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

Knowledge and due consideration of the natural history of valvular heart disease are prerequisites for their operative therapy. Presumptive mortality and morbidity of the surgical intervention must be weighted against the expected prognosis under medical treatment alone. The timing of the operation depends on these considerations. Mitral stenosis and the chronic forms of mitral and aortic incompetence have similar natural histories and for both signs and symptoms are good indicators for an eventual progression of the condition. The length of the period during which the patient is free of complaints may be quite variable but a critical change in the natural history comes about once the disease causes signs and symptoms. Surgical repair is indicated when the patient reaches stage III according to the NYHA-classification. The prognosis is worst for aortic stenosis, in particular due to the danger of sudden death. Patients with high pressure gradients are at particularly high risk; this holds even true for those patients which are not yet suffering from any complaints. The prognosis becomes even more serious, when signs such as dyspnea, anginal pain, or syncopal attacks occur. Prognosis and indication for surgical intervention cannot be evaluated reliably by considering only the clinical signs without knowledge of hemodynamic parameters. Acute mitral and aortic incompetence, in paricular when they occur during baterial endocarditis, must be observed very closely because of their most serious prognosis; if necessary, emergency surgery must be carried out in these cases.
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PMID:[Natural history in patients with mitral- and aorticvalve-disease (author's transl)]. 32 60

In a 24-month period, 27 patients with idiopathic hypertrophic subaortic stenosis (IHSS), ages 65-80 years, were observed. Diagnoses were made by echocardiography (24 patients), cardiac catheterization (one patient), and both methods (two patients). The most common symptoms were angina (17 patients), dyspnea (13 patients), and syncope (11 patients). Two patients were asymptomatic, while another complained only of vague retrosternal chest discomfort with exertion. One asymptomatic patient had a completely normal physical examination, but electrocardiography (ECG) demonstrated a pattern of left ventricular hypertrophy. Another patient had an inconsistent apical holosystolic murmur. Two patients had alpha streptococcal endocarditis; neither was known to have pre-existing valvular disease. Fourteen patients had ECG criteria for left ventricular hypertrophy (LVH). Three patients were known to have associated aortic valve disease. The symptoms of IHSS may be nonspecific; asymptomatic patients with and without cardiac murmurs may be observed. Coexisting valvular disease, coronary artery disease, and bacterial endocarditis were documented. Patterns of myocardial infarction on ECG were not seen in these 27 patients.
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PMID:Idiopathic hypertrophic subaortic stenosis in the elderly. 56 40

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

The endocardial fibroelastosis (EFE) is the most frequent cardiomyopathy. This disease is characterised by endocardial hyperplasia due to proliferation of elastic and collagenous fibres. There are primary and secondary forms. Within the primary form, the infantile form is the most frequent and of greatest importance to the pediatrician. This form is more a syndrom than a distinct disease. It is a reaction of the endocard due to several noxes. Lately a possible viral etiology is being discussed e.g. Parotitis, Coxsackie or other viruses. Clinical criteria for diagnosis are: cardiomegaly, left ventricular hypertrophy seen in 97% in the ECG, the absence of a murmur (or a soft apical mumur) absence of cyanosis and absence of systemic disease. Differential diagnosis is mainly between fibroplastic parietal endocarditis (FPE), cardiovascular collagenosis (CC) and endomyocard fibrosis (EMF). In FPE thrombosis is frequent and typically there is eosinophilia. CC is found in South Africa and is characterised by edema and fibrinoid necrosis. MEF is present mainly in Uganda, Nigeria and South India, characterised by endocardial fibrosis, valve involvement and eosinophilia. The obstructive hypertrophic cardiomyopathy is characterised by a pronounced cardiomegaly, insufficient weight gain as well as dyspnea and cyanosis. Catheterization shows a gradient across one or both of the outflow tracts due to hypertrophic subaortic or subpulmonic stenosis. Therapy of EFE consists in treating the cardiac decompensation and according to the severity of the disease, in steroids.
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PMID:[Endocardial fibroelastosis (E.F.) and its differential diagnosis]. 94 82

Homograft aortic valve replacement was done in 103 patients and prosthetic aortic valve replacement in 106 between January 1962 and December 1973. Patients who received homograft and prosthetic valves were compared with respect to age, sex, preoperative functional impairment, infection, dyspnea, angina, hemodynamics, chest X-ray, electrocardiogram, associated operations, early and late mortality, and valve failure. Combined total mortality was 28% (12% operative, 8% first postoperative year, 8% late). Ten percent of valve required replacement. One year after operation, 70% of survivors were asymptomatic, 27% were improved, and 3% were unchanged or between homograft and prosthetic valve replacement. Valve-related failure and infections were more common after homograft aortic valve replacement. Emboli, hemorrhage, and hemolysis were commoner after prosthetic valve replacement. Fungal infections occurred in five homograft patients but in no patient with a prosthetic aortic valve. Severe properative symptoms or recent endocarditis was associated with greater mortality and valve failure in both the homograft and the prosthetic series. Increased mortality and failure was also seen in patients with either preoperative aortic regurgitation with high left ventricular end-diastolic pressure and low cardiac index, or aortic stenosis with cardiomegaly or roentgenographic evidence of congestive heart failure. Therefore, in two series of patients at equal risk, mortality and valve failure were similar for homograft and prosthetic aortic valve replacement.
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PMID:Homograft and prosthetic aortic valve replacement: a comparative study. 99 28

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

A 31-year-old male with tetralogy of Fallot (TF) and total occlusion of the right coronary orifice complicated with infective endocarditis successfully underwent total repair of TF and coronary artery bypass graft (CABG). The patient had severely suffered from symptoms including breathlessness, palpitation (SVT) and chest pain. The coronary arteriography revealed occlusion of the right coronary orifice. The preoperative course was further complicated by endocarditis with vegetation of the aortic valve that did not respond to antibiotics. Concomitant surgical procedures consisting of TF repair, CABG to the right coronary artery with saphenous vein graft and vegetectomy of the aortic valve were carried out. The postoperative course was uneventful though he underwent cholecystectomy for symptomatic gall stones after TF repair. The patient is now in NYHA class II.
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PMID:[A case report of tetralogy of Fallot associated with total occlusion of the right coronary artery and complicated with infective endocarditis]. 148 44

Two cases of pneumothorax secondary to pulmonary septic infarctions occurred in the course of tricuspid endocarditis in intravenous drug misusers. This unusual complication must be considered in patients with right sided endocarditis who develop pleuritic chest pain, haemoptysis, or breathlessness.
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PMID:Pneumothorax secondary to septic pulmonary emboli in tricuspid endocarditis. 149 75

A 50-year-old male alcoholic addict, examined because of diarrhoea with fever was found to have Campylobacter jejuni in blood and stool cultures. After administration of broad-spectrum penicillin all acute symptoms disappeared but he lost 8 kg within 3 months and his general state health gradually deteriorated. After 3 months he suddenly developed leg oedema, dyspnoea and bouts of fever up to 38.8 degrees C. A loud cardiac murmur was now heard. Echocardiography demonstrated vegetations on the regurgitant aortic valve. Endocarditis being suspected he was at first treated with penicillin G (15 mega IU/d) and gentamycin (160 mg/d). The fever regressed, but after 8 days the blood culture grew Campylobacter fetus subspecies fetus. Antibiotic treatment was switched to imipenem, twice daily 500 mg, in accordance with sensitivity test results. Further blood cultures were sterile. Despite this the cardiac status deteriorated, the aortic regurgitation reaching grade IV. The valve was replaced with a bioprosthesis and the patient quickly improved postoperatively. Antibiotic treatment was stopped and the cardiovascular status became normal. The patient has now been free of symptoms and recurrence for 7 months.
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PMID:[Acute aortic insufficiency following endocarditis due to infection with Campylobacter fetus subspecies fetus]. 151 29


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