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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several lipid-related reactions involving coagulation and fibrinolytic mechanisms have been described. Many of these reactions have been related to the development of atherosclerosis and thromboembolism. In this article, I review the antiphospholipid antibody syndrome, the tissue factor pathway inhibitor, the involvement of fatty acids in fibrinolysis, and the Lp(a) lipoprotein.
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PMID:Lipid-related clotting reactions of clinical significance. 145 82

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

The authors describe a healthy young male smoker with familial history of recurrent thromboembolism who presented with severe, rapidly progressive lower limb ischemia and abnormal results from liver function tests. An arteriogram of the lower extremities showed bilateral infrainguinal atherosclerotic arterial occlusions. The laboratory findings, in addition to abnormal liver function findings, included moderately elevated antiphospholipid antibodies and hemostatic abnormalities involving elevated fibrinogen, lipoprotein (a) levels, and deficient fibrinolysis. He underwent bilateral femoral thrombectomy, which was followed by a meticulous anticoagulation, and had gradual improvement of ischemic symptoms and liver functions. This is, to their knowledge, the first reported case in the English literature of premature lower extremity atherosclerosis and antiphospholipid syndrome associated with elevated lipoprotein (a) levels and documented complex hemostatic abnormalities contributing to systemic thrombosis.
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PMID:Massive lower extremity arterial thrombosis and acute hepatic insufficiency in a young adult with premature atherosclerosis associated with hyperlipoprotein(a)emia and antiphospholipid syndrome. A case report. 766 91

The occurrence of cardiac manifestations and their relationship with the lupus anticoagulant (LA) in SLE was studied in 74 patients who were followed up for 22 years (median), of which 16 years were after the initial LA testing. Pericarditis was the most common cardiac event occurring in 16 (22%) patients but it did not correlate with LA. Valvular heart disease, coronary artery disease, left ventricular failure and/or cor pulmonale were observed in 16 (22%) patients. Taken together, their occurrence was associated with a history of leg ulcers (odds 3.8, P = 0.028) but not with LA or other common clinical manifestations of the antiphospholipid syndrome. Valvular heart disease in five patients was significantly associated with LA (P = 0.05). Cor pulmonale due to chronic pulmonary embolism was present in two patients with LA. Myocardial infarctions in five patients occurred late in the course of disease but in relatively young patients (mean 43 years). Fatal myocardial infarction in the absence of atherosclerosis in two LA-positive patients supports a pathogenetic role for LA in these cases. In conclusion, of the various cardiac complications in SLE, valvular heart disease and cor pulmonale appear to be connected with the antiphospholipid syndrome. Both conditions should be actively sought in patients with LA to decrease possible adverse events (arterial emboli and right ventricular failure) affecting the patients' prognosis.
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PMID:Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus. 795 2

The objective of this study was to determine the prevalence and clinical significance of elevated antiphospholipid antibodies (APA) in a large series of patients admitted to a department of Internal Medicine. At the end of entry phase, 1014 patients were tested (488 males-526 females, mean age: 66.7 years, range 18-97). Seventy-two (7.1%) patients were found APA positive at least once: 44 males and 28 females, mean age 69 years, range 23 to 94. Twenty fulfilled the criteria of Primary Antiphospholipid Antibody Syndrome: 10 patients were referred for deep vein thrombosis, 3 had history of deep vein thrombosis, 1 had both arterial thrombosis and a history of venous thrombosis; 2 had thrombocytopenia; 3 had stroke, 1 had a history of a stroke. One patient had SLE according to ARA classification. The most frequent associated disease was cancer: 14 patients, 9 had evolutive malignant disease, 5 were in clinical remission of neoplasia. Other clinical conditions included chronic and/or acute alcoholic intoxication (n = 8), severe atherosclerosis (n = 4), leg ulcer (n = 4). Insufficient data are available about the evolution, but 7 patients died in the year following diagnosis. Eight patients had fluctuations in APA detection: 2 initially APA positive became negative, 5 initially negative became positive and 1 patient was alternatively positive, negative and positive without steroid treatment. Thus, as expected, APA occur in a variety of clinical disorders. The association with cancer or alcoholic intoxication deserves further investigations.
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PMID:A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. 798 47

Of 20 patients with antiphospholipid syndrome 6 were found clinically and upon special tests to have signs of ischemic heart disease. All the 6 had shifts in lipid spectrum of plasma. It is important to study coronary pathology in antiphospholipid syndrome to elucidate mechanisms underlying thrombosis and vascular atherosclerosis in human diseases.
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PMID:[The manifestations of IHD and the status of the coronary arteries in patients with the antiphospholipid syndrome]. 877 98

Vascular damage in systemic lupus erythematosus (SLE) occurs through vasculitis, premature atherosclerosis, and hypercoagulability (predominantly due to the antiphospholipid antibody syndrome). In the Hopkins Lupus Cohort, a prospective cohort study, the incidence of thrombosis is 2 per 100 person-years of follow-up. Markers of immune-complex mediated injury (high anti-dsDNA and low C3), atherosclerosis (hypertension, hyperlipidemia, homocysteine) and antiphospholipid antibodies (lupus anticoagulant or anticardiolipin) are independent predictors of thrombosis. Hydroxychloroquine use is protective against future thrombosis.
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PMID:Thrombosis and systemic lupus erythematosus: the Hopkins Lupus Cohort perspective. 879 94

The family of antiphospholipid antibodies includes antibodies binding to cardiolipin in serological test for syphilis, antibodies prolonging the clotting time in lupus anticoagulant test, antibodies reacting with plasma phospholipid-binding proteins, such as beta 2-glycoprotein I and prothrombin, and antibodies binding to oxidized low-density lipoprotein (LDL). Antiphospholipid antibodies are traditionally associated with arterial and venous thrombosis in patients with primary or secondary antiphospholipid syndrome. The recent studies, especially those on patients with myocardial infarction, extend the concept of antiphospholipid antibodies, and suggest that they play a role also in atherosclerosis. Based on the clinical studies and immunological findings, it seems that the differences in the specificity of antiphospholipid antibodies may reflect to their pathogenetic mechanisms and, finally, to their clinical consequences. The present review suggests that antibodies to oxidized LDL may not interfere directly with blood coagulation, but seem to have importance in the inflammation of the vessel wall in atherosclerosis and in vasculitis. Instead, antibodies to beta 2-glycoprotein I and to prothrombin show a closer association with thrombosis. It is possible that in the atherosclerotic plaque, the plasma proteins, such as beta 2-glycoprotein I or prothrombin, are bound to the endothelial surface and antibodies to cryptic epitopes revealed in these proteins are induced. These antibodies may contribute to the formation of atherosclerotic thrombosis by changing the balance of haemostasis toward hypercoagulative state.
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PMID:Antiphospholipid antibodies and atherosclerosis. 890 78

Patients with the antiphospholipid syndrome as well as those with a lack in the prostacyclin synthesis stimulating plasma factor (PF) are prone to develop thrombophilia and are at a higher clinical risk for vascular disease. As patients with the antiphospholipid syndrome have been reported to show elevated lipoprotein (Lp)(a) levels, we re-examined all our patients known to have an inborn or an acquired persistent deficiency of PF. Their non-affected relatives served as controls. In addition, 36 patients suffering from clinically manifested atherosclerosis as well as 16 healthy adults, all of them having elevated Lp(a) levels (> 30 mg/dl), were screened for a PF deficiency. In fact, all the patients with a deficient PF activity showed elevated Lp(a) values. While the prevalence of PF deficiency ranges about 1-2%, in 7 (19%) patients with clinically manifested atherosclerosis and 3 (19%) healthy adults with elevated Lp(a) this defect was found. The findings demonstrate an association between PF deficiency and Lp(a), indicating a biochemical interaction which needs to be further elucidated.
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PMID:Is a (n inborn) deficiency of prostacyclin synthesis stimulating plasma factor associated with increased lipoprotein(a)? 898 34

Anticardiolipin antibodies (aCL) in the sera of patients with antiphospholipid syndrome (APS) recognize an altered structure of beta 2-glycoprotein I (beta 2-GPI) interacting with solid-phase negatively charged phospholipids. beta 2-GPI bound to Cu2+-oxidized plasma lipoproteins, i.e. oxidized very low-density lipoprotein (oxVLDL), oxidized low-density lipoprotein (oxLDL), or oxidized high-density lipoprotein (oxHDL). beta 2-GPI inhibited in vitro uptake, i.e. cell surface binding, cellular association, and proteolytic degradation of oxLDL by murine macrophage J774A.1 cells. The binding of oxLDL to the macrophages was inhibited by the addition of polyinosinic acid (poly (I)), a competitor of the scavenger receptor, but not by another polyanionic acid, polycytidylic acid (poly (C)). Conversely, the binding of oxLDL was significantly increased by the simultaneous addition of human beta 2-GPI and monoclonal aCL derived from NZW x BXSB F1 (WB F1) mice, an animal model of APS, or anti-beta 2-GPI antibodies from BALB/c mice immunized with human beta 2-GPI. These findings indicate that beta 2-GPI may be an antiatherogenic protein and that the autoimmune response against beta 2-GPI may have a role in the development of atherosclerosis in APS.
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PMID:Involvement of beta 2-glycoprotein I and anticardiolipin antibodies in oxidatively modified low-density lipoprotein uptake by macrophages. 906 34


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