UMLS:C0004153 - FACTA Search

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 order to determine if cystathionine beta-synthase (CBS) could separate groups of patients with various vascular disease, CBS activity was studied in cultured human skin fibroblasts from 30 subjects being either controls, atherosclerotic patients or patients having suffered a deep venous thrombosis. We found a tendency to a negative correlation between age and CBS activity in the control group only (r = -0.58, P = 0.08), with a tendency to lower CBS activities in the young patients with atherosclerotic (4.9) or venous disease (5.3) compared to the young control group (10.2). This could implicate higher levels of p-homocysteine with increased age as well as in young patients with atherosclerotic or thrombotic disease causing vascular damage. The results are important for the further discussion of the role of homocysteine as a risk factor for developing atherosclerotic and thrombogenic vascular disease and for finding a suitable screening method as prevention is by vitamin supplement only.
Atherosclerosis 1998 Aug
PMID:Age and cystathionine beta-synthase activity in cultured fibroblasts from patients with arterial and venous vascular disease. 971 28

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease resulting from the thromboembolic obstruction of the segmental and/or large size pulmonary arteries, subsequently leading to pulmonary arterial hypertension. Incomplete resolution of acute pulmonary emboli and thrombus organization are believed to be important for the development of the disease. Primary pulmonary hypertension (PPH) is a further disease that at present is poorly understood but shows a clinical picture similar to CTEPH. Since lipoprotein(a) [Lp(a)]. a genetically determined risk factor for atherosclerosis and thrombosis, has been found increased in plasma of patients with deep vein thrombosis and pulmonary embolism, we measured plasma Lp(a) levels in 40 patients with CTEPH and 50 patients with PPH and compared them to 50 matched controls. The median for Lp(a) plasma levels was significantly higher in CTEPH patients (26.6 mg/dl) than in PPH patients (9.6 mg/dl) and controls (7.2 mg/dl). Increased plasma Lp(a) could, therefore. play a significant role in the mechanisms of ongoing thrombosis and thrombus organization in CTEPH, while its possible role in PPH can be limited to a small number of patients.
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PMID:Plasma Lp(a) levels are increased in patients with chronic thromboembolic pulmonary hypertension. 971 43

Antiplatelet drugs have been demonstrated to reduce the incidence of myocardial infarction (MI), stroke or vascular death in patients with vascular disease. There are no data suggesting that antiplatelet therapy acts differently in older people than in younger people and recommendations based on randomised clinical trials are probably generalisable to older people. Aspirin (acetylsalicylic acid) has been shown to reduce the incidence of non-fatal MI, nonfatal stroke and vascular death in patients with acute MI, a previous MI, angina pectoris or peripheral occlusive arterial disease (POAD), and to reduce cardiovascular morbidity and mortality in patients with a prior ischaemic stroke or transient ischaemic attack (TIA). It has also been shown to reduce the incidence of thrombus formation after coronary artery bypass graft surgery and percutaneous transluminal angioplasty, and in patients with atrial fibrillation and heart valve replacements. Deep vein thrombosis and pulmonary embolism after surgery are also prevented by aspirin. The available data allows the following recommendations to be made. Aspirin 160 to 325 mg daily should be administered to older men and women without contraindications to aspirin who have acute MI, prior MI, unstable or stable angina pectoris, ischaemic stroke, TIA or POAD, and continued indefinitely to reduce the risk of MI, stroke or vascular death. Aspirin should be started in patients before or immediately after revascularisation, and after heart valve replacement. Older men and women with nonvalvular atrial fibrillation who have contraindications to oral anticoagulant therapy but no contraindications to aspirin should be treated with aspirin 325 mg daily. It is reasonable to treat older men and women without contraindications to aspirin with aspirin 160 to 325 mg daily if they are at high risk for developing new coronary events. The incidence of stroke, MI or vascular death in patients after a stroke or TIA is reduced by ticlopidine. Therefore, ticlopidine 250 mg twice daily may be used in older men and women with a history of stroke or TIA who do not respond to or who cannot tolerate aspirin. Patients at high risk for coronary artery stent thrombosis benefit from combined therapy with aspirin plus ticlopidine. The annual incidence of ischaemic stroke, MI or vascular death was significantly reduced by clopidogrel in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial. Therefore, clopidogrel 75 mg daily may be used in older men and women with symptomatic atherosclerosis who do not respond to or who cannot tolerate aspirin to reduce the incidence of ischaemic stroke, MI or vascular death. It should be noted that the acquisition cost for either ticlopidine or clopidogrel is considerably greater than that for aspirin. Most data indicate that the combination of aspirin and dipyridamole is not more effective than aspirin alone in preventing vascular events, and available data do not support the use of sulfinpyrazone in patients with vascular disease.
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PMID:Antiplatelet agents in the prevention of cardiovascular morbidity and mortality in older patients with vascular disease. 1049 69

Heparin, a mixture of glycosaminoglycans of various sizes, is a potent natural anticoagulant. Low molecular weight heparins (LMWH) contain only the polymers of smaller size, which appear to possess most of the antithrombotic potential. Pharmacological differences between the two suggest a number of advantages with LMWH therapy. Our objective was to establish the utility of LMWHs in comparison to the current practice of anticoagulation in surgical patients. Articles were obtained through MEDLINE and CURRENT CONTENTS queries. The searches were limited to English and French-language articles and included published overviews containing relevant individual trials. We examined the current literature, consisting of 1,730 published reports from 1979-1998, regarding the biochemistry, pharmacology, physiology, and clinical applications of LMWH in comparison with current therapy. Studies were selected based on their relevance to LMWHs, the size and methods of trials, and their application to clinical care. Peer-reviewed published data were critically evaluated by independent extraction by several authors. Established rules for levels of evidence were used to objectively evaluate the strength of evidence supporting recommendations in each clinical area. LMWHs provide superior anticoagulation in the prophylaxis of DVT following orthopedic, general, and trauma surgery. Further studies should establish which other patients may benefit from such prophylaxis. Current evidence does not support the use of LMWHs in patients with mechanical heart valves or those on mechanical cardiac support devices; however, it may have a role in the maintenance of vascular graft patency. Further studies should examine the role of LMWHs in transplant atherosclerosis, and in patients requiring long-term anticoagulation at high risk for bleeding with warfarin therapy. The economic implications of LMWH administration remain unclear. On the basis of the information presented in this review, LMWHs are promising new agents in prophylaxis and treatment of both arterial and venous thrombosis. In the near future, LMWHs are likely to supplant UFH and perhaps warfarin in many applications.http://link.springer-ny.com/link/service/journals/00547/bibs/8n4p203.html</hea
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PMID:Low Molecular Weight Heparin: An Evaluation of Current and Potential Clinical Utility in Surgery. 1055 62

Homocysteine is a non-protein-forming sulphur amino acid that plays an important role in remethylation and trans-sulphuration processes. In recent years, a high plasma homocysteine concentration has been implied as a possible pathophysiological factor in atherosclerosis and artery and deep vein thrombosis, probably through generation of H(2)O(2), enhanced platelet activity and increased production of macrophage-derived tissue factor. Furthermore, an increase of polymorphonuclear leukocyte (PMN) activity mediated by homocysteine-generated H(2)O(2) has also been reported. Because some preliminary experimental results in our laboratory did not confirm this effect of homocysteine on PMNs, we investigated the effect of homocysteine on the activity of PMNs, measured by their luminol-dependent chemiluminescence. Moreover, we also studied the effect of homocysteine in a luminol-hypochlorite chemiluminescent system. Our results clearly indicate that homocysteine at micromol/L concentrations (10-100 micromol/L) slightly inhibits neutrophil chemiluminescence, while it strongly inhibits the luminescence of the luminol-hypochlorite system. Therefore, the hypothesis that homocysteine induces an increase of H(2)O(2)-mediated neutrophil activity is not supported and, probably, the common opinion that views the H(2)O(2) generated by homocysteine as a possible mechanism for cardiovascular damage should be reconsidered.
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PMID:Effect of homocysteine on polymorphonuclear leukocyte activity and luminol-dependent chemiluminescence. 1093 39

The aim of this study was to examine potential links between antiOxLDL antibodies and the clinical and biological features of secondary antiphospholipid syndrome (II APLS) associated with systemic lupus erythematosus (SLE). A cohort study was done of 98 SLE patients followed-up for 1 y, including 18 with definite II APLS and 13 patients with definite primary APLS (I APLS). IgG anticardiolipin, IgG anti beta2 GPI, lupus anticoagulant, VDRL and IgG antiOxLDL were measured in all 98 study subjects. High antiOxLDL titers were found in seven (39%) of the 18 patients with II APLS vs 10 (12.5%) of the 80 patients without APLS (P < 0.01; OR = 4.45; 95% CI = 1.4-14.1) and none of the 13 patients with I APLS (P < 0.02). The mean antiOxLDL titer was not significantly higher in the SLE patients with than without II APLS (P > 0.05). A high antiOxLDL titer was correlated with deep venous thrombosis (P < 0.01; OR = 5.77; 95% CI = 0.54-61) but not with arterial thrombosis (P > 0.05; OR = 1; 95% CI = 0.29-3.09), thrombocytopenia, central nervous system involvement, livedo reticularis, or a positive Coombs test. The antiOxLDL antibody titer was correlated with the IgG anticardiolipin antibody titer (r = 0.235; P = 0.02) and with the IgG anti-beta2 GPI antibody titer (r = 0.224; P = 0.026). AntiOxLDL elevation was found in 17% of SLE patients and was significantly associated with II APLS and venous thrombosis. We found no evidence suggesting that antiOxLDL may be associated with atherosclerosis.
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PMID:Anti-oxidized low-density-lipoprotein (OxLDL) antibodies in systemic lupus erythematosus with and without antiphospholipid syndrome. 1140 65

Numerous clinical studies in Western and Asian countries suggest that individuals with elevated blood levels of homocysteine have an increased risk of atherosclerosis, myocardial infarction, cerebral infarction, and deep vein thrombosis. Homocysteine is also known to induce both atherogenic and thrombogenic mediators in cultured vascular cells so that homocysteine may influence the damage of endothelial cells, promote smooth muscle cell growth, induce atherogenic mediators and thrombus formation after coronary angioplasty. The association between homocysteine and restenosis after percutaneous coronary intervention (PCI) has been discussed. In this study, the relationship between plasma homocysteine levels and restenosis after PCI to investigate whether plasma homocysteine levels may be a predictor of restenosis after PCI was examined. One hundred consecutive patients who underwent successful PCI were enrolled and plasma homocysteine level was measured in all patients prior to PCI. Plasma for homocysteine level was obtained in 99 of 100 patients who had angioplasty. The mean plasma homocysteine concentration in the enrolled patients was 13.61 +/- 6.04 micromol/L. The minimum and maximum of plasma homocysteine were 4.40 micromol/L and 50.00 micromol/L, respectively. In healthy subjects, the normal reference range of homocysteine level is 5-15 micromol/L However, recent data suggest that some patients may be at increased cardiovascular and cerebrovascular risk at levels as low as 12 micromol/L. For this reason, both cut off points of homocysteine level > or = 15 micromol/L or > or = 12 micromol/L to identify the high homocysteine level group were used. Of 99 patients, high homocysteine level (> or = 15 micromol/L) was established in 9 patients with restenosis versus 20 patients without restenosis. If the cut off point of homocysteine level > or = 12 micromol/L was used, high homocysteine level was established in 14 patients with restenosis versus 39 patients without restenosis. From both cut off points of homocysteine level, there was no correlation between plasma homocysteine level and the restenosis group. (p>0.05).
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PMID:Homocysteine and restenosis after percutaneous coronary intervention. 1200 4

The purpose of this study was to check whether antiphospholipid antibodies (aPL) could be an independent risk factor for atherosclerosis. Eighty-five subjects were studied: 45 with primitive antiphospholipid antibody syndrome and 40 controls affected by deep vein thrombosis secondary to known causes. The two groups were homogeneous for age, sex, and risk factors for atherosclerosis. All the subjects submitted to echo-color doppler of the carotid arteries, femoral arteries, and abdominal aorta. The cases were then subdivided into three subgroups on the basis of the positivity to the three subpopulations of aPL. Results demonstrate that there is no correlation between aPL and atherosclerosis. The different positivity to aPL does not modify this conclusion.
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PMID:Are antiphospholipid antibodies an independent risk factor for atherosclerosis? 1212 Oct 50

Plasma D-dimer concentration rises more than 100-fold during acute deep vein thrombosis, but there are no prospective data concerning D-dimer as a risk factor for incident venous thrombosis in a general population. Incident venous thrombosis was ascertained in 2 prospective observational studies, the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study. Of 21 690 participants enrolled between 1987 and 1993, after 8 years of follow-up, D-dimer was measured using baseline stored plasma of 307 participants who developed venous thrombosis and 616 who did not. Relative to the first quintile of the distribution of D-dimer, the age-adjusted odds ratios for future venous thrombosis for the second to fifth quintiles of D-dimer were 1.6, 2.3, 2.3, and 4.2, respectively (P for trend <.0001). Following added adjustment for sex, race, body mass index, factor V Leiden, prothrombin 20210A, and elevated factor VIII coagulant activity (factor VIII:c), these odds ratios were 1.5, 2.1, 1.9, and 3.0, respectively (P for trend <.0001). Among those with idiopathic thrombosis or secondary thrombosis unrelated to cancer, the adjusted fifth quintile odds ratios were 3.5 and 4.8, respectively. By contrast, D-dimer in the fifth versus first quintile was not related to occurrence of cancer-associated thrombosis (odds ratio, 1.1). Odds ratios for elevated D-dimer were consistently elevated in subgroups defined by age, sex, race, duration of follow-up, and thrombosis type (deep vein thrombosis or pulmonary embolus). D-dimer is strongly and positively related to the occurrence of future venous thrombosis.
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PMID:Fibrin fragment D-dimer and the risk of future venous thrombosis. 1465 70

Cardiovascular disease is the leading cause of death in women. In pooled analysis, observational studies have shown a 50% reduction in death and myocardial infarction among users of hormone replacement therapy (HRT) for the primary and secondary prevention of cardiovascular disease. The first randomized trial of HRT for secondary prevention of heart disease found no benefit to therapy (Heart and Estrogen/progestin Replacement Study ). Even after 6.8 years of follow-up, there was still no cardiovascular benefit from the use of HRT (HERS II). HRT was associated with a 50% increased risk of heart attacks within the first year as well as an increased risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) (relative risk 2.89) and gallbladder disease (RR 1.38). The Estrogen Replacement and Atherosclerosis trial found no evidence that HRT slowed the progression of subclinical angiographic disease either. This was despite a favorable effect on high-density lipoprotein and low-density lipoprotein. The first randomized trial of HRT for the primary prevention of heart disease found no overall benefit (Women's Health Initiative). The combination of estrogen and progestin resulted in a 29% increase in heart attacks, 41% increase in stroke, a doubling of thrombotic events (DVT and PE), as well as a 26% increase in breast cancer. The risk for thrombotic events was greatest in the first year whereas the risk of breast cancer increased progressively with duration of therapy. HRT is no longer recommended for the primary or secondary prevention of cardiovascular disease or stroke. It may still be considered for short-term relief of menopausal symptoms in women without high-risk conditions, but alternatives exist.
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PMID:Hormone Replacement Therapy for Primary and Secondary Prevention of Heart Disease. 1268 16

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