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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of aspirin in the primary prevention of diet-induced atherogenesis in cynomolgus monkeys was studied. The diet consisted of 2% cholesterol and 10% butter by weight for 24 wk. Six monkeys received only the atherogenic diet and five monkeys received the diet plus aspirin, 81 mg/monkey per day. Aspirin did not affect plasma cholesterol levels or aortic atherosclerosis. Platelet aggregation to arachidonic acid was almost completely suppressed. Aspirin decreased significantly the number of coronary vessels with atherosclerotic involvement, and the number of coronary vessels narrowed by 20% or more. Thus, aspirin appears to exert a protective effect in the primary prevention of diet-induced coronary atherosclerosis in a primate model.
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PMID:Aspirin inhibits development of coronary atherosclerosis in cynomolgus monkeys (Macaca fascicularis) fed an atherogenic diet. 10 14

Fifty-nine patients with stage I (according to A. L. Myasnikov's classification) coronary atherosclerosis and 23 healthy persons of the same age were tested for the content of rosette-forming T- and B-lymphocytes, immunoglobulin classes, lymphocyte blast-cell transformation reaction to the phage and antigen from the normal and atherosclerotic aorta, and the changes in these indices under the effect of miscleron (in 23) and acetylsalicylic acid (in 10 persons). A tendency to an increase in the content of B-lymphocytes and G and A immunoglobulins and intensification of the lymphocyte blast-cell transformation reaction to an antigen from the sclerotic aorta, and a tendency to a decrease in the content of T-lymphocytes in patients with atherosclerosis were noted. The normalizing effect of miscleron therapy on these indices with parall improvement in the values of lipid metabolism were also established. Acetylsalicylic acid did not change the values of lipid metabolism and had not effect on the blood immunoglobulin content.
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PMID:[Change in the immunological indices in arteriosclerosis]. 31 38

The initial hemorheologic values and their dynamics in various periods after reconstructive operations were studied in 70 patients with atherosclerosis of the abdominal aorta. The rheologic blood properties proved to be considerably changed in atherosclerotic affection of the abdominal aorta. The causes of the hemorheologic disorders in this pathological condition are marked changes in regional hemodynamics and the character of the blood flow and significant disorders of protein, lipid and carbohydrate metabolism. Study of the effect of aspirin on the rheologic properties of blood in this contingent of patients showed the expediency of its use both in preoperative management and in the postoperative period. Aspirin reduces significantly the degree of blood platelet aggregation and the seeming viscosity of blood.
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PMID:[Blood rheological disorders in atherosclerotic lesion of the abdominal aorta and their correction by the use of aspirin]. 37 Apr 36

Groups of New Zealand white male rabbits were fed atherogenic diets containing 1% cholesterol. The diets of experimental groups were supplemented additionally with either aspirin, phenylbutazone, mefenamic acid, flufenamic acid, oxyphenylbutazone or aminopyrine. Blood cholesterol and phospholipids were measured at 3--4 week intervals. After 12 weeks the animals were sacrificed and the severity of atherosclerosis in the thoracic aorta was measured. In separate experiments, rabbit platelets were incubated with each of the drugs individually and conversion of [14C]arachidonic acid to thromboxanes and related compounds was assayed. Inhibition of collagen and arachidonic acid-induced platelet aggregation by each drug was also measured. All drugs inhibited thromboxane synthesis and platelet aggregation in varying degrees with flufenamate and aspirin being most and aminopyrine least effective. The pattern of metabolite formation from [14C]arachidonate was consistent with a block in the cyclooxygenase reaction. Phenylbutazone, flufenamic acid and oxyphenylbutazone produced significant reductions in atherosclerotic plaque formation without major changes in blood cholesterol levels or blood cholesterol--phospholipid ratios. Aspirin and aminopyrine were ineffective. The results indicate that the effectiveness of anti-inflammatory drugs as inhibitors of thromboxane synthesis and platelet aggregation in vitro does not afford a sufficient predictive index of their anti-atherogenicity in vivo. The significance of these findings is discussed in terms of the possible involvement of cyclooxygenase derivatives in atherogenesis.
Atherosclerosis 1979 Feb
PMID:Anti-inflammatory drugs in experimental atherosclerosis. Part 4. Inhibition of atherosclerosis in vivo and thromboxane synthesis and platelet aggregation in vitro. 45 16

The central role of the thrombocytes in the initial atherogenesis and the secondary formation of the thrombus on sclerotically changed walls of the vessels is the basis of all experiments to perform a primary or secondary prevention of the atherosclerosis with thrombocyte aggregation inhibitors. Of the numerous thrombocyte-inhibiting substances acetyl salicylic acid, dipyridamol and sulfinpyrazone proved most suitable for clinical purposes. Apparantly for methodical reasons experiments of a primary prevention of the atherosclerosis with aggregation inhibitors have hitherto not be performed. On the other hand, in numerous quantitatively very different studies on patients with manifest cerebral, coronary and peripheral arteriosclerosis the influencibility of the course of the disease was tested by thrombocyte inhibitors. Since correct prospective studies are connected with enormous organisational expenditure and must extend for a longer period many extensive examinations have not yet finished. In the present survey the hitherto existing reports from literature are critically summarized, taking into particular consideration the per ipheral angioorganopathies and first informations on an own study concerning the prophylaxis of the diabetic angiopathy with Micristin are given. The present state of knowledge allows the conclusion that the well founded theoretical concept is apparantly confirmed by practice. However, the successes observed could be statistically ascertained only in individual cases, so that at present a final estimation of the prophylactic value of these preparations is not yet possible.
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PMID:[Inhibitors of platelet aggregation in the therapy of arteriosclerosis obliterans]. 48 16

Cardiovascular disease is a major cause of death. There is evidence that this disease is predicted and its progression influenced by various factors (e.g. hyperlipidaemia). In this review, we consider aspects of platelet structure and function which may explain how this cell type contributes to the pathogenesis of vascular disease. The platelet also contains bioamines (serotonin, 5-HT; histamine) which are potent vasoactive substances. Studies involving patients with peripheral vascular disease (PVD) where abnormalities in platelet function (platelet aggregation and platelet shape change) and in bioamine status (vascular, platelet and plasma bioamine concentrations) are reviewed. We also discuss how platelet activation (in vitro) and plasma lipids influence intraplatelet bioamine status. Finally, we report in vitro evidence of the effect of two drugs prescribed to PVD patients: aspirin and naftidrofuryl. Aspirin is an ineffective inhibitor of 5-HT-induced whole blood platelet aggregation whereas naftidrofuryl is effective in the presence or absence of aspirin. By identifying and altering the factors which contribute to the pathogenesis of atherosclerosis we will be better equipped to prevent, reverse or retard this process.
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PMID:Serotonin, histamine and platelets in vascular disease with special reference to peripheral vascular disease. 134 86

Thromboxane A2 (TXA2) biosynthesis was studied in healthy subjects, patients with chronic cerebral infarction, patients under chronic aspirin treatment and patients with atrial fibrillation. Urinary 11-dehydro-TXB2, as a major metabolite of TXA2, was measured by radioimmunoassay. The extent of carotid atherosclerosis was determined by B-mode ultrasonography. The mean +/- SD urinary excretion in patients with cerebral infarction and distinct carotid-atherosclerotic lesions (1,725 +/- 239 ng/g creatinine, n = 6) was significantly higher (p less than 0.01) than in healthy subjects (911 +/- 239 ng/g creatinine, n = 44) and patients with cerebral infarction who had no distinct carotid lesion (1,050 +/- 191 ng/g creatinine, n = 6). The urinary excretion of healthy subjects was higher (p less than 0.01) in smokers (1,063 +/- 244 ng/g creatinine, n = 17) than in non-smokers (815 +/- 183 ng/g creatinine, n = 27). Aspirin largely suppressed 11-dehydro-TXB2 excretion (266 +/- 114 ng/g creatinine, n = 7). Three of 5 patients with atrial fibrillation showed very high values. Our results indicated that platelet activation occurs in the atherosclerotic lesions, and that urinary 11-dehydro-TXB2 is the appropriate analytic target for detecting platelet activation.
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PMID:Urinary 11-dehydro-thromboxane B2: a quantitative index of platelet activation in cerebral infarction. 139 73

The adherence of monocytes to the arterial endothelium followed by its migration into the arterial intima is the earliest event in atherogenesis. The vasoconstrictive peptide, Endothelin-1 (ET-1), is elevated in patients with atherosclerosis. We were interested to know whether ET-1 was a chemoattractant for blood monocytes. Using the modified membrane filter technique for chemotaxsis assessment, ET-1 increased monocyte chemotaxis in a dose-dependent manner. Ca2+ channel blockers, Nifedipine, Diltiazem and Verapamil (5 microM), reduced ET-1 chemotaxsis more than 60% (P < 0.001). Aspirin and Indomethacin (1 mM and 100 microM, respectively) reduced migration by 23% (P < 0.05). Alpha-Lipoic acid, Probucol and Neomycin (100 microM) were also migration inhibitory (37%, P < 0.01). These results suggest that ET-1 is a strong chemoattractant for blood monocytes; Ca2+ influx is probably the major stimulus for the accelerated migration induced by ET-1.
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PMID:Chemotaxis of human blood monocytes toward endothelin-1 and the influence of calcium channel blockers. 147 72

This study was conducted to investigate acute effects of smoking on platelet function, endothelial cells and plasma lipids and to follow these parameters after Aspirin ingestion. Twelve fasting smokers each inhaled the smoke of one cigarette. Blood was drawn before and 10 min after smoking. Plasma nicotine, measured by gas chromatography, increased from 13.48 before smoking to 78.41 nM after smoking. Platelet aggregation to thrombin and ADP increased significantly (P less than 0.001). The platelet aggregate ratio decreased from 0.95 to 0.75 (P less than 0.005). Plasma beta-thromboglobulin also increased in post-smoking samples as measured using radioimmunoassay. 'Circulating endothelial cells' increased significantly after smoking (P less than 0.005). Triglycerides decreased (P less than 0.005) in plasma and in the VLDL fraction (P less than 0.05). Both post-smoking plasma free fatty acids and free glycerol increased, respectively, as compared with respective values. Lipase activity ascribable to lipoprotein lipase and hepatic lipase, absent in pre-smoking plasma samples, could be detected in post-smoking plasma without heparin injection. At least 1 week later, the subjects returned to follow an identical protocol except that they had ingested Aspirin (650 mg) 10-14 h before blood sampling. The same parameters were measured before and after smoking the same cigarette. Except for plasma nicotine, all the smoking-induced changes were abolished by ingestion of Aspirin. The results of this study indicate an interrelationship between platelet hyperactivity, endothelial injury and plasma lipids. They also demonstrate an inhibition of the major smoking-induced changes by Aspirin in the presence of high plasma nicotine levels. It is concluded that Aspirin may offset several of the deleterious acute effects of smoking. However, our conclusions cannot be, in any way, extended for long-term effects of both smoking and Aspirin treatment. Based on these data, it is suggested that there may be some links between platelet hyperactivity, endothelium injury and plasma lipids.
Atherosclerosis 1992 Apr
PMID:Acute influence of smoking on platelet behaviour, endothelium and plasma lipids and normalization by aspirin. 146 56

Of the major risk factors for atherosclerosis, high factor VII and fibrinogen levels, genetic predisposition, gender and age cannot be influenced. Reduction of high blood pressure reduces the cerebral but not the coronary vascular risk and correction of dyslipidaemia correlates with cardiovascular risk. Other major risk factors (tobacco consumption, obesity, sedentary lifestyle and diabetes) can also be modified. Aspirin in doses of approximately 300 mg/day may be recommended for the primary prevention of myocardial infarction (MI), but only in those patients with a moderate to high risk of cardiovascular disease. Aspirin reduces the risk of fatal and nonfatal MI by about 50% and also decreases the overall mortality rate among patients with unstable angina. A lower dose of aspirin (150 mg/day) also reduces mortality by 23% in the acute phase of MI. In doses of 300 mg/day, aspirin is useful in the secondary prevention of MI and reduces the overall mortality rate by 15%. Various antiplatelet agents, including aspirin (alone or combined with dipyridamole) and ticlopidine, have proved useful in the prevention of thrombosis in aorto-coronary grafts, provided treatment begins at the latest 6 hours after surgery. The usefulness of antiplatelet drugs has been well established in the prevention of immediate reocclusion following coronary angioplasty, but not in the prevention of late reocclusion. Aspirin and ticlopidine are also beneficial in extracorporeal circulation techniques. In patients with a synthetic cardiac valve prosthesis, antivitamin K-anticoagulants are still indispensable lifelong, but their antithrombotic effect can be reinforced by dipyridamole or aspirin. Diuretics probably provide the best primary protection against cerebrovascular accidents, although medium doses of aspirin may be considered in elderly people at high risk of such accidents. Aspirin (alone or combined with dipyridamole) and ticlopidine may be recommended for the secondary prevention of cerebral ischaemic accidents. Aspirin (with or without dipyridamole) and ticlopidine reinforce the treatment of obliterative arterial disease in the lower limbs.
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PMID:Risk factors, interventions and therapeutic agents in the prevention of atherosclerosis-related ischaemic diseases. 172 14


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