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)

A 38-year-old female was admitted to our hospital because she was suffered from severe dyspnea on effort. She had a history of nasal bleeding, endocarditis, fever, proteinuria, and alopecia at the age of 16, and was diagnosed as SLE. She was suffered from recurrent cerebral infarctions at the age of 35 and 38, and then mitral regurgitation was pointed out. Preoperative examination revealed non-active phase of SLE and UCG showed massive mitral regurgitation. Operative findings showed thrombosed verrucca circumferentially on the mitral valve. Mitral valve replacement (B-S #27) was done with using a felt strip in order to reinforce the mitral annular tissues. Histological findings of the verrucca showed Libman-Sacks endocarditis. Postoperative course was uneventful. Surgical treatment for Libman-Sacks endocarditis is extremely rare.
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PMID:[A case of mitral valve replacement for Libman-Sacks endocarditis]. 156 50

A 53-year-old male was admitted to the hospital because of Candida albicans endocarditis. He had had a thoracoplasty due to pulmonary tuberculosis and showed severe restructive lung function. In 1987 and '89, trachiostomy was made because of respiratory failure. The patient was well until nine months earlier, when he consulted a physician because of fever. The investigations failed in finding the cause of the fever. He was administered antituberculosis agents and antiinflammatory drugs but had a fever every day. Two months before admission, a cardiac ultrasonographic study showed evident vegetations with mitral regurgitation. From the above course and examinations, a diagnosis of Candida albicans endocarditis was made. Infusions of CEZ, TOB, PIPC and miconazole for more than one month was ineffective. In November, 1990, he was referred to our medical center for the purpose of operation. A blood culture proved Candida albicans infection. An intravenous administration of fluconazole 400 mg/day was begun. However, there was pulmonary bleeding probably due to heparin used for prevention of atrial thrombosis and he developed fever, hypoexemia, ventricular tachycardia, and hyponatremia. He underwent mitral-valve replacement with a SJM valve. Culture of the vegetated mitral valve again proved Candida albicans. After operation, hypoexemia, ventricular tachycardia, hyponatremia were improved gradually. However he had an eosinophilia, eruption, and dyspnea. We suspected a drug eruption of fluconazole. Lymphocyte stimulating test of fluconazole proved positive. After the episode, he had no symptoms and was discharged.
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PMID:[A case of Candida albicans endocarditis with impaired lung function]. 162 49

Endovascular infections that involve the right side of the heart present their own unique etiologies, pathophysiologies, clinical manifestations, and therapeutic issues. The pathology of the vegetations of right-sided endocarditis is identical to that of left-sided endocarditis. These vegetations are irregular, friable masses of varying size the contain platelets, fibrin, RBCs, and microorganisms. These lesions serve as a nidus for deep-seated infection and produce sustained bacteremia. Right-sided endocarditis occurs in 5% to 10% of all cases of endocarditis. The most common predisposing factors are IV drug abuse and congenital heart disease. S. aureus is the most common pathogen. The clinical manifestations include fever, chills, rigor, dyspnea, pleuritic pain, productive cough, and hemoptysis. The cardiac manifestations can be notably absent early in the course of the disease, with only 20% of patients initially showing a significant murmur on physical examination. Peripheral embolic lesions can be seen. Echocardiography is helpful in identifying vegetations on the tricuspid valve in a significant proportion of patients. The chest radiograph is characteristic, showing features typical of multiple septic pulmonary emboli. The radiograph shows multiple, small, fuzzy, patchy, peripherally located densities that can change rapidly on serial films. Complications of right-sided endocarditis include pulmonary infarction, pulmonary abscess, progressive right-sided heart failure, and renal abnormalities. The treatment of right-sided endocarditis includes prolonged therapy, with high doses of IV bactericidal antibiotics. Four weeks of antibiotic therapy is generally required, but newer regimens using combination antibiotic therapy can be successful in sensitive strains of viridans group streptococci and S. aureus. Surgical resection of the tricuspid valve is recommended for organisms that do not respond to initial antibiotic therapy, fungal endocarditis, resistant relapsing organisms, or coexistent infection with S. aureus and P. aeruginosa. The prognosis of right-sided endocarditis is generally favorable when compared with left-sided endocarditis. The prognosis is especially favorable in IV drug abusers infected with S. aureus. Patients infected with fungal organisms, Pseudomonas or Serratia, have a worse prognosis. The presence of significant right-sided heart failure also imparts a worse prognosis.
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PMID:Endovascular infections arising from right-sided heart structures. 173 55

A 47-year-old man was hospitalized in May, 1990, because of breathlessness and continuous fever which appeared about 4 weeks after he had had his periodontic tooth removed in December, 1989. He had been diagnosed as having ventricular septal defect (VSD) at the age of 6 years. When he was hospitalized, he was in a condition of class IV by NYHA classification, with a white blood cell count of 17,300/mm3, an increase in CRP, a red blood cell sedimentation rate of 108 mm/hr, and positive alpha-streptococcus in blood culture. His cardiothoracic ratio was 64% with signs of pulmonary congestion on a chest X-ray film. Echocardiography revealed the presence of VSD and huge vegetations on the tricuspid, mitral and aortic valves. He was considered to have active infective endocarditis (AIE) which had presumably been provoked by VSD and the tooth removal. Penicillin G at a daily dose of 20 million units and gentamicin at a daily dose of 80 mg were intravenously administered to treat the alpha-streptococcus infection for about 4 weeks. Furosemide was used for congestive heart failure. Since, although his cardiac function appeared to have been improved, the signs and symptoms of the infection persisted, triple valve replacement for the tricuspid, mitral and aortic valves and patch closure of the VSD were performed 4 weeks after the hospitalization. The operation revealed inflammatory lesions extending from the endocardium of the right ventricle to the mitral valves through the VSD, and huge vegetations on the tricuspid, mitral and aortic valves. The operation was successful and the inflammatory areas gradually disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of ventricular septal defect associated with active infective endocarditis which was successfully treated by triple valve replacement and ventricular septal defect patch closure]. 174 71

During January 1982 to June 1989, there were 105 evaluable adult cases of native valve infective endocarditis admitted to Department of Medicine, Siriraj Hospital. The incidence was approximately 2.6 per 1,000 admissions. The male to female ratio was 1.4 and the mean age was 31.6 years. Thirty (28.5%) were cases associated with intravenous drug abuse. All non-addicts had pre-existing cardiac lesions susceptible to endocarditis especially rheumatic mitral regurgitation, aortic regurgitation, VSD and PDA. The clinical features of cases without intravenous drug abuse were low grade fever for few weeks, malaise, dyspnea and heart murmur. The addicts with endocarditis presented with acute febrile illness and pulmonary symptoms. Mucocutaneous embolic lesions were detected in one third of the patients. Echocardiography detected vegetations in 50 per cent of the patients. Streptococci were the most common causative agent in 93 per cent of non-addicts whereas the same percentage in addicts were caused by S. aureus. Most of the patients were treated with beta lactams (pen G, ampicillin or cloxacillin) alone or combined with aminoglycosides (streptomycin or gentamicin) for a duration from 10 days to 16 week. Six cases had valve replacement operation due to intractable heart failure and valve ring abscess, 2 had embolectomy of major arteries and 2 had craniotomy due to intracerebral hemorrhage. The overall case fatality rate was 14 per cent. The causes of death were heart failure, cerebral complications and severe pulmonary infections. Clinical response was observed sooner in non-addict patients.
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PMID:Native valve infective endocarditis at Siriraj Hospital, 1982-1989. 179 80

Clinical characteristics of 60 (41 males, 19 females) patients with echocardiographically proven mitral valve prolapse were analysed, with special interest in the associated thoracic skeletal abnormalities. There was a male preponderance (2.2:1) and 91.7% of patients were symptomatic--atypical chest pain, palpitations, exertional dyspnoea and easy fatiguability being the major symptoms. Sixty seven percent had an asthenic body habitus, and 55% had high-arched palate. Thoracic scoliosis (55%), straight back syndrome (50%), flat chest (46.7%), and pectus excavatum (20%) were seen in association with the condition, with 81.7% having any one or combination of these features. Lateral chest radiography showed pancaking of heart shadow in 48.3%. Isolated non-ejection systolic click(s) was the major cardiac auscultatory finding (61.7%), while 60% showed pansystolic prolapse on echocardiography. Electrocardiographic ST-T-U changes in the inferior and/or lateral chest leads were seen in 46.7%, while 16.7% had cardiac arrhythmias. None had infective endocarditis, heart failure or cerebral embolic events. The findings corroborate the view that thoracic skeletal anomalies may be regarded as non-auscultatory features of this syndrome.
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PMID:Mitral valve prolapse syndrome and associated thoracic skeletal abnormalities. 130 Oct 49

Four patients with infective endocarditis caused by Actinobacillus actinomycetemcomitans seen at the National Taiwan University Hospital between January 1985 and December 1990 are reported. There were two men and two women with a mean age of 40 years. Three had had a xenograft replacement, the other one had prolapse of mitral valve. Carious teeth were noted in two. The most common presenting symptoms were fever, cough, dyspnoea, and weight loss and the duration of symptoms before diagnosis varied from 2 weeks to 2 months. Peripheral stigmata of endocarditis were not present in any patient. Laboratory investigation revealed haematuria and anaemia in three patients, and elevated erythrocyte sedimentation rates in all four. None had leucocytosis. Echocardiography was performed more than once for each patient and vegetation was demonstrated in only one. Blood culture became positive after 7-10 days of incubation. One of the isolates was resistant to penicillin. The diagnosis was delayed due to the indolent clinical course, non-specific presentation, and the slow growth of the organism. However, all patients were cured clinically and bacteriologically after 6 weeks of intravenous antibiotic therapy which included penicillin, cefamandole, chloramphenicol, or aztreonam, with or without an aminoglycoside. All patients were free of evidence of recurrence after 6-25 months of follow-up.
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PMID:Actinobacillus actinomycetemcomitans endocarditis: a report of four cases and review of the literature. 180 Oct 59

A 58-year-old man was admitted to hospital because of exertional dyspnoea and a cardiac murmur not previously heard. For one year he was known to have left-sided fibrinous pleuritis. For 5 years he had been taking methysergide for cluster headaches. From 1950-1980 he had worked with asbestos-containing insulating material. Erythrocyte sedimentation rate was greatly increased to 117/136 mm and there was an hypochromic anaemia (Hb 10.4 g/dl). The cholestasis enzymes were elevated (gamma-GT 88 U/l; alkaline phosphatase 511 U/l). Computed tomography of the thorax demonstrated left-sided pleural thickening of up to 3 cm. Endocarditis was excluded (sterile blood culture; normal echocardiogram). There was no evidence of an infectious, immunological or malignant cause for the pleural fibrosis. One year after pleurectomy and having discontinued methysergide all biochemical tests were normal.
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PMID:[Pleural fibrosis as a side effect of years-long methysergide therapy]. 189 55

Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mitral valve prolapse, panic disorder, and chest pain. 189 9

We present a case history of 29-year old female with infective endocarditis, who was admitted 15 months after neurosurgical treatment of disruption of cerebral aneurysm. The diagnosis of organic heart disease had been established in her childhood. 6 months after discharge from neurosurgery she developed marked dyspnoea on exertion and became febrile (up to 39.0 C). The presumptive diagnosis of infective endocarditis was established 6 months later, when she developed the symptoms and signs of severe anaemia with ESR 170 mm/hr although blood cultures were negative. The patient underwent treatment with Penicillin and Debecillin. On admission to our Institute echocardiography showed a very large, mobile vegetation in the left ventricle, connected to the anterior leaflet of mitral valve. Decision of mitral valve replacement was made, but rupture of the next cerebral aneurysm was the reason of unexpected, sudden death of the patient. The postmortem examination revealed 7 x 4 cm large vegetation, with the mass of 7.0 g. Histologically the vegetation consisted of mass of fibrin strands, platelets and blood cell with inflammatory cells. On its base the signs of the process of organization were marked. This vegetation was the largest one that we found in literature on this subject.
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PMID:[Unusually large vegetation on the mitral valve in a patient with bacterial endocarditis]. 194 48


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