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)

The whole blood and plasma viscosity changes in course of acute myocardial infarction were examined. The examination were performed at the beginning of acute phase of myocardial infarction (period 1), at second to third day (period 2) and after about 10 days of infarction episode (period 3). 77 patients (mean age 56.8 +/- 9.8 years) suffered from myocardial infarction were examined. The whole blood viscosity at following shear rates [s-1]: 0.116; 1.0; 4.59; 150 and plasma viscosity were performed. Besides the viscometric examinations the total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, glucose and fibrinogen as well as blood morphology and ESR were determined. All rheological measurements were carried out at the temperature of 37 degrees C immediately after blood drawing. The control group consisted of 110 healthy persons (aged 56.6 +/- 10 years). Some persons of control group have got risk factors of atherosclerosis as: obesity, artery hypertension and cigarette smoking. The following additional parameters were investigated: hematocrit, the artery pressure, the body mass index, total cholesterol concentration, serum LDL-cholesterol, HDL-cholesterol, fibrinogen and blood morphology. The corrected whole blood viscosity was adjusted to 45% of hematocrit. It was stated that the native whole blood viscosity was disturbed at all periods of disease. The corrected whole-blood viscosity in all periods of acute myocardial infarction comparing with controls increased. The greatest rise of corrected whole blood viscosity was especially observed in second period of acute myocardial infarction. Plasma viscosity in patients with acute myocardial infarction is increased in all periods. The greatest rise of plasma viscosity was in second period of disease. The rheological blood and plasma disturbances were connected with increase of total cholesterol, LDL-cholesterol, triglycerides and fibrinogen. These disturbances of blood and plasma viscosity may play a role in promoting myocardial infarction factors.
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PMID:[The whole blood and plasma viscosity changes in course of acute myocardial infarction]. 1264 42

Cardiovascular disease (CVD) is still the major cause of the morbidity and mortality in hemodialysis (HD) patients. The characteristics of major arterial changes, atherosclerosis and related risk factors in HD patients remain unclear. We aimed to evaluate the atherosclerotic process in asymptomatic HD patients and healthy volunteers, and to determine the association between the risk factor(s) and the atherosclerotic process in these groups. 92 HD patients (female: 43, male: 49) and 62 age and sex matched healthy volunteers (female: 27, male: 35) were enrolled in this study. Diabetics, smokers, and patients with symptomatic CVD were excluded. The right and left carotid intima-media thicknesses (CIMTs) were measured and plaque structures were studied by B-mode ultrasound. The mean CIMT in patients and control group were 0.79 +/- 0.16 mm and 0.54 +/- 0.09 mm, respectively. Mean CIMT in HD patients was thicker (p < 0.001) and the presence ratio of plaque was higher in patients group (n=38, %61.2 vs n=9, %17.3) (p < 0.001). Calcified type of plaque was more frequent in HD patients than control group. Age (r=0.48, p < 0.001), left ventricular mass (r=0.42, p < 0.05), and homocysteine (r=0.46, p < 0.01), mean hematocrit (r=-0.36, p < 0.05), plasma CRP (r=0.50, p < 0.001), ESR (r=0.43, p < 0.01) and albumin (r= -0.34, p < 0.05) levels were correlated with the CIMT measurements and plaque presence, significantly. -CIMT as an atherosclerotic process indicator is thicker in asymptomatic HD patients than healthy subjects. We concluded that in addition to various classical risk factors, uremic environment may also contribute to acceleration of the atherosclerotic process.
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PMID:Increased incidence of carotid artery wall changes and associated variables in hemodialysis patients without symptomatic cardiovascular disease. 1511 96

The objective of this study was to determine the lipoprotein profile of limited cutaneous systemic sclerosis (LcSSc). Fasting lipids were determined in 24 female patients and 24 healthy age-matched and sex-matched controls. Exclusion criteria were conditions that induce an altered lipid profile. Lipoprotein levels of risk were determined in accordance with the National Cholesterol Education Program (NCEP). Significantly lower levels of high-density lipoprotein (HDL) cholesterol (47.6+/-12.4 mg dL(-1) vs. 58.2+/-12.3 mg dL(-1); P=0.003) and total cholesterol (197.0+/-40.7 mg dL(-1) vs. 222.0+/-34.0 mg dL(-1); P=0.02) were observed in LcSSc patients than in controls. The presence of anti-centromere antibodies (ACA) was also associated with lower HDL levels (45.0+/-12.1 mg dL(-1)) compared to ACA-negative patients and controls (50.2+/-12.6 and 58.2+/-12.3 mg dL(-1), respectively, P=0.01). The only clinical variable associated with low HDL levels was pulmonary hypertension (PH) (33.6+/-2.3 mg dL(-1) vs. 49.6+/-11.9 mg dL(-1), P=0.01). No significant correlation was observed among HDL levels and ESR (r=-0.313; P=0.14), CRP (r=-0.296; P=0.16), or BMI (r=-0.263; P=0.21). Remarkably, a higher percentage of risk HDL levels was identified in LcSSc patients (41.6%) than in healthy controls (8.3%) (P=0.02). Our data suggest that LcSSc patients, particularly those who are ACA positive, have an adverse lipid profile characterized by low HDL levels, a known independent risk for CAD in women. The relevance of this finding for the development of atherosclerosis in this disease must be confirmed by epidemiological studies.
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PMID:Lipoprotein profile in limited systemic sclerosis. 1628 68

Early diagnosing and modification or elimination of atherosclerosis risk factors with the descendants of the ill with past ischemic stroke (IS) might reduce risk of subsequent stroke incidence in the family, or myocardial infarction or other disease being atherosclerosis - derivative. This subject seems to be essential because it concerns young people. The purpose of the present study is identification and assessment of metabolic atherosclerosis risk factors with adult progeny of the ill with past IS at young age. There were examined 43 adult children of the parents who fell ill at young age (between 39 and 55 years in case of men and 60 years in case of women) with IS. The test group included 21 men and 22 women aged from 19 to 39 years (average age - 26.3 years). The reference group consisted of 40 persons, including 18 men and 22 women aged from 22 to 39 years (average age - 26.8 years). The persons from reference group were corresponding (in respect of structural aspects, such as age and sex) to the test group, their parents had negative history towards atherosclerosis - derivative illnesses. None of the patients under examination was a cigarette smoker. Examination of both groups consisted in conducting anamnesis, measurement of body weighing and height, blood pressure as well as evaluation of biochemical atherosclerosis risk factors. Blood testing (blood serum or plasma) consisted of blood cell count and ESR as well as blood glucose level, creatinine, urea, transaminase and bilirubin levels as well as total cholesterol, LDL cholesterol and HDL cholesterol fractions, apolipoprotein B, apolipoprotein AI, lipoprotein (a), triglycerides, homocysteine, folate, fibrinogen, von Willebrand factor and C-reactive protein level. Among persons whose parents were affected, at young age, with IS higher average level of BMI (24.2 +/- 3.8 kg/m2) was detected as compared with that in the reference group (22.4 +/- 2.5 kg/m2), LDL cholesterol fraction (2.7 +/- 0.8 mmol/l vs 2.4 +/- 0.6 mmol/l) and triglycerides (1.1 +/- 0.4 mmol/l vs 0.8 +/- 0.4 mmol/l) as well as lower level of apolipoprotein Al (1.5 +/- 0.2 g/l vs 1.6 +/- 0.2 g/l). Average values of other factors in the blood serum were not significantly different in both with compared groups. In case of women, whose parents were affected with IS, higher levels of the following indicators were detected: BMI (24.3 +/- 3.9 kg/mz vs 21.5 +/- 2.3 kg/m2), total cholesterol (5.1 +/- 0.7 mmol/l vs 4.4 +/- 0.5 mmol/l, LDL cholesterol (2.7 +/- 0.6 mmol/l vs 2.1 +/- 0.4 mmol/l), apolipoprotein B (1.0 +/- 0.1 g/l vs 0.8 +/- 0.1 g/l), lipoprotein (a) (0.3 +/- 0.2 g/l vs 0.2 +/- 0.1 g/l) and triglycerides (1.0 +/- 0.4 mmol/l vs 0.7 +/- 0.2 mmol/l). In group of men whose parents were affected with IS lower levels of apolipoprotein Al (1.3 +/- 0.2 g/l vs 1.5 +/- 0.2 g/l) and of von Willebrand factor (71.4 +/- 23.9% vs 87.1% +/- 16,8%) were detected. Descendents of the ill with past IS should be treated as higher risk group especially when supranormative values of metabolic atherosclerosis risk factors are detected with them. In case of persons with positive family history of IS, having higher values of metabolic atherosclerosis risk factors, it is necessary to apply intensive actions towards change of their life styles, and if necessary - also to include pharmacological treatment.
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PMID:[Assessment of metabolic atherosclerosis risk factors in progeny of patients with past ischemic stroke]. 1620 32

Atherosclerosis-related vascular complications in beta-thalassemia/hemoglobin E (beta-thal/Hb E) patients may result from iron induced oxidation of lipoproteins. To identify the specific site of oxidative damage, changes in lipid fluidity at different regions in LDL and HDL particle were investigated using two fluorescence probes and two ESR spin probes. The magnitude of increased lipid fluidity in thalassemic lipoproteins was dependent on the location of the probes. In hydrophobic region, the rotational correlation times for 16-doxyl stearic acid and DPH anisotropy were markedly changed in LDL and HDL of the patients. In the surface region, there was only a slight change in the order parameter (S) for 5-doxyl stearic acid and TMA-DPH anisotropy. Lipid fluidity at the core of LDL and HDL showed good correlation with oxidative stress markers, the ratio of CL/CO, and the level of alpha-tocopherol, suggesting that hydrophobic region of thalassemic lipoprotein was a target site for oxidative damage.
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PMID:Lipid fluidity at different regions in LDL and HDL of beta-thalassemia/Hb E patients. 1702 20

Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis, but the underlying mechanisms are unclear. The size and number of lipoprotein particles may be better predictors of atherosclerosis than conventional cholesterol measurements. We measured lipoprotein subclasses by nuclear magnetic resonance spectroscopy (NMR), coronary artery calcification by electron beam computed tomography, and insulin resistance by homeostasis model assessment in 105 patients with SLE and 77 control subjects. VLDL particles were larger (50.0+/-8.5 versus 47.7+/-8.5 nm, P=0.01) and concentrations of large high-density lipoprotein (HDL) particles lower (10.1+/-5.3 versus 11.3+/-5.1 nmol/L, P=0.03) in patients with SLE than controls. In patients with SLE, small LDL concentration was associated with body mass index (rho=0.27), insulin resistance (rho=0.34), C-reactive protein (CRP; rho=0.30), and erythrocyte sedimentation rate (ESR; rho=0.20); all P<0.05. Large HDL concentration was inversely associated with insulin resistance (rho=-0.29), disease activity (rho=-0.23), and ESR (rho=-0.39); all P<0.05. VLDL concentrations correlated with CRP (rho=0.22), ESR (rho=0.24), disease damage (rho=0.20), and corticosteroid exposure (rho=0.29); all P<0.05. Neither the concentration of lipoprotein subclasses nor particle size was associated with coronary artery atherosclerosis. There were only minor differences in the NMR lipid profiles of patients with SLE and controls. Lipoprotein subclasses were associated with metabolic variables, inflammatory markers, and corticosteroid use but not with coronary artery atherosclerosis in SLE.
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PMID:Lipoprotein subclasses and particle size determined by nuclear magnetic resonance spectroscopy in systemic lupus erythematosus. 1842 45

Nephrogenic systemic fibrosis (NSF) is a rare disorder in patients with chronic kidney disease characterized by an increased tissue deposition of collagen. Its pathogenesis remains unclear. Prior studies indirectly suggested a possible impact of chronic inflammation and accelerated atherosclerosis--a common feature in kidney diseased patients--whereas recent data focused almost exclusively on gadolinium (Gd)-based MR contrast agents. Usually NSF develops a maximum of 2-3 months after Gd. Longer intervals have not yet been described. Therefore, we present the first case with an extraordinary long time course in terms of chronic inflammation. A 52-year-old Caucasian woman with end-stage renal disease was admitted to our hospital with progressive muscle weakness and skin induration resulting in growing immobility. Her past medical history revealed a secondary HPT, multiple vascular complications, a seronegative rheumatoid arthritis, and a pituitary gland adenoma. The latter conditions led to multiple MR examinations with Gd-based contrast agents, the last one more than 4 years ago. Numerous laboratory tests were performed including ESR, CRP, intact parathyroid hormone (iPTH), serum ferritin, cyclic-citrullinated peptide antibodies (CCP), ANA, ANCA, immunoelectrophoresis, and serology for hepatitis as well as human immunodeficiency virus. Eventually a skin biopsy of her left thigh was obtained. The laboratory investigation showed persistently elevated levels of CRP, ESR, serum ferritin, and iPTH, whereas all other parameters were inconspicuous. The hisology displayed typical signs of nephrogenic systemic fibrosis. NSF can occur at any time after Gd exposure in the long term. Gd is a necessary, but not the sole cause of NSF. Certain other cofactors such as chronic inflammation and accelerated atherosclerosis seem to be involved.
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PMID:Chronic inflammation and accelerated atherosclerosis as important cofactors in nephrogenic systemic fibrosis following intravenous gadolinium exposure. 1855 Dec 45

The pathophysiological process of natural human aging has not been studied adequately due to the lack of an appropriate human model. Since recent investigations have suggested that inflammation possibly contributes to the pathogenesis of age-related disorders including atherosclerosis, cancer, and diabetes mellitus, the term "inflammaging," a combination of "inflammation" and "aging," has been coined. Werner syndrome (WS), caused by the loss of function of RecQ3 DNA/RNA helicase, is a typical progeroid syndrome mimicking natural aging, although it is extremely rare outside of Japan. We sought to examine WS patients from an immunological/inflammatory perspective. Sera from 14 mutation-proven WS patients (ages: 33-70 years) and 21 healthy Japanese adults ages 15 to 95 years were examined with ELISA for soluble Fas ligand (sFasL) to compare conventional inflammation markers. With natural aging, a statistically significant correlation (p < 0.0001) was observed in the serum level of sFasL. The sFasL in WS, a level comparable to that in healthy elderly ages 83 to 95 years, had significantly increased (p < 0.05) compared to that in young healthy individuals ages 15 to 70 years. A significant correlation was noted between the serum levels of conventional inflammation markers such as CRP (p < 0.025), ESR (p < 0.024), and WBC count (p < 0.0085). In conclusion, an increased level of serum sFasL in natural aging and WS patients may suggest a common pathophysiological mechanism: inflammation. WS may be a good model for analyzing inflammaging.
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PMID:Elevation of soluble Fas (APO-1, CD95) ligand in natural aging and Werner syndrome. 2010 15

Osteoporosis and vascular disease are commonly found together in elderly people. Several common mechanisms and risk factors have been suggested to contribute to the development of osteoporosis and atherosclerosis. The present cross-sectional study was performed to determine whether the degree of bone turnover is correlated to carotid intima-media thickness (CCA-IMT), as a marker of subclinical atherosclerosis. We selected 50 outpatients (mean age 71.7 +/- 12.3), underwent to eco-Doppler evaluation of extracranial carotid tract, without history of calcium and/or vitamin D supplementation, or antireabsorptive therapy. CCA-IMT was measured by high-resolution B-mode ultrasonography. Bone turnover was evaluated by analysing serum levels of C-terminal telopeptide of type I collagen (sCTX), and bone-specific alkaline phosphatase. We also evaluated the vitamin D status by determination of the serum concentration of 25-hydroxyvitamin D [25(OH)D]. We found a prevalence of hypovitaminosis D [serum 25(OH)D levels <30 ng/mL, mean value 10.7 +/- 5.8] of 91.8%, and an increased bone resorption, with mean sCTX levels higher than reference values (mean 1.18 +/- 0.57 ng/mL). A significant positive correlation was found between CCA-IMT and age (r = 0.480, P = 0.001), erythrocyte sedimentation rate (ESR: r = 0.438, P = 0.001), high-sensitivity C-Reactive Protein (HsCRP: r = 0.482, P = 0.011), serum creatinine (r = 0.305, P = 0.031), and sCTX (r = 0.389, P = 0.006). In a multivariate linear regression, CCA-IMT was independently predicted by age (beta = 0.34, P = 0.001), ESR (beta = 0.37, P = 0.005), and sCTX (beta = 0.32, P = 0.006). The preliminary results of our study seem to indicate that after adjustment for established cardiovascular risk factors, sCTX independently predict an increased CCA-IMT in the elderly population.
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PMID:Carotid intima-media thickness and bone turnover: the role of C-terminal telopeptide of type I collagen. 2018 21

Epidemic studies have shown that rheumatoid arthritis (RA) patients have shorter life expectancy than healthy persons, primarily due to cardiovascular events. The aim of our study was to explore inhibitory effects on atherosclerosis of RA patients by TNF-inhibitor etanercept (ETN). We studied six RA patients with moderate or high disease activity as defined by the European League Against Rheumatism (EULAR) disease activity score (DAS28-ESR) in spite of treatment with methotrexate (MTX) 8 mg/week. We measured their pulse wave velocity (PWV) before and after treatment with ETN 25 mg/week for one year. There were no additional medications other than ETN that might influence on atherosclerosis. Their PWV decreased in five of six patients and the average decreased from 1474.8 cm/sec to 1432.5 cm/sec. The average of DAS28-ESR score was significantly decreased from 5.56 to 2.87 and they achieved good response by the EULAR criteria. There were no significant changes in the blood pressure, serum lipid (total cholesterol and triglyceride) and HbA1c ; all values were within normal limits before and after ETN treatment. It is suggested that the improvement of PWV is due to anti-inflammatory effects, leading inhibition of atherosclerosis, of ETN in RA patients.
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PMID:[Anti-atherosclerotic effects of etanercept in rheumatoid arthritis patients]. 2279 May 78


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