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)

Much new information has been gleaned about the morphology, biochemistry and function of platelets. The pathophysiology of atherosclerosis and thromboembolic disorders appears to be related to abnormal platelet function. Endothelial damage, thromboxane A2, Thrombin, adenosine diphospate and epinephrine may each promote platelet aggregation, whereas prostacyclin impairs aggregation. Aspirin, sulfinpyrazone and dipyridamole have been used as antiplatelet agents, and specific indications are being developed to guide their selection.
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PMID:Antiplatelet therapy. 702 99

Aspirin and dipyridamole have been used to treat the thromboembolic complications of atherosclerosis. We studied the effects of these drugs on the rate of endothelial healing after a standard de-endothelializing injury of the thoracic aorta. Twenty-five rabbits received 13.5 mg/kg/day of aspirin and 15 mg/kg/day of dipyridamole one week before injury and for the period of endothelial regrowth. There were 25 control animals. Mean serum aspirin salicylate levels were 12 micrograms/dL at the time of injury and 15 micrograms/dL at death. Areas of endothelial regrowth were measured by Evans blue dye at 1, 4, 7 and 14 days after injury. The percentage of endothelial regrowth was measured by computer-assisted morphometry. Antiplatelet treatment retarded endothelial regrowth by 66% at four days, 22% at seven days, and 28% at 14 days. Antiplatelet drugs must be used cautiously, as re-endothelialization of injured arteries is retarded.
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PMID:Aspirin and dipyridamole inhibit endothelial healing. 713 4

The model was established in male rabbits with experimental atherosclerosis, which was induced by diet cholesterol (0.5 g per day for 8 weeks), by means of intravenous injection of one unit of pituitrin (P.P.). To evaluate the effects of aspirin, heparin and viper venom (VV) on this model, 26 male rabbits were divided randomly into four groups: group A (GA) as control, group B (GB) treated with heparin (10mg, i.v.), group C (GC) with VV (0.08 arginine esterase activity units), group D (GD) with both heparin and VV. Aspirin (30 mg) was given orally before experiment. The results showed that the rate of coronary thrombosis was 11.26% in GA, 8.10% in GB, 9.17% in GC, and 7.56% in GD respectively. The difference between each of three treated groups and the control one was significant (P < 0.005, 0.05, 0.001, respectively). Such a difference can also be found between GA and that without oral aspirin (11.26% vs 16.39%, P < 0.001). The beneficial effects of heparin and VV may be due to their inhibitory effects on different steps of thrombosis, i.e., heparin can prolong the coagulation time, and VV can inhibit platelet aggregation and decrease the concentration of plasma fibrinogen. It is concluded that heparin, viper venom, and especially their combination would be useful in the treatment of human acute coronary syndromes.
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PMID:A new animal model of coronary thrombosis and effects of antithrombotic agents. 755 40

We examined the effect of beraprost sodium (BPS), a stable prostaglandin I2 (PGI2) analogue, on restenosis after balloon angioplasty in the atherosclerotic artery in rabbits. Regional atherosclerosis was induced in the femoral artery of New Zealand white rabbits by balloon deendothelialization and 2% cholesterol diet. After establishment of atheroma in the femoral artery, angioplasty was performed. In all, 65 rabbits were assigned to the following six subcutaneous drug treatment groups: control group (n = 13, saline 0.25 ml/kg); BPS low-dose group (n = 11, BPS 50 micrograms/kg twice daily); BPS high-dose group (n = 12, BPS 100 micrograms/kg twice daily); 2-day BPS high-dose group (n = 11, BPS 100 micrograms/kg twice daily for 2 days after angioplasty); aspirin (ASA) group (n = 10, ASA 30 mg once daily); and BPS+ASA group (n = 8, BPS 50 micrograms/kg twice daily plus ASA 30 mg once daily). Administration of each drug was started 30 min before balloon angioplasty and was continued until 4 weeks thereafter, except in the 2-day BPS high-dose group. Re-examination 4 weeks after the angioplasty showed significant (p < 0.05) preservation of the luminal diameter in the BPS high-dose and 2-day BPS high-dose groups (1.30 +/- 0.15 and 1.25 +/- 0.09 mm, respectively) as compared with that in the control group (0.83 +/- 0.10 mm); however, the luminal diameter in the BPS low-dose, ASA, and BPS+ASA groups (0.94 +/- 0.18, 1.06 +/- 0.11, and 1.05 +/- 0.15 mm, respectively) was not significantly different from that in the control group.
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PMID:Inhibition of restenosis by beraprost sodium (a prostaglandin I2 analogue) in the atherosclerotic rabbit artery after angioplasty. 756 40

Recent evidence has led us to propose that transforming growth factor-beta (TGF-beta) is a key inhibitor of atherosclerosis. We show here that a population of patients with advanced atherosclerosis all have less active TGF-beta in their sera than patients with normal coronary arteries, with a fivefold difference in average concentration between the two groups. This correlation with atherosclerosis is much stronger than for other known major risk factors and it may therefore have important diagnostic and prognostic significance. Aspirin medication correlates with an increase in active TGF-beta concentration, indicating that therapeutic interventions for TGF-beta are possible.
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PMID:The serum concentration of active transforming growth factor-beta is severely depressed in advanced atherosclerosis. 758 46

Lower extremity vascular grafts, either vein or synthetic, fail for diverse reasons. Technical defects or poor surgical judgment doom a graft beyond any benefit pharmacotherapy can offer. Graft failure due to spontaneous thrombosis particularly affects prosthetic conduits, and use of antiplatelet agents (dextran, ASA) or anticoagulants (heparin, warfarin) is probably useful in this setting. An effective way to inhibit vein graft or anastomotic intimal hyperplasia remains elusive. Perhaps the most permanent and longstanding influence on lower extremity graft survival can be made through risk factor intervention aimed at arresting the progression of atherosclerosis. Aggressive treatment of hyperlipidemia, hypertension, smoking, and other known risk factors should be routinely and aggressively pursued in patients with lower extremity grafts, either autogenous or prosthetic. Lower extremity graft patency is optimally ensured by technically adept insertion of a proper autologous conduit in a well-selected patient. Pharmacotherapy may have a significant adjunctive role in the maintenance of graft patency, especially in high-risk settings such as limb salvage with associated poor outflow, a marginal vein graft, or the obligatory use of prosthetic material.
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PMID:Pharmacologic intervention to prevent graft failure. 763 20

Thromboxane A2 biosynthesis was studied in healthy subjects, in patients in whom the extent of carotid atherosclerosis was determined, and in patients receiving chronic aspirin treatment, to determine what factors activate platelets to develop carotid atherosclerosis. Urinary 11-dehydrothromboxane B2, a major metabolite of thromboxane A2, was measured by radioimmunoassay after purification by reverse-phase HPLC. The extent of carotid atherosclerosis was determined by real-time B-mode ultrasonography. The severity of carotid atherosclerosis in each subject was evaluated by plaque score, which was computed by summing the maximum thickness of plaque measured in millimeters. Urinary excretion of 11-dehydrothromboxane B2 in healthy subjects was higher (P < 0.01) in cigarette smokers (1063 +/- 244 ng/g creatinine) than in non-smokers (815 +/- 183 ng/g creatinine). Aspirin significantly suppressed 11-dehydrothromboxane B2 excretion (266 +/- 114 ng/g creatinine). In the 24 patients in whom the plaque score was measured, multivariate analysis indicated a significant positive correlation between urinary excretion of 11-dehydrothromboxane B2 and plaque score, age, smoking and hypercholesteremia. Our results indicate that risk factors such as age, hypercholesteremia, atherosclerosis and smoking activate platelets in vivo to develop carotid atherosclerosis.
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PMID:Risk factors for carotid atherosclerosis and platelet activation. 806 12

Patients with atherosclerotic carotid artery stenosis commonly have arterial disease elsewhere, especially coronary artery disease. The aim of the medical treatment is to reduce the incidence of stroke, myocardial infarction and vascular death. Both primary and secondary prevention of these vascular events requires control of vascular risk factors, particularly lowering elevated blood pressure, lowering of elevated blood cholesterol and stopping smoking. Aspirin and ticlopidine are effective in reducing vascular events in patients with atherosclerosis, with a relative reduction of about 25% for the composite outcome event "stroke, myocardial infarction or vascular death". Whether low dose (less than 100 mg/d), medium (300 mg/d) or high dose (1,000 mg/d or more) of aspirin confer the same degree of protection against vascular events is unclear. The gastrointestinal side effects are greater for the high dose than for the medium dose, but the difference between the medium dose and the low dose is very small. Ticlopidine conveys a modest risk of reversible severe neutropenia and is often used as a second-line drug, but this is a controversial issue. Heparin is often used as a short-term preventive treatment in patients with transient ischaemic attacks or minor stroke, especially in those with "crescendo" transient ischaemic attacks, progressing stroke, severe carotid stenosis or intraluminal thrombus.
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PMID:[Medical treatment of atherosclerotic carotid stenoses]. 815 33

The ageing of connective tissues involves modifications of collagen, which are currently generating much interest amongst protein researchers. Protein glycation, a non-enzymic reaction involving sugar, appears to play a role in the evolution of age-related physical changes and diabetic complications-retinopathy, neuropathy, renal failure and atherosclerosis. Our studies show that the glycation of human corneal and scleral collagen produces increases in the collagen intermolecular spacing-these increases are similar to those we previously reported on the ageing of collagen in these tissues. The present investigation employs X-ray diffraction to look at the structural effects of various substances that are believed in inhibit protein glycation. Aspirin-like compounds and certain vitamins successfully prevented the sugar-induced molecular changes from occurring in corneal and scleral collagen, suggesting that such compounds could have a useful role in this aspect of ageing.
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PMID:Vitamins and analgesics in the prevention of collagen ageing. 883 72

Atherosclerosis is a complex progressive process with high morbidity and frequent dramatic mortality. The experience from the developed countries justifies the effectiveness of atherosclerosis prevention. The combination of nonpharmacologic, antiaggregatory and antihyperlipemic prevention reaches currently the effectiveness of surgical intervention, with the exception of sudden events. On the other hand the surgical intervention does not restore the process of atherosclerosis and requires the same secondary prevention if the long term prognosis is to be improved. The review presents the guidelines on nonpharmacologic, antihyperlipemic (up to the combination of statin with fibrates) and the antiaggregatory prevention with the initial dose of ASA being 200 mg and a long term dose being > or = 30 mg of ASA/d treatment. (Tab. 4, Fig. 3, Ref. 25.)
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PMID:[Prevention and therapy of atherosclerosis]. 892 7


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