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)

Lipoprotein(a) (Lp(a)) has close structural homology with plasminogen and, at least in vitro, may interfere with fibrinolysis. Any changes in the serum Lp(a) concentration during and following myocardial infarction (MI) and whether the serum Lp(a) level is affected by streptokinase (SK) are therefore of interest. Serum Lp(a) levels immediately before and 3 h after completion of an intravenous infusion of SK in 39 patients with acute MI were not significantly different (median 31.3 mg/dl before and 35.9 mg/dl after). Furthermore, SK added during the serum Lp(a) assay did not affect the result, except at very high concentrations of SK (1000 units/ml). Serum Lp(a) and fasting lipids were measured daily for 3 days following definite MI in 13 patients and then after 14 and 42 days. There was no significant change in serum Lp(a) following MI. In marked contrast, C-reactive protein levels in these patients increased steeply immediately following MI. Thus, there was no early 'acute-phase response' in serum Lp(a) levels after MI. However, greater variation in its concentration was observed at day 14 than at other times. Serum cholesterol, apolipoprotein B and apolipoprotein A1 concentrations decreased significantly following MI, whereas a significant transient increase in serum triglycerides occurred. Forty-two days after MI all lipid and lipoprotein values had regained their day 1 levels, except for apo A1, which remained depressed.
Atherosclerosis 1993 Oct
PMID:The immediate effect of streptokinase on serum lipoprotein(a) concentration and the effect of myocardial infarction on serum lipoprotein(a), apolipoproteins A1 and B, lipids and C-reactive protein. 828 Jan 86

Studies suggest that thrombosis is important in the progression of atherosclerotic lesions. The biochemical markers prothrombin fragment 1-2 and fibrinopeptide A reflect in vivo thrombin generation and activity, respectively. As such, they are markers that might be associated with cardiovascular risk. From the Cardiovascular Health Study, a cohort study of 5201 persons over 65 years of age, 399 persons free of clinical cardiovascular disease (CVD) at the baseline examination were selected for study of specialized markers of hemostasis. We report the cross-sectional relationships of the thrombin markers to CVD risk factors and measures of subclinical CVD. The range of fragment 1-2 2 was 0.12 to 0.85 nmol/L. The range of fibrinopeptide A was 0.9 to 44.1 micrograms/L. High levels of fragment 1-2 and fibrinopeptide A were associated with age, with levels higher in women than men. Fragment 1-2 was associated with smoking; high levels of triglyceride, creatinine, and C-reactive protein; and low levels of glucose. Fibrinopeptide A was associated with high C-reactive protein and apolipoprotein(a) and lower ankle-brachial index. There were no significant associations of the thrombin markers with race, fibrinogen, alcohol consumption, diabetes, or most measures of subclinical CVD. Study findings support a hypothesis that there are physiological interrelationships between cardiac risk factors, hemostasis, inflammation, and progression of atherosclerosis.
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PMID:Correlates of thrombin markers in an elderly cohort free of clinical cardiovascular disease. 879 70

Serum amyloid A (SAA) proteins comprise a family of apolipoproteins synthesized in response to cytokines released by activated monocytes/macrophages. Acute-phase protein concentrations have been advocated as objective biochemical indices of disease activity in a number of different inflammatory processes. Clinical studies in large groups of patients with a variety of disorders confirmed the rapid production and exceptionally wide dynamic range of the SAA response. It is as sensitive a marker for the acute-phase as C-reactive protein (CRP). Recent studies indicate that SAA is the most sensitive non-invasive biochemical marker for allograft rejection. Further studies comparing the measurement of SAA to CRP could reveal other indications for its specific use. These studies are now more feasible given newer assays to measure this acute-phase reactant. Observations that the acutephase response is tightly coupled to lipoprotein abnormalities and the fact that acute-SAA proteins are mainly associated with plasma lipoproteins of the high density range suggested a possible role of this apolipoprotein (apo SAA) in the development of atherosclerosis. The expression of SAA mRNA in human atherosclerotic lesions and the induction of acute-phase SAA by oxidized low-density lipoproteins strengthen the hypothesis that SAA might play a role in vascular injury and atherogenesis.
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PMID:Human serum amyloid A (SAA) protein: a prominent acute-phase reactant for clinical practice. 881 53

Insulin-dependent diabetic patients with nephropathy have a high risk of cardiovascular disease. Chronic inflammation is a part of the pathogenesis of atherosclerosis, and presently we have studied the relation between the inflammatory state, measured as levels of interleukin-6 and C-reactive protein and fibrinogen in diabetic nephropathy. Thirty-three insulin-dependent diabetic patients with diabetic nephropathy (urinary albumin excretion rate (AER) > 300 mg/24-h) and 22 patients with incipient diabetic nephropathy (AER 30-300 mg/24-h) were compared with 14 non-diabetic controls and 17 diabetic patients with normal AER (<30 mg/24-h). Fibrinogen was significantly higher in diabetic nephropathy than in non-diabetic controls and diabetic patients with normal AER (median 8.1, range (5.4-15.6) mu mol/l vs. 6.6 (5.0-12.1) mu mol/l, p < 0.05, and 6.2 (5.0-9.0) mu mol/l, p < 0.005, respectively), while C-reactive protein did not deviate between groups. Interleukin-6 was significantly elevated in all insulin-dependent diabetic patients (diabetic nephropathy (3.2 (1.0-14.5) pg/ml, p < 0.005), incipient nephropathy (3.7 (1.0-22.9) pg/ml, p < 0.005) and diabetic patients with normal AER (2.7 (1.0-9.0) pg/ml, p < 0.05) compared with nondiabetic controls (1.2 (1.0-6.2) pg/ml)). When fibrinogen was adjusted for interleukin-6, C-reactive protein or both, the level of fibrinogen was still higher in patients with diabetic nephropathy than in patients without nephropathy (p < 0.05), which suggests that inflammation is not the only mechanism that increases fibrinogen levels in patients with diabetic nephropathy.
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PMID:Elevated fibrinogen and the relation to acute phase response in diabetic nephropathy. 890 98

The plasma level of fibrinogen is associated with the risk of ischaemic heart disease (IHD) and the severity of atherosclerosis. It has been suggested that an increased plasma level of fibrinogen is a coronary risk indicator because it reflects the inflammatory condition of the vascular wall. An inflamed vascular wall may increase the production of the cytokines interleukin 6 (IL6), interleukin 1-beta (IL1-beta), and tumour necrosis factor alpha(TNF-alpha), which have a major role in the regulation of synthesis in the liver of acute phase proteins, including fibrinogen. Smoking has also been reported to increase the levels of fibrinogen and C-reactive protein (CRP). This may indicate that smoking induces an inflammatory reaction, probably of the pulmonary bronchi and alveolae. Therefore, we anticipated that with both types of inflammation the levels of acute phase proteins and cytokines would be related. We have investigated the contribution of inflammation to the plasma levels of fibrinogen in 34 patients with severe coronary artery disease (CAD) and 30 healthy controls comparable for age and smoking habits. We did not find a parallel in the effects of smoking and ischaemic heart disease on the plasma levels of fibrinogen, CRP, IL6, IL1-beta and TNF-alpha. Cardiovascular disease had its most important effect on the plasma fibrinogen level, while smoking appeared to increase the CRP levels, while both CAD and smoking seemed to affect the IL6 levels. Our results indicate that both smoking and CAD induce an inflammatory condition but that the increase of plasma levels of different inflammatory markers is complex. Although the acute phase reaction is the main regulatory mechanism of fibrinogen, the increase of fibrinogen in our group of CAD patients could not be fully explained by increased inflammation.
Atherosclerosis 1996 Apr 05
PMID:Association of plasma fibrinogen levels with coronary artery disease, smoking and inflammatory markers. 912 93

A total of 274 patients with abdominal aortic aneurysms due to atherosclerosis (AAA) and 16 patients with inflammatory abdominal aortic aneurysms (IAAA) were reviewed to compare and contrast the clinical characteristics of the 2 groups. The AAA group comprised 243 men and 31 women with a mean age of 69.2 +/- 0.4 (range 51-86) years. The IAAA group comprised 15 men and 1 woman with a mean age of 67.4 +/- 2.0 (range 53-81) years. Most patients with IAAA (12/16; 75.0%) had pain at presentation, whereas only 37 out of 274 patients (13.5%) with AAA had pain (p < 0.001). Fifty out of 274 patients (18.2%) with AAA were asymptomatic, the most common principal complaint being a pulsatile tumor, which was found in 150 out of 274 patients (54.7%; p < 0.005 vs IAAA). Regarding laboratory findings of inflammation, preoperative erythrocyte sedimentation rate values were elevated in 15 out of 16 (93.8%) patients, and C-reactive protein values were elevated in 13 out of 16 (81.3%) patients with IAAA. The incidence of perioperative complications was similar in the 2 groups. The 30-day postoperative mortality among AAA patients was 6.2% (17/274 cases), including 12 cases of non-ruptured and 5 cases of ruptured AAA; in contrast, no early deaths occurred among patients with IAAA. The cumulative 5-year survival rate was 80.2% for IAAA patients and 74.6% for AAA patients (NS). The results of our review suggest that careful diagnosis and intra- and postoperative management could lead to patients with IAAA having a similar survival rate to those with AAA.
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PMID:Inflammatory abdominal aortic aneurysms and atherosclerotic abdominal aortic aneurysms--comparisons of clinical features and long-term results. 915 71

Cardiovascular complications account for more than 50% of death in hemodialysis patients. Strong and independent predictors of mortality or cardiovascular complications are low levels of serum albumin, high plasma C-reactive protein and lipoprotein(a), plasma proteins that are described to function as negative or positive acute phase reactants. Further prominent and known risk factors that contribute to the increased incidence of atherosclerosis in hemodialysis patients are disorders in lipoprotein metabolism and elevated plasma fibrinogen concentrations. The latter has also been described to increase following acute or chronic inflammation. The main metabolic abnormality of the lipoprotein profile is a delayed catabolism of triglyceride-rich apoB-containing lipoproteins caused by a decreased activity of lipolytic enzymes. Inhibition of lipoprotein lipase activity by cytokines or parathyroid hormone impedes conversion of very-low-density lipoprotein to low-density lipoprotein, resulting in remnant accumulation and hypertriglyceridemia. Another acute phase condition, namely, acute myocardial infarction, results in a similar pattern of dyslipidemia and coagulation disorder. In summary, the acute phase response deeply influences serum lipids and lipoproteins as well as other atherogenic acute phase proteins in hemodialysis patients. Appreciation of acute phase lipoprotein changes is essential for accurate diagnosis of dyslipidemias, proper design of future clinical studies, and correct interpretation of published data.
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PMID:Inflammation, dyslipidemia and vascular risk factors in hemodialysis patients. 935 Jun 81

Non-insulin-dependent diabetes mellitus (NIDDM) is commonly associated with hypertriglyceridaemia, low serum HDL-cholesterol concentrations, hypertension, obesity and accelerated atherosclerosis (metabolic syndrome X). Since a similar dyslipidaemia occurs with the acute-phase response, we investigated whether elevated acute-phase/stress reactants (the innate immune system's response to environmental stress) and their major cytokine mediator (interleukin-6, IL-6) are associated with NIDDM and syndrome X, and may thus provide a unifying pathophysiological mechanism for these conditions. Two groups of Caucasian subjects with NIDDM were studied. Those with any 4 or 5 features of syndrome X (n = 19) were compared with a group with 0 or 1 feature of syndrome X (n = 25) but similar age, sex distribution, diabetes duration, glycaemic control and diabetes treatment. Healthy non-diabetic subjects of comparable age and sex acted as controls. Overnight urinary albumin excretion rate, a risk factor for cardiovascular disease, was also assayed in subjects to assess its relationship to the acute-phase response. Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001). There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X. C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group. We conclude that NIDDM is associated with an elevated acute-phase response, particularly in those with features of syndrome X. Abnormalities of the innate immune system may be a contributor to the hypertriglyceridaemia, low HDL cholesterol, hypertension, glucose intolerance, insulin resistance and accelerated atherosclerosis of NIDDM. Microalbuminuria may be a component of the acute-phase response.
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PMID:NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X. 2212 8

Hyperhomocysteinemia is associated with severe, premature atherosclerosis and thromboembolism. The mechanisms involved in the atherogenic and thrombotic complications of hyperhomocysteinemia are not understood. It has been suggested that hyperhomocysteinemia predisposes to atherosclerosis by injuring the vascular endothelium. Whether hyperhomocysteinemia is independently associated with changed endothelial function, either in the absence or the presence of clinically manifest atherosclerotic disease, is, however, not known. Therefore we investigated, both in patients with peripheral arterial occlusive disease and in healthy individuals, whether plasma protein markers of endothelial function differed between subjects with, and subjects without hyperhomocysteinemia. We studied 80 individuals under the age of 56 years: healthy individuals with (n = 20) and without (n = 20) hyperhomocysteinemia and patients with peripheral arterial occlusive disease with (n = 20) and without (n = 20) hyperhomocysteinemia. The following endothelium-derived proteins were measured as markers of endothelial cell function: von Willebrand factor (vWf) and von Willebrand factor propeptide (vWf: AgII), tissue-type plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), cellular fibronectin (cFN) and thrombomodulin (TM). In addition we assessed C-reactive protein (CRP). vWf, vWf: AgII, tPA and CRP were significantly higher in the patients with peripheral arterial occlusive disease than in the healthy individuals. No differences in marker protein plasma levels were found between individuals with, and those without hyperhomocysteinemia, apart from vWf, which was significantly raised in hyperhomocysteinemic as compared to normohomocysteinemic patients. We did not find any evidence for an independent association between hyperhomocysteinemia and protein markers of endothelial cell function in healthy subjects.
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PMID:Endothelial marker proteins in hyperhomocysteinemia. 940 14

In a prospective study, the role of various hemostatic factors known to be associated with thrombotic risk was investigated in 71 patients with peripheral arterial occlusive disease (PAOD, stages II through IV, Fontaine; aged 68 +/- 13 years). Laboratory investigations were done before; 1, 24, and 48 hours after; and 3 and 6 months after percutaneous transluminal angioplasty (PTA). Thirty of 71 (42.3%) patients developed restenosis (> 50% reduction of the lumen diameter) at the site of PTA within 6 months, verified by color-coded duplex sonography. Significantly increased levels of thrombin-antithrombin III complexes (P < .01), prothrombin fragments 1 + 2 (P < .01), and D-dimers (P < .01) were found 1 hour, as well as 24 to 48 hours, after PTA. Fibrinogen (P < .01) and von Willebrand factor (P < .01) were significantly higher 48 hours after PTA. Restenotic patients as a whole had higher plasma fibrinogen (3.46 +/- 1.12 versus 2.95 +/- 0.62 g/L, P < .01) and C-reactive protein (25.4 +/- 46.7 versus 7.9 +/- 6.9 mg/L, P < .05) at baseline, as well as higher fibrinogen (P < .05) and prothrombin fragments 1 + 2 (P < .01) during months 3 to 6 after PTA. There was a nonsignificant tendency for higher values of von Willebrand factor (206 +/- 98% versus 184 +/- 100%, P = .2) at baseline in patients with restenosis, whereas tissue plasminogen activator, plasminogen activator inhibitor, coagulation screening tests, blood cell counts, and serum lipids showed no significant difference between the two groups. The relative risk for developing restenosis within 6 months while having high fibrinogen (> 2.8 g/L) or C-reactive protein at baseline was 2.80 (95% CI: 1.30-6.02, P < .01) and 1.96 (95% CI: 1.07-3.58, P < .05), respectively. Patients with critical limb ischemia (stage III/IV, Fontaine) had significantly higher fibrinogen and von Willebrand factor at repeated points of time, as well as significantly higher C-reactive protein and lower creatinine clearance at entry. In the logistic regression risk factor analysis, baseline plasma fibrinogen, C-reactive protein concentration, and the severity of the arterial disease were significantly predictive of restenosis. Our results indicate that high procoagulant factors and persistent thrombin generation of the hemostatic system might promote restenosis, particularly in patients with extended atherosclerosis. This finding suggests that new treatment strategies should be taken under consideration for patients with PAOD and PTA.
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PMID:Role of hemostatic risk factors for restenosis in peripheral arterial occlusive disease after transluminal angioplasty. 940 13


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