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)

Breddin thrombagglutination test is followed up in patients with hypercoagulation states--atherosclerosis, atherosclerotic myocardiodysthrophia, angina pectoris gravis and acute myocardial infarction and hypocoagulation states--esential and symptomatic thrombopenia. TAT is positive in 88% of the patients with atherosclerosis and in patients with angina pectoris gravis and myocardial infarction TAT is Vth stage in 100%. TAT is zero stage in 91% in patients with thrombopenia and only in 9%-I stage. The term "zero stage" is introduced.
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PMID:[Thrombagglutination test (TAT) in hyper- and hypocoagulation]. 122 97

The present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial infarction was compared with 28 control subjects. The patient groups showed elevated levels of Factor VII procoagulant activity (FVII:C) and more markedly elevated Factor VII antigen (FVII:Ag) levels than the control group; therefore they had a decreased FVII:C to FVII:Ag ratio. The increased Factor VII level in the patient groups was caused by elevated Factor VII zymogen levels, and not by activated Factor VII. Since FVII:C levels strongly correlated with the titer of thrombin-antithrombin III complexes in all patients, the hypercoagulable state accompanying severe coronary atherosclerosis seems to underlie the increase of FVII and TAT in the stable phase of myocardial infarction.
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PMID:Elevation of factor VII activity and mass in coronary artery disease of varying severity. 174 7

Veins and arteries grafted into the aorto-to-coronary position undergo degenerative processes, subintimal fibrous hyperplasia and diffuse atherosclerosis. We examined the influence of various crystalloid and cardioplegic solutions on the endothelium of human saphenous veins and internal mammary arteries, bovine internal mammary veins and arteries and rabbit carotid arteries, using light microscopy, TEM, SEM, immunological techniques and quantitative permeability measuring methods. Immersion or perfusion of vessel segments for various periods of time led to an ultrastructural endothelial cell damage, to an increased endothelial permeability for macromolecules, partly to an endothelial cell loss. Addition of high concentrations of heparin impaired this effect. Under influence of various solutions an increased plaque development under stimulation with atherogenic stimuli was observed.
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PMID:[Early and late damage in bypass vessels induced by crystalloid and cardioplegic solutions]. 178 83

Endothelial characteristics and the macrophage foam cell nature of early naturally occurring lesions in the aorta and coronaries of the pigeon have been well characterized. However, the characteristics of pigeon atherosclerosis at other vascular sites have not been extensively studied. The present study was designed to compare atherosclerosis in the brachiocephalic artery with that in the coronaries and aorta. Forty-six White Carneau (WC) pigeons (26 female, 20 male) ranging in age from 2.5 to 7 years were necropsied after fixation under deep anesthesia by perfusion at 160 mm Hg with buffered glutaraldehyde. Arteries stained with Sudan IV for gross evaluation were subsequently processed for SEM and TEM. The occurrence of sudanophilia in the proximal brachiocephalic artery was greater in females (22/26) than in male (2/20). The endothelium, as studied by SEM, was intact over all normal and sudanophilic areas. Cell morphology varied with location in the vessel and gradually changed from polygonally shaped cells with prominent margins and protruding nuclei in the proximal brachiocephalic artery to elongated, flattened cells in distal regions. These regional differences were consistently observed, and did not correlate with age, gender, or areas of lipid accumulation. Unlike lesions in the coronary arteries and at the celiac bifurcation of the aorta, a relative paucity of white blood cells over diffuse sudanophilic areas was observed. This lack of adherent monocytes correlated with lesion ultrastructure. Connective tissue in the intima of the sudanophilic brachiocephalic arteries was disorganized, reflecting both an increase in matrix components and the presence of massive pools of extracellular lipid. Intracellular lipid was minimal and when present was confined to random droplets in the cytoplasm of intimal smooth muscle cells. Monocyte-derived foam cells, characteristic to other vascular beds, were absent from the brachiocephalic artery lesions. These results document differential lesion composition in the WC pigeons and suggest a gender-related susceptibility for brachiocephalic artery atherosclerosis in pigeons.
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PMID:Morphologic characteristics of naturally occurring atherosclerosis in the brachiocephalic artery of the pigeon. 202 38

1. Cholesterol feeding of rabbits impairs the endothelium-dependent relaxation (EDR) evoked by acetylcholine (ACh) in the aorta. The experiments described in this paper were undertaken to examine the influence of age upon this phenomenon. 2. Rabbits aged 8 weeks and 46 weeks were fed a diet containing 2% cholesterol and other lipids for 4 weeks. Age-matched control animals were fed a standard rabbit diet. The concentrations of cholesterol and triglycerides in plasma were measured and the extent of atherosclerosis was estimated by staining the aortae with Sudan Red. Light and electron microscopy were undertaken also. 3. Rings of aorta were prepared for recording isometric tension. They were contracted with noradrenaline (NA) and EDR elicited by adding ACh. 4. The young rabbits showed weight gain, hypercholesterolaemia, prominent Sudan Red staining, together with scanning and transmission electron microscopic (SEM and TEM) features of cholesterol-induced atherosclerosis. The older animals showed significant weight loss and hypercholesterolaemia. The aortae of these animals showed no significant sudanophilia or light microscopic features of atherosclerosis. The SEM appearances were similar to the young animals fed cholesterol. 5. EDR to ACh was significantly impaired in both groups of cholesterol-fed rabbits. The maximal relaxations to ACh in young control and cholesterol-fed rabbits were 46.4 +/- 2.9% and 24.0 +/- 4.3% (mean +/- s.e. mean, n = 8, P less than 0.05) of the contractile response to NA (1 mumol 1(-1]. The corresponding results in the age control and cholesterol-fed rabbits were 31.8 +/- 3.9% and 9.1 +/- 1.5% (n = 9, P less than 0.05). 6. The young rabbits were far more susceptible to cholesterol-induced atherosclerosis than older animals and these changes were accompanied by loss of EDR. In the older animals and these changes were accompanied by loss of EDR. In the older animals the loss of the latter property was not accompanied by a significant degree of atherosclerosis although hypercholesterolaemia was present.
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PMID:Impairment of endothelium-dependent relaxation: an early marker for atherosclerosis in the rabbit. 326 Aug 4

Endothelia lining the 2 surfaces (arterial and ventricular) of the posterior cusp of aortic valves from normocholesterolemic, New Zealand white rabbits were found to display pleomorphic surface features characterized by differences in cellular shape and orientation to the direction of blood flow, microappendage populations (microvilli and blebs), nuclear contours and the surface reactions of cationic dyes (RR, AB) and peroxidase-conjugated lectins (Con A, Limulin, WGA). With the aid of SEM and TEM, the cells lining the arterial surfaces appeared relatively smooth and flattened with a moderate to heavy reaction of the carbohydrate cell coat at the blood interface. By contrast, the contours of the endothelia lining the ventricular surfaces were noticeably raised with numerous plasmalemmal microappendages and only a moderate dye/lectin reaction. Observations of similar endothelial populations from diet-induced, hypercholesterolemic rabbits (500 mg/dl) revealed a variety of dramatic changes in the cells lining the arterial surfaces of the valvular cusps. No severe changes were observed in the endothelia of the ventricular surfaces. Such findings are suggestive further of the importance of the interaction between the environment and the endothelial cell coat as influencing factors in the onset of intramural lipid infiltration.
Atherosclerosis 1985 Mar
PMID:Surface responses of aortic valve endothelia from diet-induced, hypercholesterolemic rabbits. 399 84

Lacunar infarcts are related to occlusion of penetrating arteries. Lipohyalinosis affects the smaller arteries 40-200 microns in diameter, and atherosclerosis involves larger arteries 200-850 microns in diameter. We hypothesized that the processes of thrombus formation might be different among these two kinds of lacuner infarcts, including those caused by lipohyalinosis and atherosclerosis. We studied acute coagulation and fibrinolytic activation in lacunar infarct patients which were divided into two groups according to their size: smaller lacunar group and larger lacunar group. Then we divided lacunar infarct patients into two groups in terms of the progression of motor deficits: those who showed the progression and those did not. And coagulation and fibrinolytic activation were compared each other. One hundred and twenty four patients were enrolled in this study, including 34 control subjects, 39 patients with smaller lacune (3 mm-10 mm in diameter), 28 patients with large lacune (10 mm-20 mm), and 23 patients with atherothrombotic infarcts confirmed by angiography. The levels of TAT activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.009, p < 0.0001, respectively), whereas those in small lacune were not. Also, the levels of D-dimer activity in large lacune and atherothrombotic infarcts were significantly higher than those in control subjects (p = 0.0003, p < 0.0001, respectively), whereas those in small lacune were not. The progression of motor deficits were more frequently recognized in large lacune than in small lacune: three patients out of 39 small lacune patients and 22 patients out of 28 large lacune patients (difference was significant, p = 0.001). The level of TAT activity in patients who showed progression of motor deficits was significantly higher than that in those who did not (p = 0.0002), whereas the difference of the levels of D-dimer activity in two groups did not reach significant differencial levels. The process of thrombin and fibrin formation in large lacunar infarcts which are related to microatheroma and atheroscrelosis appears to be different from that in small lacunar infarcts. Antiplatelet and anticoagulation therapy should be tailored to large lacunar infarct patients.
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PMID:[Coagulation and fibrinolytic activation in lacunar infarct patients]. 1068 30

Chlamydia pneumoniae has been detected in atherosclerotic plaques by various means. Chlamydiae are able to cause persistent infections. Serologically elevated antibody titers are found in severe chronic obstructive pulmonary disease. In atherosclerosis and pulmonary emphysema, inflammatory reactions can be seen by means of light microscopy. Specimens from patients with obliterative arteriosclerosis undergoing thrombendarteriectomy and with advanced emphysema undergoing lung volume reduction surgery were examined using scanning (SEM) and transmission (TEM) electron microscopy, and using immunofluorescence with monoclonal antibodies and antiserum against chlamydiae. SEM shows spherical bodies (SBs) with a diameter from 0.3 microm to 0.6 microm on the surface of the alveoli and bronchioles, as well as in atherosclerotic plaques. In atherosclerosis and emphysema, SBs reveal a double membrane, adherence to collagen fibers, tissue destruction, as well as intracellular and interstitial localization in TEM. They show in parts a densely packed central structure. SBs are seen both in alpha-1-antitrypsin deficiency emphysema and smoker's emphysema. Using immunofluorescence microscopy, spots are seen in corresponding distributions to the SBs. Morphological findings are typical for aberrant chlamydiae seen in persistent infections. Chronic infection and bacterial colonization associated with progressive disease seems to be relevant not only in atherosclerosis but also in pulmonary emphysema.
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PMID:The role of chlamydia in the pathogenesis of pulmonary emphysema. Electron microscopy and immunofluorescence reveal corresponding findings as in atherosclerosis. 1099 81

There is evidence that the coagulation system is activated in patients with peripheral arterial occlusive disease (PAOD). The beneficial effects of the vasoactive drug prostaglandin E1 (PGE1) may rely in part on the modulation of the coagulation system. The study was designed to evaluate the effects of PGE1 on hemostatic and fibrinolytic variables in patients with intermittent claudication. Therefore molecular markers of thrombin (prothrombin fragment 1+2, PTF 1+2; thrombin-antithrombin III complexes, TAT) and fibrin formation (fibrinopeptide A, FPA) and markers of the fibrinolytic activity (fibrin degradation products, D-dimers) were determined before and immediately after the first PGE1 dose (60 microg in 100 ml NaCl over 2 h i.v.) as well as after 4 weeks of daily infusion therapy in 12 PAOD patients and in eight control patients before and after a single placebo infusion. Plasma levels of PTF1+2, TAT, FPA and D-dimers tended to decrease after the initial dose of PGE1. Infusion therapy with PGE1 for 4 weeks led to a decrease of all hemostatic and fibrinolytic parameters with most pronounced changes for PFT1+2, D-dimers and plasminogen activator inhibitor-1 decreasing by 11% (P<0.05), 20% (P<0.05), and 7% (P<0.05), respectively. These variables remained unchanged in controls with placebo infusion. In summary, infusion therapy with PGE1 in patients with PAOD reduces thrombin formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin deposition involved in the pathogenesis of atherosclerosis.
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PMID:Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1. 1109 Feb 53

To determine the presence of a 'hypercoagulable state' as assessed by indices of thrombin and plasmin generation and of the amount of fibrin that is lysed, in patients with stable coronary, cerebral and peripheral arterial disease a population-based cross-sectional study was performed. From a population-based cohort comprising 7983 men and women aged 55 years and over, we randomly selected 127 subjects with a history of myocardial infarction, 124 with a history of stroke and/or transient ischemic attack, 131 patients with peripheral arterial disease and 263 control subjects in the same age group without arterial disease. Subjects using anticoagulant drugs were not selected. F1+2, TAT, and PAP were not associated with a history of cardiovascular events, nor with peripheral arterial disease. In contrast, positive associations were found for D-Dimer. Mean D-Dimer level was 40 microg/l (95% CI 35, 44) in control subjects; 53 microg/l (47, 61) in those with a history of myocardial infarction and 51 microg/l (45, 58) in those with a history of stroke and or transient ischemic attack. D-Dimer increased gradually with increasing severity of peripheral atherosclerosis; a decrease in ankle/arm systolic blood pressure ratio of 0.1 was associated with an increase in D-Dimer of 3.9 microg/l (p<0.01). This was more pronounced in subjects with higher F1+2, TAT and PAP concentration. In conclusion, the markers of onset of coagulation F1+2, TAT and PAP are not associated with the presence of arterial disease, but increased levels of these markers are necessary for the positive association between D-Dimer and arterial disease.
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PMID:Activation products of the haemostatic system in coronary, cerebrovascular and peripheral arterial disease. 1124 39


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