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Query: UMLS:C0004153 (
atherosclerosis
)
77,401
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The three major epicardial coronary arteries of a set of 472 autopsy cases divided into four groups: a) non-diabetics and non-hypertensive, 322 subjects; b) hypertensive, 75 subjects; c) diabetics, 57 subjects and d) hypertensive and diabetic, 17 subjects, were studied. Classical pathomorphological procedures and an atherometric system (AS), suitable to characterize the atherosclerotic lesions, was used searching for differences between the level of
atherosclerosis
into these four groups and its eventual progression according to the time of evolution of these diseases. Raw data processing was full automated and some univariate and multivariate statistical procedures (means, standard deviations,
ANOVA
, MANOVA and principal components analysis) were performed using two commercial statistical packages: "NCSS" and "SYSTAT". The most remarkable findings were the following: Diabetes and hypertension have both strong impact upon the rate at which the atherosclerotic process takes place in subjects affected by these diseases. The time of evolution of both diseases correlates positively and independently of age with the velocity of the atherosclerotic process at the three coronary arteries. The impact of diabetes seems to be stronger and is particularly expressed by the severe plaques (Z) while the effect of hypertension is specially observable at the fibrous plaques (Y). There seems to be no significant interaction (synergism) between the two risk factors upon the measurement of the atherosclerotic lesions, that is, they have an additive effect. Two simple underlying factors can be used to account for interindividual differences. These two factors are "dominated", respectively, by fibrous (Y) and severe plaques (Z).
...
PMID:Atherosclerosis in diabetes and hypertension. A comparative morphometric study of their progression using an atherometric system. 180 26
In order to evaluate the effect of the angiotensin I-converting enzyme inhibitor, captopril, on lipid metabolism, we measured serum lipoperoxides concentration ( LPX ) as well as plasma levels of renin activity (PRA), aldosterone (PAC) and bradykinin ( PBK ) before and after captopril administration in 15 hypertensive patients. Captopril significantly lowered the LPX (p less than 0.05 by repeated measures
ANOVA
) from the control value of 3.25 +/- 1.16 (mean +/- S.D.) to 2.92 +/- 0.94, 2.83 +/- 1.10, and 2.89 +/- 1.31 nmol/ml 30, 60, and 120 min after the administration, respectively. A significant reduction of blood pressure (p less than 0.0001) and PAC (p less than 0.01) was observed following captopril administration, while PBK increased significantly (p less than 0.001) from a baseline level of 10.85 +/- 4.07 to 13.95 +/- 5.29, 16.25 +/- 6.85, and 15.71 +/- 7.65 pg/ml 30, 60, and 120 min after captopril administration, respectively. There was no significant correlation between changes in serum LPX and in mean blood pressure, PRA and PAC, though a significant inverse relationship was found between changes in serum LPX and in PBK 120 min after the administration (r = -0.576, p less than 0.05, n = 13). Although the mechanisms by which serum LPX is decreased by captopril are not clear, it is suggested from the results that captopril is a beneficial antihypertensive agent for preventing LPX -induced
atherosclerosis
in hypertensive patients.
...
PMID:[The effects of the angiotensin I-converting enzyme inhibitor, captopril, on serum lipoperoxides level and the renin-angiotensin-aldosterone and kallikrein-kinin systems in hypertensive patients]. 637 99
To further characterize the role of monocytes in atherogenesis, we studied the influence of a qualitatively, well-defined hemodynamic flow field on the deposition pattern of monocytes in the thoracic aorta of normal (N, n = 6) and hypercholesterolemic (H, n = 10) rabbits. Pairs of H rabbits were sacrificed after 1, 2, 4, 7 and 10 weeks of cholesterol feeding. Complete deposition patterns of adherent cells were quantified over 500 mm2 of aortic endothelium around the lesion-susceptible intercostal orifices using an en face light microscopic technique. Adherent cells were almost exclusively monocytes by morphological criteria and non-specific esterase staining. The mean density of adherent cells in normal rabbits was 1.28 +/- 1.21 (S.D.) per mm2 of endothelium and increased nearly 5-fold by 7 weeks of cholesterol feeding. High local densities of adherent monocytes (up to 34 cells/mm2) were noted over early fatty lesions present in one 4 week and all 7 and 10 week H rabbits. Adherent cell densities near intercostal orifices prior to lesion formation were approximately 50% greater than in non-orifice regions in both the normal and the 1 and 2 week H rabbit groups. These differences were statistically significant at P < 0.05 by
ANOVA
. We conclude that preferred adherence of monocytes occurs around intercostal orifices in normolipidemic and early cholesterol-fed rabbits before lesions develop at these lesion-prone sites. Monocyte deposition appears to be governed not only by the arterial flow field but also by cholesterol feeding since higher numbers of adherent monocytes were found on both early fatty streaks and nonlesioned endothelium in rabbits fed cholesterol for longer than 4 weeks.
Atherosclerosis
1995 Jul
PMID:Deposition pattern of monocytes and fatty streak development in hypercholesterolemic rabbits. 748 25
The Yucatan miniswine has been recommended as an animal model of advanced
atherosclerosis
. Atherosclerotic plaques developed in this model demonstrate foam cells, widespread fibrosis, and calcification, features suggestive of human
atherosclerosis
. We have observed the occurrence of intraluminal projections that appear peculiar to this animal model. Forty-three miniswine, weighing between 20 and 30 kg, were rendered atherosclerotic with a combination of balloon endothelial injury of the aortoiliac segments and dietary supplementation with 2% cholesterol and 15% lard. Endothelial injury was created by retrograde balloon catheter injury of the aorta and both external iliac arteries via cutdowns on the femoral arteries. Serum cholesterol prior to starting the diet and at 1, 2, and 6 weeks following initiation of the diet was 2.0 +/- 0.4, 11.6 +/- 4.0, 15.9 +/- 5.0, and 16.4 +/- 4.2 mM, respectively (p < .0001,
ANOVA
). Angiographically significant lesions were apparent in 33 of 37 (89%) animals (occlusion 20/37, stenosis 17/37) at 6 weeks postinjury. In three of six (50%) animals followed up to 16 weeks postinjury, trabecular areas were seen in the external iliac arteries on angiography. Light and electron microscopy demonstrated that these areas were covered with normal endothelium and projected into the lumen or bridged with the adjacent arterial wall. Foam cells and calcification were not seen in these lesions. This finding is not typical of human
atherosclerosis
and appears peculiar to this type of animal model.
...
PMID:Intraluminal endothelium-covered bridges in chronic fat-fed balloon-injured Yucatan miniswine. 789 41
Platelet activation and platelet-derived growth factor (PDGF) play a pivotal role in the pathogenesis of
atherosclerosis
. Evidence has been accumulating that in the evolution of chronic arterial obstructive disease (CAOD) platelets are also crucially important. The aim of the present study was, therefore, to assess plasma levels of PDGF in patients with different degrees of CAOD according to Fontaine. Twenty patients (17 men, 3 women, mean age sixty-eight +/- seven years) with intermittent claudication (Fontaine stage II) entered the study and their PDGF levels were assessed by radioimmunoassay. Ten additional patients (7 men, 3 women, mean age seventy-three +/- seven years) with more severe CAOD (leg pain at rest/skin ulcers) were also studied. Ten healthy subjects (6 men, 4 women, mean age fifty-four +/- six years) comprised the control group. Patients in stage II were reinvestigated after sixty days of a "training" procedure. Patients with both intermittent claudication and more severe disease had higher levels of PDGF than controls (controls 165.9 +/- 119.1 pg/mL; Fontaine stage II 403.5 +/- 218.4; Fontaine stage III/IV 578.1 +/- 637.2:
ANOVA
P = 0.04) with no difference between the two groups of patients. After the training period, PDGF levels were significantly higher than at baseline (863.7 +/- 819.6 pg/mL vs 403.5 +/- 218.4) but without significant improvement of physical performance. The elevation of PDGF levels in blood from CAOD patients could be the result of marked platelet activation due to interaction with a widely damaged peripheral vasculature. The same was not true for coronary heart disease, in which normal values of PDGF in venous blood were found.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Platelet-derived growth factor (PDGF) in patients with different degrees of chronic arterial obstructive disease. 816 Oct 7
Free radical-induced injury to the arterial wall has been implicated in the pathogenesis and progression of
atherosclerosis
. To model the in vitro effects of free radicals on endothelial cell function, protein and lipid synthesis were measured after exposing cells to a superoxide generating system of xanthine (X = 100 microM) and xanthine oxidase (XO = 0.2 units). Total protein synthesis, measured by [35S]methionine uptake, decreased by 87.65 +/- 2.04% over 4 hr compared to controls (P < 0.05). Examination of lipid synthesis by high-performance liquid chromatography in cells prelabeled with either [3H]oleic acid or [3H]sodium acetate revealed alterations in all lipid classes. Phospholipid and neutral glyceride synthesis significantly decreased in a time- and dose-dependent fashion compared to controls (two-way
ANOVA
). In contrast, cholesterol synthesis and lipid peroxidation increased in a time- and dose-dependent fashion. When X = 200 microM and XO = 0.3 units, there was a statistically significant increase in cholesterol synthesis and lipid peroxidation within 24 hr (Tukey's HSD). We conclude that there is evidence of endothelial cell injury as measured by decreases in protein, glyceride, and phospholipid synthesis. The concurrent increases in lipid peroxidation and cholesterol synthesis may explain the relationship between free radical injury and the pathogenesis of
atherosclerosis
.
...
PMID:Free radical-induced alterations in endothelial cell function. 827 66
Patients with primary hyperparathyroidism have increased bone turnover, but it is less well documented how brief periods of excess parathyroid hormone (PTH) (endogenous or exogenous) affect bone metabolism. In the present double blind study, we examined the effect of either ethylenediaminetetraacetatic acid (EDTA) or placebo on serum levels of PTH and biochemical markers of bone turnover in 15 women and 39 men (aged 41 to 81 years) suffering intermittent claudication due to
atherosclerosis
. Disodium EDTA was administered as 20 repeated infusions of 3 grams during a period of 5-9 weeks. Serum calcium and serum phosphate decreased following treatment (p < 0.001) and remained unchanged in the placebo group. However, the differences between the groups were insignificant (
ANOVA
p = 0.13 and p < 0.10, respectively). PTH increased 2 1/2 fold following EDTA treatment (p < 0.001,
ANOVA
). The change in serum PTH was inversely correlated with the change in serum calcium (r = -0.53, p < 0.01). In the EDTA group, urinary hydroxyproline/creatinine and calcium/creatinine increased after treatment (
ANOVA
p < 0.001 and p < 0.05, respectively). Serum bone alkaline phosphatase decreased significantly in the EDTA group immediately after treatment (p < 0.001,
ANOVA
) and returned to baseline level at three months while only an insignificant decrease in serum osteocalcin was seen following treatment. We conclude that EDTA treatment increases endogenous PTH secretion considerably and leads to increased bone resorption. However, no changes in osteoblastic markers indicating increased activation of bone remodeling could be demonstrated. Our findings support that chelation therapy with EDTA is accompanied by bone loss.
...
PMID:Effects of intravenous EDTA treatment on serum parathyroid hormone (1-84) and biochemical markers of bone turnover. 829 6
The aim was to investigate the atherogenic potential of lipoprotein(a) (Lp(a)) and to further our understanding of the atherogenic process by measuring rates of transfer into the intima-inner media (i.e., intimal clearance) and rates of loss from the intima-inner media (i.e., fractional loss) of Lp(a) and LDL using cholesterol-fed rabbits with nonlesioned (n = 13) or atherosclerotic aortas (n = 12). In each rabbit, 131I-Lp(a) (or 131I-LDL) was injected intravenously 26 h before and 125I-Lp(a) (or 125I-LDL) 3 h before the aorta was removed and divided into six consecutive segments of similar size. The intimal clearance of Lp(a) and LDL was similar and markedly increased in atherosclerotic compared with nonlesioned aortas (
ANOVA
, effect of
atherosclerosis
: P < 0.0001). Fractional losses of labeled Lp(a) and labeled LDL in atherosclerotic aorta were on average 25 and 43%, respectively, of that in nonlesioned aortas (
ANOVA
, effect of
atherosclerosis
: P < 0.0001). Fractional loss of Lp(a) was 73% of that of LDL (
ANOVA
, effect of type of lipoprotein: P = 0.07). These data suggest that the development of
atherosclerosis
is associated with increased influx as well as decreased fractional loss of Lp(a) and LDL from the intima. Accordingly, Lp(a) may share with LDL the potential for causing
atherosclerosis
.
...
PMID:Preferential influx and decreased fractional loss of lipoprotein(a) in atherosclerotic compared with nonlesioned rabbit aorta. 875 69
Circulating levels of the adhesion molecule P-selectin (CD62P) are increased in the plasma of patients with
atherosclerosis
, but its relationship to the anatomical location of symptomatic disease or extent of symptomatic disease is unknown. The influence of the risk factors for
atherosclerosis
on soluble P-selectin is also unclear. To clarify these questions we analysed plasma samples from 170 patients with symptomatic peripheral vascular disease and 119 asymptomatic controls who were, as a group, age- and sex-matched. Soluble P-selectin (ELISA) was increased in 83 patients with symptomatic disease of the iliac and/or femoral arteries alone (P < 0.05,
ANOVA
) but not in 37 patients with symptomatic carotid artery disease alone compared with controls. Soluble P-selectin was equally raised in 120 patients with disease at one arterial site and in 50 patients with disease at two or more arterial sites (both P < 0.05) compared with controls. Smoking and
atherosclerosis
were both independent predictors of raised soluble P-selectin. We conclude that increased soluble P-selectin may have value as a marker of peripheral vascular disease of the iliac and/or femoral arteries in group comparisons only, as the poor discrimination and wide variation of data make comparisons at the individual level difficult.
...
PMID:Soluble P selectin in peripheral vascular disease: relationship to the location and extent of atherosclerotic disease and its risk factors. 903 60
We measured the capacity of human plasma to induce cholesterol efflux from Fu5AH rat hepatoma cells in four groups of men with or without non-insulin-dependent diabetes mellitus (NIDDM) and coronary artery disease (CAD). Plasma from men with both NIDDM and CAD (n = 47) had the lowest efflux capacity (17.3 +/- 3.6%) whereas healthy control subjects with neither diabetes nor CAD (n = 25) had the highest capacity (19.8 +/- 3.4%). The groups with CAD but no diabetes (n = 44) and with NIDDM but no CAD (n = 35) had intermediate efflux values (18.5 +/- 3.8 and 18.5 +/- 3.9%, respectively). In a 2 x 2 factorial
ANOVA
, the differences were significant with respect to the presence of CAD (P = 0.038) and NIDDM (P = 0.041), with no interaction between the factors. The concentration of HDL particles containing apolipoprotein (apo) A-I but no apo A-II (LpA-I) was not related to efflux capacity in univariate or multivariate analyses. A multivariate regression analysis showed that when controlled for the presence of NIDDM and CAD, the concentration of particles containing both apo A-I and apo A-II (LpA-I:A-II) and plasma phospholipid transfer protein activity were both positively, independently, and significantly (P < 0.001) related to cholesterol efflux capacity.
Atherosclerosis
1996 Dec 20
PMID:Cholesterol efflux from Fu5AH hepatoma cells induced by plasma of subjects with or without coronary artery disease and non-insulin-dependent diabetes: importance of LpA-I:A-II particles and phospholipid transfer protein. 912 15
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