebral insult in 1; of the 14 patients in group II who died early, none died from excessive bleeding, 4 from decreased cardiac output of uncertain cause, 5 from left ventricular inflow obstruction (produced by a Starr-Edwards ball-valve prosthesis in 4 and from a Starr-Edwards disc prosthesis in 1), 1 from left ventricular outflow obstruction (by a porcine bioprosthesis), 2 from technical mishaps (incision into left ventricular free wall with rupture in 1 and ligation of the left circumflex coronary artery with resulting acute myocardial infarction in 1) and 2 died suddenly for reasons not determined. Of the 6 patients dying greater than 60 days after operation, 4 died from chronic congestive cardiac failure, 1 from a cerebral embolus and 1 from prosthetic valve endocarditis.
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PMID:Mitral valve stenosis and pure tricuspid valve regurgitation: comparison of necropsy patients having simultaneous mitral and tricuspid valve replacements with necropsy patients having simultaneous mitral valve replacement and tricuspid valve anuloplasty. 376 18

Necropsy findings were examined in 20 male patients with end-stage renal disease associated with longstanding spinal cord injury and treated with maintenance hemodialysis. All patients exhibited cardiovascular abnormalities. Fibrinous pericarditis was found in 50% of the patients. Left and right ventricular hypertrophy was present in 45% and 20% of the cases, respectively. The respective incidences of left and right ventricular dilatation were 40% and 30%. Cardiac amyloidosis was noted in 25% of the cases, whereas myocardial fibrosis was found in 45% of the patients. Valvular abnormalities were limited to one case of aortic stenosis and two cases of mitral ring dilatation. No evidence of infective endocarditis was observed despite the high incidence of infections in this population. Whereas 45% of the patients exhibited some degree of coronary arteriosclerosis, none exhibited evidence of acute myocardial infarction and only one showed pathologic changes consistent with old myocardial infarction. Aortic atherosclerosis was noted in the majority of patients.
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PMID:Cardiovascular pathology in dialysis patients with spinal cord injury. 622 12

Coronary embolism is an uncommon but distinct clinical entity. It can be diagnosed clinically, and should be suspected when acute myocardial infarction occurs in association with an underlying condition which predisposes to embolism. The most common are valvular heart disease, a prosthetic heart valve, infective endocarditis, cardiomyopathy with mural thrombus and arrhythmia. The diagnosis may be obscured by atypical symptoms and transient ECG changes. The diagnosis is supported by the demonstration of normal coronary arteries by selective coronary arteriography. Treatment with long-term anticoagulants may prevent further emboli. Additional antiplatelet drugs are also necessary in patients with prosthetic heart valves.
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PMID:Diagnosis of coronary embolism: a review. 635 70


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