Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

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

The Committee reviewed cardiac involvement in the antiphospholipid antibody syndrome. The Committee's recommendations are: Valve abnormalities: anticoagulation is recommended for symptomatic patients with valvulopathy. Prophylactic antiplatelet therapy may be appropriate for asymptomatic patients (recommended by 13/17 experts in an independent review). Committee members disagreed whether corticosteroid therapy is helpful, but agree that distinguishing among presumptive valvulitis (valve thickening on echocardiogram), valve deformity and vegetations is important, as treatment implications may differ. Occlusive arterial disease (angina, myocardial infarction): the Committee recommends aggressive treatment of all risk factors for atherosclerosis (hypertension, hypercholesterolaemia, smoking) and liberal use of folic acid, B vitamins and cholesterol-lowering drugs (preferably statins). Hydroxychloroquine for cardiac protection in APS patients may be considered. The Committee also recommends warfarin anticoagulation for those who have suffered thrombosis in the absence of atherosclerosis, but recognizes that developing data may support the use of antiplatelet agents instead. Intracardiac thrombi: the Committee recommends intensive warfarin anticoagulation, and consultation with cardiac surgeons when appropriate. Ventricular dysfunction: the Committee has no recommendations on this aspect of cardiac disease. Pulmonary hypertension: the Committee recommends intensive anticoagulation with warfarin and clinical trials of bosentan, epoprostenol and other new agents.
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PMID:Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee consensus report. 1289 91