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

Mitral valve replacement is considered when there is severe mitral stenosis, severe mitral insufficiency or a combination of the two. Ordinarily, surgical replacement is considered only for patients who are in functional classes III or IV and do not respond to medical management. Patients with symptomatic mitral stenosis should be treated with mitral commissurotomy whenever possible. Patients selected for commissurotomy should have a pliable valve, no other major valve dysfunction, sinus rhythm, no systemic embolism and good left ventricular function. Early operation is not ordinarily required. Mitral insufficiency may require mitral valve replacement in six rather common settings: rheumatic disease, rupture of mitral chordae tendineae, postinfarction rupture of a papillary muscle, intractable infective endocarditis, floppy mitral valve and malfunction of a prosthetic valve. Rupture of mitral chordae tendineae can usually be recognized from the history, physical examination, echocardiogram and angiocardiogram. Severe left ventricular papillary muscle dysfunction is usually due to cardiac infarction, and occurs within the first 9 days of infarction. When only a papillary muscle tip is ruptured the patient may survive long enough for a mitral valve replacement. In infective endocarditis, operation is more often needed because of congestive heart failure than because of refractory infection. Evidence of mitral stenosis or insufficiency in a patient with a previously implanted prosthetic valve usually indicates an urgent need for study and early operation. Uncommon causes of mitral incompetence that may require valve replacement are endocardial fibroelastosis, Marfan's syndrome, calcified mitral anulus, osteogenesis imperfecta, methysergide-induced heart disease and carcinoid heart disease.
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PMID:Indications for surgical replacement of the mitral valve. With particular reference to common and uncommon causes of mitral regurgitation. 37 33

The pathological features of 12 acinar cell neoplasms of the pancreas are described; these comprise 11 carcinomas, of which seven were pure acinar cell growths and four were mixed acinar and ductal carcinomas, and one adenoma. These tumors occurred in a series of 105 during the period 162-75. Thrombotic endocarditis developed in three out the 11 carcinoma cases. The distinctive histological features of these neoplasms and the means of differentiating them from anaplastic carcinomas and certain other carcinomas, for example, islet cell carcinoma, oat cell carcinomas, and carcinoid tumours, are discussed. The poor prognosis of pancreatic cancers is emphasized, and reasons are put forward for believing that future epidemiological studies may need to take account of the histological types of pancreatic carcinoma.
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PMID:Acinar cell neoplasms of the exocrine pancreas. 84 59

The gross surgical pathologic features of the pulmonary valve were reviewed in 116 patients (63 male and 53 female) who had undergone a cardiac operation with pulmonary valve excision at our institution during the period 1973 through 1987. Although the mean age was 12 years, subjects ranged in age from 3 months to 73 years, and 25 patients, including 19 with congenital heart disease, were older than 20 years of age. Among 105 patients who had pure pulmonary stenosis, 61 (58%) had tetralogy of Fallot, 18 had isolated pulmonary stenosis, 23 had other congenital cardiac anomalies, and 3 had carcinoid heart disease. Five patients had pure pulmonary regurgitation (four with tetralogy and one with infective endocarditis), and four had combined pulmonary stenosis and regurgitation (two with congenital cardiac anomalies and two with carcinoid heart disease). In two patients, the valve was neither stenotic nor regurgitant. Thus, congenital heart disease accounted for 110 of the 116 cases (95%), and tetralogy of Fallot was the most commonly observed form (65 cases). Bicuspid pulmonary valve was the most common anomaly and was present in 58% of patients with tetralogy but in only 17% of those with isolated pulmonary stenosis.
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PMID:Surgical pathology of the pulmonary valve: a study of 116 cases spanning 15 years. 259 25

Of multiple etiologies for pure tricuspid regurgitation, the causes may be divided into those associated with anatomically abnormal and anatomically normal tricuspid valves. Conditions associated with anatomically abnormal valves include rheumatic, floppy, Ebstein's anomaly, carcinoid, infective endocarditis, papillary muscle dysfunction, and other rarer causes such as radiation, hypereosinophilic syndrome, and endomyocardial fibrosis. Conditions associated with anatomically normal tricuspid valves include multiple causes of cor pulmonale (chronic obstructive pulmonary disease, primary pulmonary hypertension, and pulmonary hypertension due to mitral stenosis). Of 45 necropsy patients with clinically documented pure tricuspid regurgitation, conditions producing pulmonary hypertension (cor pulmonale, mitral stenosis) were the most frequent etiology (47 percent), followed by floppy (16 percent), rheumatic (11 percent), idiopathic dilated cardiomyopathy (9 percent), Ebstein's anomaly (7 percent), and miscellaneous conditions (10 percent). Of multiple causes of pure mitral regurgitation, tricuspid valve anular circumference and leaflet area are useful measurements in establishing etiology: dilated anuli (greater than 12 cm) are associated with Ebstein's anomaly, floppy valves, and multiple causes of pulmonary hypertension. Increased leaflet areas are associated with floppy valves and Ebstein's anomaly. Anular insertion site separates floppy tricuspid valves from Ebstein's anomaly. Of 21 purely regurgitant operatively-excised tricuspid valves, the etiologies were: rheumatic (43 percent), "functional" due to pulmonary hypertension from mitral stenosis (38 percent), Ebstein's anomaly (9 percent), infective endocarditis (5 percent), and floppy (5 percent). In contrast to etiology of pure mitral regurgitation, rheumatic disease is the leading cause for operative excision of purely regurgitant tricuspid valves. Comparison of systolic pulmonary arterial pressures and tricuspid valve morphology disclosed that pulmonary arterial pressures greater than or equal to 55 mm Hg and tricuspid valve anuli greater than 12 cm were associated with anatomically normal tricuspid valves and that pulmonary arterial pressures less than or equal to 40 mm Hg and tricuspid anuli less than 12 cm were associated with anatomically abnormal tricuspid valves.
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PMID:Etiology of pure tricuspid regurgitation. 353 6

Despite recent renewed interest in the detection of tricuspid valve regurgitation by echocardiographic and Doppler techniques, little morphologic information is available on dysfunctioning tricuspid valves. This report describes 45 necropsy patients with clinical and morphologic evidence of pure (no element of stenosis) tricuspid regurgitation and provides morphometric observations (anular circumference, leaflet area) of the tricuspid valve useful in determining the etiology of pure tricuspid regurgitation. Of 45 patients, 24 (53%) had pure tricuspid regurgitation resulting from an anatomically abnormal valve (prolapse in 7, papillary muscle dysfunction in 6, rheumatic disease in 5, Ebstein's anomaly in 3, infective endocarditis in 2, carcinoid tumor in 1), and 21 (47%) had an anatomically normal valve with systolic pulmonary artery hypertension (cor pulmonale in 12, mitral stenosis in 9). Anular circumference was dilated (greater than 12 cm) in patients with various causes of pulmonary hypertension, floppy valve and Ebstein's tricuspid anomaly. Leaflet area was increased in floppy valve and Ebstein's anomaly. Of the 45 patients, 24 had pulmonary systolic artery pressure measurements available for correlation with tricuspid valve morphology. Pulmonary artery pressures accurately predicted morphologically normal from abnormal valves in 16 patients (89%). Morphologic overlap occurred in six patients with pulmonary pressures of 41 to 54 mm Hg. Of these six, the additional knowledge of normal or dilated anular circumference correctly separated valves with normal and abnormal leaflets.
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PMID:Etiology of pure tricuspid regurgitation based on anular circumference and leaflet area: analysis of 45 necropsy patients with clinical and morphologic evidence of pure tricuspid regurgitation. 395 62

Clinically significant cardiovascular abnormalities may occur as secondary manifestations of noncardiac neoplasms. The principal cardiac effects of noncardiac tumors include the direct results of metastases to the heart or lungs, the indirect effects of circulating tumor products (causing nonbacterial thrombotic endocarditis, myeloma-associated amyloidosis, pheochromocytoma-associated cardiac hypertrophy and myofibrillar degeneration, and carcinoid heart disease), and the undesired cardiotoxicities of chemotherapy and radiotherapy.
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PMID:Cardiac effects of noncardiac neoplasms. 640 9

Little morphologic information is available on operatively excised pulmonic valves. The causes of pulmonic stenosis are limited to a few conditions: (1) rheumatic and (2) nonrheumatic (congenital, carcinoid, infective endocarditis). Congenital causes of pulmonic stenosis constitute well over 95% of these conditions. Congenital types of pulmonic stenosis include acommissural dome-shaped, dysplastic, and bicuspid. Rare acquired causes of pulmonic stenosis include carcinoid, rheumatic, and infective endocarditis. Of the acquired causes of pulmonic stenosis, carcinoid is the most common condition. In contrast, causes of pure pulmonic regurgitation are multiple. Two major categories of pure pulmonic regurgitation include (1) conditions associated with anatomically abnormal valve cusps (congenital, rheumatic, carcinoid, trauma, and infective endocarditis) and (2) conditions associated with anatomically normal cusps (elevated pulmonary artery systolic pressures, idiopathic dilated pulmonary trunk, and Marfan's syndrome).
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PMID:Pathology of pulmonic valve stenosis and pure regurgitation. 770 86

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis are reviewed. In over 90% of stenotic tricuspid valves, the etiology is rheumatic disease. In isolated tricuspid stenosis, the etiology is either carcinoid or congenital. Rare causes of tricuspid stenosis include active infective endocarditis, metabolic or enzymatic abnormalities (Fabry's, Whipple's disease), and giant blood cysts.
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PMID:Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I. 772 Feb 97

Cardiovascular emergencies in oncology patients include all of the usual cardiac problems, as well as complications of cancer and its therapy. Pericardial effusions and tamponade, cardiac masses, and extrinsic compression of the heart and great vessels by tumor masses, or fluid collections may all occur. Certain tumors may secrete mediators that are directly toxic to the heart; for example, catecholamines are secreted by pheochromocytomas and serotonin is secreted by carcinoid tumors. Tumors can also cause arrhythmias due to the mediators they secret or to direct mechanical irritation of the heart or pericardium. Cancer therapy is also associated with cardiac emergencies. Perioperative myocardial ischemia or infarction, as well as arrhythmias, may complicate surgery. Pericardial effusions and tamponade can follow surgery, radiation, or chemotherapy. Chemotherapy with anthracyclines, mitoxantrone, and trastuzumab may prompt acute and chronic heart failure. 5-Fluorouracil causes coronary spasm in some patients, leading to angina, myocardial infarction, arrhythmias, and/or sudden death. Cyclophosphamide, particularly in high doses, may produce acute myopericarditis. Radiation may cause acute pericardial disease and late sequelae such as myocardial infarction, acute valvular insufficiency, or effusive constrictive pericarditis. Endocarditis also occurs in cancer patients in association with vascular access devices and immune compromise. This review will discuss each of these complications of cancer and its therapy.
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PMID:Cardiovascular emergencies in the cancer patient. 1086 14

Appetite suppressants fenfluramine, dexfenfluramine, and phentermine have been used alone or in combination as an alternative to diet and surgery in the management of obesity. This therapy was halted in 1997 after reports of valvular lesions affecting almost one third of patients treated with these drugs. Fortunately, most cases of appetite suppressant-related valve disease are mild or moderate and rarely required valve repair or replacement. Follow-up studies have suggested improvement in valvulopathy after discontinuation of the treatment. The mechanism of valve disease induced by these drugs is speculative and may be related to their serotonergic effects. Echocardiographic features are similar to carcinoid heart disease and valvulopathy associated with ergot use. Most cases require only follow-up and endocarditis prophylaxis; surgery is rarely needed.
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PMID:Appetite suppressants and valvular heart disease. 1235 24


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