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)

A 38 year old woman with systemic lupus erythematosus (SLE) was admitted because of epigastralgia and fever. The diagnosis of SLE was made 22 years ago based on Raynaud's phenomenon, butterfly rash, hair loss, photosensitivity and positive antinuclear antibody. She had episodes of consciousness disturbance, transient visual disturbance of the left eye, and a necrosis of the left big toe. She underwent artificial arthroplasty of bilateral femoral heads 11 years ago, when multiple aseptic necroses of thirteen bones were found, and when anti-cardiolipin (CL) antibody was found to be positive. An echogram of abdomen suggested an obstruction of superior mesenteric artery (SMA) when she was admitted. Selective angiography revealed a complete obstruction of SMA and splenic artery, and incomplete obstruction of celiac artery. Conservative treatment with urokinase infusion and prednisolone 50 mg/day was not effective, and small intestine and right colon were resected on the 23rd hospital day. The pathological examination showed thrombosis of SMA. There was no evidence of arteritis or atherosclerosis. Anti-CL antibody and lupus anticoagulant were positive on admission, but the level of both anti-DNA antibody and complement was normal. Therefore, it was suggested that the thrombosis was related with anti-phospholipid antibody. The characteristic clinical feature were multiple aseptic bone necroses and thromboses of several arteries. We discussed the relationship of thrombosis and the etiology of multiple bone necrosis in this case with anti-phospholipid antibody.
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PMID:[A systemic lupus erythematosus patient with multiple aseptic bone necroses, thrombosis of superior mesenteric artery and anti-phospholipid antibody]. 144 87

Patients with systemic lupus erythematosus may develop premature atherosclerosis, notably coronary artery disease. A group of 10 patients with peripheral vascular disease presenting with intermittent claudication or gangrene were studied from a group of 563 patients followed prospectively at the Wellesley Hospital Lupus Clinic. These 10 patients were compared with the next lupus clinic patient matched for age and sex, with respect to demographic characteristics and risk factors. The patients and controls did not differ significantly in lupus activity criteria count, partial thromboplastin time, the number with antibody to cardiolipin, number receiving steroids or mean steroid dose, family history of atherosclerosis, hyperlipidaemia, smoking, hypertension or use of oral contraceptives. The risk factors for developing peripheral vascular disease were a longer duration of systemic lupus erythematosus and a longer duration of use of steroids. Eight of the 10 patients had coexistent coronary artery disease or transient ischaemic attack.
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PMID:Peripheral vascular disease in patients with systemic lupus erythematosus. 154 39

The antiphospholipid syndrome was diagnosed in 19 of 1078 patients treated between 1987 and 1991. All patients with antiphospholipid syndrome had either anticardiolipin antibody (16/19) or lupus anticoagulant (10/19); three patients had thrombocytopenia, eight patients had a prolonged partial thromboplastin time, and 10 patients had an elevated erythrocyte sedimentation rate. The most common site of involvement was the cerebral circulation (nine patients), manifested by transient ischemic attacks or stroke. Eight patients had upper extremity disease, characterized by symptoms of Raynaud's phenomenon, with angiographic lesions involving the brachial, radial, ulnar, and/or digital arteries. Lower extremity disease occurred in seven patients, with clinical presentations similar to those of atherosclerosis and varying angiographic patterns. In comparison with the population having atherosclerosis, patients with arterial manifestations of antiphospholipid syndrome were more likely to be women (13 of 19 versus 411 of 1078, p less than 0.02), were significantly younger (46.2 years versus 63.6 years, p less than 0.0001), did not smoke (1 of 19 patients versus 700 of 1078, p less than 0.0001), had a higher percentage of upper extremity involvement (8 of 18 versus 13 of 1078, p less than 0.0001), and had a higher incidence of early graft failure (9 of 12 grafts versus 13 of 371 grafts, p less than 0.0001). The syndrome is associated with the repetitive failure of vascular reconstructions and occlusion of native vessels. Antiphospholipid syndrome should therefore be suspected in young, female, nonsmokers with vascular disease, especially those with involvement of the upper extremity, cerebrovascular disease with normal findings on extracranial carotid angiography, and premature graft failure.
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PMID:Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis. 172 74

Coronary artery disease has emerged as an important cause of death in young patients with SLE. We report three cases of acute myocardial infarction in young lupus patients who underwent emergent coronary angiography. One patient had a large coronary aneurysm and died five months later from myocarditis. The other two patients underwent coronary angioplasty. The difficulty in distinguishing coronary arteritis from premature atherosclerosis and its relevance to methods of treatment is discussed.
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PMID:Evaluation and treatment of acute myocardial infarction complicating systemic lupus erythematosus. 173 66

Acute myocardial infarction is a potentially fatal complication of SLE. Reported mechanisms include atherosclerosis, arteritis and coronary arterial spasm. The following case report presents a fourth possible cause; intracoronary thrombus with angiographically normal coronary arteries in a patient with active lupus and AMI.
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PMID:Myocardial infarction due to intracoronary thrombi without significant coronary artery disease in systemic lupus erythematosus. 186 45

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Fifty-six patients, 49 females and 7 males, with the confirmed diagnosis of systemic lupus erythematosus were examined by M-mode, 2--D and Doppler echocardiography. Pericardial effusion was found in 15 patients (27%), while pericardial thickening was suspected in 6 additional patients (37.5% altogether). Two patients had the signs of a pericardial tamponade, but both of them were uraemic. Libman-Sacks endocarditis was suspected in 4 patients (7.5%) because of verrucous changes in the aortic or mitral valve and regurgitant jet. Slight to moderate left ventricular hypocontractility was present in 3 patients (5%), while 3 additional patients had borderline values of the left ventricular contractility parameters. Left ventricular hypertrophy, usually mild, was found in 21 patients (37.5%). Echocardiographic signs of pulmonary hypertension were present in 2 patients (3.6%). It has been concluded that pericardial affection is frequent during the course of systemic lupus erystematosus, while a diffuse myocardial involvement is rare, except the consequences of arterial hypertension and accelerated coronary atherosclerosis. Libman-Sacks endocarditis still represents a diagnostic problem. For a more precise definition of cardiac involvement in systemic lupus erythematosus, a comparative analysis of the disease activity and immunosuppressive therapy is needed.
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PMID:[Echocardiographic analysis of changes in the heart in patients with systemic lupus erythematosus]. 207 23

The importance of a prothrombotic state as a cause of ischemic stroke in young adults is ill defined. We examined 46 unselected patients under age 50 years with cerebral ischemia for anticardiolipin antibody (aCL) and lupus anticoagulants (LA), over a 3-year-period. Age- and sex-matched patients with other neurologic diseases served as a noncerebral ischemia comparison group to test whether (1) stroke/transient ischemic attacks (TIA) in young people is associated with aCL and/or LA, and (2) their presence is specific to cerebral ischemia. In the stroke/TIA group, 21 patients had aCL or LA and 25 had neither, whereas in the control group, 2 patients had aCL and 24 had neither. Equal numbers of stroke/TIA patients with and without antiphospholipid antibodies (aPL) had other stroke risk factors. Patients with aPL and cerebral ischemia, however, had a more frequent history of multiple events than those without them. These antibodies occur with undue frequency in young patients with stroke/TIA and are not associated with a concurrent diagnosis of systemic lupus in most cases. A coexistent aPL-associated prothrombotic state may be a key determinant of whether patients with atherosclerosis, mitral valve prolapse, or other structural lesions experience recurrent ischemia.
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PMID:Antiphospholipid antibodies and cerebral ischemia in young people. 211 4

Myocardial infarction has rarely been reported in patients with systemic lupus erythematosus but may develop late in the disease usually as a result of severe and accelerated atherosclerosis or coronary arteritis. A 32-year-old man with untreated and unrecognized systemic lupus erythematosus, in the absence of conventional coronary risk factors (except family predisposition) and definite extracardiac manifestations of systemic lupus erythematosus had a silent myocardial infarction early in the course of the disease. A coronary arteriogram revealed multiple stenosis of the left anterior descending artery and critical stenosis of the right coronary artery. It is our belief that lupus vasculitis is a likely contributing factor in the development of obstructive coronary disease in this patient.
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PMID:[Silent myocardial infarct as a main manifestation of systemic lupus erythematosus]. 232 60

Dyslipoproteinemia, a feature of systemic lupus erythematosus may contribute to premature atherosclerosis. In order to develop an experimental model for this dyslipoproteinemia we measured plasma concentrations of lipoproteins in juvenile NZB/W (lupus) and NZB/B (control) mice. Additionally to evaluate the effects of a diet rich in n - 3 fatty acids we measured lipoprotein concentrations in mice on normal or menhaden oil-enriched diets. The lupus mice had elevated triglycerides compared to the controls, similar to that seen in human SLE patients (161 +/- 31 vs 113 +/- 13 mg/dl, P less than 0.003). In contrast, the menhaden oil diet fed NZB/W mice had triglycerides similar to the NZB/B control fed group. In the NZB/W murine SLE model, dyslipoproteinemia is an early sign of disease as has been shown in man, therefore this model will be useful in elucidating the mechanism of dyslipoproteinemia in SLE.
Atherosclerosis 1989 Oct
PMID:Dyslipoproteinemia in murine systemic lupus erythematosus. 259 28


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