Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1969 to 1974, 19 cases of Serratia marcescens endocarditis were observed in the San Francisco Bay Area. Seventeen patients were intravenous drug users, and Serratia caused 14% of all addict-associated endocarditis in San Francisco. Serratia strains were nonpigmented and had typical antibiotic sensitivities, except that 9 of the isolates exhibited colonial variation, with each variant having different antibiotic sensitivities. Aortic or mitral valves were involved in 13 patients, and heart failure developed in 9 of these. Twelve patients had embolic episodes to brain, iliofemoral arteries, or lung. Five of 6 patients with tricuspid valvulitis were cured by antibiotics either with (1) or without excision of the valve. All 12 patients with aortic or mitral valvulitis treated medically died; 11 had unremitting sepsis. Aortic valve replacement and antibiotics were effective in 1. Gentamicin combined with either carbenicillin or chloramphenicol was the most effective treatment regimen.
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PMID:Serratia marcescens endocarditis: a regional illness associated with intravenous drug abuse. 110 90

We reviewed the autopsy material of 169 patients with rheumatoid arthritis (RA) and studied the cardiac changes is these patients. Systemic vasculitis was observed in 26 cases (15.38%) among 169 patients with RA. In 17 cases (10%) we found vasculitis of the subepicardial and/or intramural coronary vessels. Coronary arteritis or arteriolotis has led to multifocal small, and/or large myocardial infarctions in 10 cases (5.9%) and was the cause of progressive cardiac insufficiency, the direct cause of death. Multifocal circumscribed myocardial infarction reported in rheumatoid disease. In 8 cases rheumatoid nodules were found in the myocardium, 3 of them related to vasculitis. We suggest that rheumatoid nodules are the most severe form of necrotizing granulomatous vasculitis. Pathognomic nodular rheumatoid pericarditis was seen in 3 cases and diffuse rheumatoid pericarditis in another case. Pathognomic nodular valvulitis was found in 7 cases. Rheumatoid nodules localized to the epi-, myo-, or endocardium were observed on 9 patients. Generalized secondary amyloidosis was observed in 32 (18.93%) of the 169 patients with RA. Secondary amyloidosis was prevalent in the heart in 29 of 32 cases (relative frequency: 90.62%).
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PMID:Cardiac changes in rheumatoid arthritis. 136 61

Described in this paper are pathomorphological alterations to the heart postmortem recorded from 100 deceased with rheumatoid arthritis. Vasculitis of subepicardial or intramural rami of coronary arteries was recorded from twelve cases and had caused multiple myocardial necrosis in ten of these. These developments had led to progressive cardiac insufficiency which actually then was the direct cause of death. Formal pathogenesis of vasculitis-related multifocal myocardial necrosis in concomitance with rheumatoid arthritis had never been described in the literature before, although such reference would have been justified for the clinical consequences for which it deserves to be emphasised as a nosological entity in its own right. Isolated rheumatic nodes were detected in the myocardium of five of the decreased and could be attributed to rheumatic arteritis in two cases. Those myocardial rheumatic nodes, according to the author's view, represent the severest form of necrotising rheumatic vasculitis. Pathognomonic pericarditis was found in four cases (2 pericarditis nodularis and 2 pericarditis rheumatica). Pathognomonic nodular valvulitis was identified in another four cases. Systemic secondary amyloidoses were found to be present in 24 of the above 100 deceased with chronic polyarthritis. The heart was involved in 23 of these 24 cases (95.8%).
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PMID:[Heart alterations in chronic polyarthritis]. 176 83

A 40 year old man with a history of myocardial infarction and hypertension presented with transient cerebral ischaemic attacks, aortic regurgitation, a raised erythrocyte sedimentation rate, and thrombocytopenia. The anticardiolipin syndrome was diagnosed and he was treated with prednisolone and warfarin. He died two years later after the development of acute heart failure. At necropsy his heart showed widespread arteriolar thrombosis without vasculitis, recanalised large vessel occlusion, and a "post-inflammatory" valvulitis of the aortic valve.
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PMID:Findings at necropsy in the heart of a patient with anticardiolipin syndrome. 275 75

The clinical characteristics and prognosis of 16 cases of mitral regurgitation (MR) secondary to Kawasaki disease (KD) were studied, and its pathogenesis was discussed. The observation period ranged from 3 years and 17 months to 15 years. Six of the 16 patients died, and 10 are alive. MR has disappeared spontaneously in 2 of these survivors. Thirteen of the 16 patients were male and 3 were female, there being a predominance in male, which is a striking contrast to rheumatic mitral regurgitation which is predominant in females. The age at the time of diagnosis ranged from 3 months to 7 years. The appearance time of MR showed two different patterns, one with early onset within a few weeks to one month after affliction with KD and the other with MR developing months or years later during the course of the follow-up. The cardiothoracic ratio was greater in those who had a progressively downhill course, and whose sigma RV1-6 decreased with time course. This was considered to be due to the decrease of the remaining functioning myocardial mass. The outcome of the patients with a severe degree of coronary arterial stenosis and occlusion observed on the coronary angiogram was poor. The prognosis of the patients with severe left coronary arterial stenosis was especially poor. MR due to KD is regarded as a new clinical entity, and its pathogenesis is thought to be due to ischemia, papillary muscle dysfunction, coronary angitis, myocardial failure and valvulitis. Incidence of MR will increase when examined by Doppler echocardiography especially in the acute stage. Our experience as well as that of others indicates the presence of valvulitis, myocarditis or left ventricular dilatation leading to MR in the acute stage.
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PMID:Mitral regurgitation in Kawasaki disease. 342 45

The pathology and clinical features of 258 cases of mitral ring calcification were reviewed. The overall incidence in patients over 50 years of age was 8.5%; it was more than twice as high in women (11.5%) as in men (4.5%) and rose sharply with age. Cardiac failure and systolic murmurs were each noted in over half the patients. Hypertension was slightly commoner than in age- and sex-matched groups without ring calcification, although the difference was not statistically significant. Small nodules of calcification were more frequent in men and heavy deposits in women. Distortion and atrial displacement of the posterior mitral cusp was present in 26% of the hearts with early ring calcification, in 56% of the hearts with moderate, and in almost all hearts with marked changes. Systolic murmurs had been heard in 73% of these cases. ;Caseation' of the calcified ring was seen in seven hearts and haemorrhagic valvulitis in three. Calcium had ulcerated through the cusp in 12 cases, with thrombotic and/or bacterial endocarditis in five. Aortic valve calcification was present in 36% of men and was quantitatively related to the severity of mitral ring calcification. In women the incidence was 30% and there was no corresponding quantitative relationship. Microscopy showed nonspecific chronic inflammatory changes adjacent to calcium in about half the cases in both sexes, with foreign body type giant cells in 6%. Similar inflammatory changes in the valve cusp were almost twice as common in women as in men. There was no evidence that previous endocarditis was responsible for mitral ring calcification, neither did parity influence its incidence. Severe coronary atherosclerosis was unrelated but severe aortic atherosclerosis was commoner in patients with calcified mitral rings. The difference, in women, was statistically significant. The higher incidence of severe degrees of ring calcification, complications, and valvular inflammation in women suggests a sex-determined difference in tissue response in the mitral area. Possible provoking factors apply to both sexes and both left side valves, and such a difference would account for the relative frequency and sex incidence of mitral ring calcification.
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PMID:Pathological and clinical study of calcification of the mitral valve ring. 543 Apr 24

Although nonspecific pericarditis, myocarditis, valvulitis, and coronary arteritis are known as cardiac lesions that accompany rheumatoid arthritis (RA), there have been few reports of the occurrence of clinically severe valvular disease. We report here the case of 69-year-old man with a 25-year history of RA who died of acute left-sided heart failure complicating to aortic steno-insufficiency and angina pectoris. Autopsy findings revealed the coincidence of a congenital bicuspid aortic valve with chronic inflammation, fibrosis and calcification; eccentric hypertrophy and myocardial fibrosis of the left ventricle; 75% luminal narrowing of the proximal portion of the coronary artery due to atherosclerosis, and narrowing of the small arteries of the cardiac muscle due to angitis. It is deduced that the coronary artery lesions, aortic valve lesions and myocardial lesions were aggravated by the bicuspid aortic valve, changes with ageing and corticosteroid therapy.
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PMID:An autopsy case of rheumatoid arthritis with aortic steno-insufficiency, angina pectoris and severe heart failure. 648 41

Thirty-three children with acute rheumatic fever were studied using echocardiography to characterize heart involvement in this disease. Among 26 subjects with a first episode of acute rheumatic fever, 18 had a clinical diagnosis of carditis and six had heart failure. Heart failure usually resulted from valvular incompetence rather than from myocardial failure in these patients. Conversely, among seven subjects with recurrent rheumatic fever, five had a clinical diagnosis of carditis and four had heart failure. Severe left ventricular dysfunction noted on echocardiography probably contributed significantly to the appearance of heart failure in two of these four subjects. Ten patients were initially believed not to have carditis: a diagnosis of mitral valvulitis was made in two of these ten on the basis of the results of the echocardiographic examination. Echocardiography, which provides important information on the cardiac status of patients with acute rheumatic fever, may help in assessing the prognosis and may be useful in the therapy of these patients.
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PMID:Clinical-echocardiographic correlations in acute rheumatic fever. 683 70

We recently encountered a 49-year-old female who developed fever due to group A streptococcal (GAS) bacteriaemia spreading to an abscess in the iliac muscle and a bacterial monarthritis of the right knee with a sterile arthritis of her left knee. Treatment was started with a six-week course of intravenous penicillin. She developed a mitral valve insufficiency and pericarditis on the tenth day of admission. In the third week heart failure developed with, on echocardiograph, a high output left ventricular failure without signs of valvulitis or myocarditis. Using a diuretic regimen she was recompensated. Because of the pericarditis with mitral valve insufficiency corticosteroids were given, which had a rapid beneficial effect. A discussion follows on the position of acute rheumatic fever versus post-streptococcal reactive arthritis in this clinical picture and the literature is updated.
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PMID:Cardiac failure following group A streptococcal infection with echocardiographically proven pericarditis, still insufficient arguments for acute rheumatic fever: a case report and literature update. 1273 24

A case of polyarteritis nodosa in the first year of life with the clinical picture dominated by pyrexia, an initial upper respiratory element, episodes of tachycardia, and sudden death three weeks after the onset is described. The necropsy showed evidence of polyarteritis nodosa, myocarditis, and valvulitis as well as congenital pyloric hypertrophy. Clinical manifestations of the latter had preceded the final illness and the two diseases were not thought to be related. The previous 19 cases reported in the first year of life are reviewed, and support is given for the concept that at this age a rash, pyrexia, upper respiratory manifestations, and progressive heart failure or sudden death are characteristic clinical manifestations and that the heart is often the site of the major lesions at necropsy. The possible role of hypersensitivity is discussed. There was no evidence for it in the present case.
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PMID:Polyarteritis nodosa and congenital pyloric hypertrophy in a 3-month-old infant. 1444 9


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