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PubMed1988

An evaluation of different doses of soluble aspirin and aspirin tablets in postoperative dental pain.

1. The efficacy of three different single doses (600, 900 and 1200 mg of soluble aspirin and aspirin tablets) was determined in a randomized placebo-controlled parallel study in 140 patients (70 females) with postoperative pain after removal of impacted third molars. 2. Patients treated with soluble aspirin 600 mg, 900 mg, 1200 mg and aspirin tablet 1200 mg reported significantly less pain (P less than 0.01) throughout the investigation period than those treated with placebo. 3. Overall pain scores after treatment with aspirin tablets 600 and 900 mg did not differ significantly from those after treatment with placebo (P greater than 0.05). 4. On a comparative dose basis, soluble aspirin was significantly more potent (P less than 0.05) than aspirin tablets.

Adolescent↗
PubMed2006

Aspirin resistance detected with aggregometry cannot be explained by cyclooxygenase activity: involvement of other signaling pathway(s) in cardiovascular events of aspirin-treated patients.

OBJECTIVES: Although the concept of aspirin resistance is extensively reported in medical literature, its precise mechanisms and clinical outcomes are largely unknown. In this study, we examined individual thromboxane biosynthesis and platelet aggregation in aspirin-treated patients, and whether the results of a platelet aggregation test influenced clinical outcomes. RESULTS: Subjects taking 81 mg of aspirin (n = 50) and controls (n = 38) were evaluated for platelet aggregation and platelet cyclooxygenase-1 (COX-1) activity by measuring collagen-induced thromboxane B2 production. For aggregometry, both light transmission (LT) and laser-light scattering methods were employed to quantitatively evaluate aggregate sizes and numbers. Aspirin treatment resulted in the inhibition of collagen-induced platelet aggregation, particularly the transition from small to large platelet aggregates. Although platelet COX-1 activity seemed to be uniformly inhibited in all patients, platelet aggregation studies showed great inter-individual differences; variation in platelet COX-1 activity only accounted for 6-20% of the individual aggregations. Factor analysis revealed the existence of a common factor (other than platelet COX-1) that explained 48.4% of the variations in platelet aggregation induced by collagen, adenosine diphosphate (ADP), and collagen-related peptide. We then prospectively enrolled 136 aspirin-treated patients in our study, and we found that being in the upper quartile level of LT, or with large aggregate formation induced by collagen, was an independent risk factor for developing cardiovascular events within 12 months [hazard ratio (HR) = 7.98, P = 0.008 for LT; HR = 7.76, P = 0.007 for large aggregates]. On the other hand, the existence of diabetes mellitus was an independent risk factor for overall outcomes (HR 1.30-11.9, P = 0.015-0.033). CONCLUSIONS: Aspirin resistance expressed as unsuppressed platelet COX-1 activity is a rare condition in an out-patient population. Other factor(s) affecting collagen-induced platelet aggregation may influence early outcomes in aspirin-treated patients.

Aged↗
PubMed1981

Studies on aspirin derivatives with very little side effect. II. Potent platelet anti-aggregant activity and no mutagenicity of aspirin-isopropylantipyrine (AIA).

The effect of a new aspirin derivative, aspirin-isopropylantipyrine (AIA), with very little gastric ulcerogenic activity and very slight acute toxicity and with analgesic, antipyretic anti-inflammatory, and platelet aggregation inhibitory activities was evaluated in vitro and ex vivo and compared with those of aspirin and isopropylantipyrine (IA). In vitro, AIA, aspirin and IA (50-200 microM) caused concentration-dependent inhibition of collagen-induced aggregation in rabbit platelets although AIA was several-fold more active than the others Arachidonic acid-induced aggregation was inhibited by all three agents (200 microM) in the following magnitude; IA greater than aspirin greater than AIA. Three agents did not influence primary ADP-induced aggregation. The in vitro effects on the release-inducing aggregants were confirmed by ex vivo experiments in rats. These demonstrated that AIA and aspirin (50 mg/kg) exhibited almost identical inhibitory potencies in the extent and the rate of collagen-induced aggregation 4 h after subcutaneous injection. AIA was still effective 24 h after administration as well as aspirin. IA was less effective, differing from the results in vitro. AIA had no effect on plasmin activity and blood flow through the common carotid artery. AIA (1 mM) maintained spreading and beating of myocardial cells in a serum-free culture. As special toxicity trials on AIA mutagenecity tests were made by the Rec-assay with Bacillus subtilis, by the plate culture with Escherichia coli, and by the Ames system with Salmonella typhimurium. AIA was found to have no mutagenic effect under any of those methods and to have no effect on the mutagenic action of 3, 4-benzopyrene under the liver microsome test using the Ames system.

Animals↗
PubMed2000

Efficacy of oral anticoagulants compared with aspirin after infrainguinal bypass surgery (The Dutch Bypass Oral Anticoagulants or Aspirin Study): a randomised trial.

BACKGROUND: Oral anticoagulants and aspirin are antithrombotic drugs that are commonly used in patients with vascular disease. We investigated whether either of these treatments prevented more effectively than the other bypass complications after infrainguinal bypass surgery. METHODS: We did a multicentre, randomised, open trial. 2690 patients who had undergone infrainguinal grafting were randomly assigned oral anticoagulants (target international normalised ratio 3.0-4.5, n=1339) or aspirin (80 mg daily, n=1351). We followed up patients for a mean of 21 months. The primary outcome was graft occlusion. FINDINGS: 308 graft occlusions occurred in the oral-anticoagulants group compared with 322 in the aspirin group (hazard ratio 0.95 [95% CI 0.82-1.11]), which suggested no overall advantage for either treatment. Oral anticoagulants were beneficial in patients with vein grafts (0.69 [0.54-0.88]), whereas aspirin had better results for nonvenous grafts (1.26 [1.03-1.55]). The composite outcome of vascular death, myocardial infarction, stroke, or amputation occurred 248 times in the oral-anticoagulants group and 275 times in the aspirin group (0.89 [0.75-1.06]). Patients treated with oral anticoagulants had more major bleeding episodes than those treated with aspirin (108 vs 56; 1.96 [1.42-2.71]). INTERPRETATION: Oral anticoagulation was better for the prevention of infrainguinal-vein-graft occlusion and for lowering the rate of ischaemic events. Aspirin was better for the prevention of non-venous graft occlusion, and was associated with fewer bleeding episodes.

Acenocoumarol↗
PubMed2005

Comparison between aspirin combined with dipyridamole versus aspirin alone within 48 hours after ischemic stroke event for prevention of recurrent stroke and improvement of neurological function: a preliminary study.

OBJECTIVES: To determine efficacy and tolerability of aspirin plus dipyridamole (combination) versus aspirin alone in acute intervention treatment after acute ischemic stoke among Thai patients. MATERIAL AND METHOD: This pilot study enrolled ischemic stroke patients within 48 hours and randomized to aspirin 300 mg/d or combination (aspirin 300 mg/d+ standard release dipyridamole 75 mg thrice a day) and followed up for 6 months. Endpoints were recurrent ischemic stroke, transient ischemic attack and vascular death. Side effects were recorded. National Institutes of Health Stroke Scale was assessed at entry and at 6 months period for determining neurological functions. RESULTS: Of 38 patients, mean age was 64.3 years. Male and female were 52.6% and 47.4% respectively. There were 18 patients in the aspirin group and 20 patients in the combination group. No patient developed end point events or no significant adverse event in both groups. The combination group showed more improvement in neurological function than the aspirin group (p-value 0.009). CONCLUSION: This pilot study showed equal efficacy and tolerability of the combination group and aspirin alone in acute intervention treatment for prevention of recurrent stroke or vascular death within 6 months.

Aged↗
PubMed1984

Comparative effects of aspirin and enteric-coated aspirin on loss of chromium 51-labeled erythrocytes from the gastrointestinal tract.

Sodium chromate Cr 51 was used to label red blood cells of 19 healthy male volunteers, whose stools were collected for four days before and four days during oral administration of either uncoated (N = 9) or enteric-coated (N = 10) aspirin. Each subject received 2.925 gm/day of aspirin, in three equal doses separated by eight-hour intervals, for a total of seven days. During drug use, stools were collected on days 4 through 7. Fecal blood content, estimated by measuring radioactivity in the stools, was significantly higher (P less than 0.001) during use of either type of aspirin than at baseline, but losses measured during use of the coated aspirin (mean, 1.54 ml/day) were significantly lower (P less than 0.001) than those measured during use of the uncoated aspirin (mean, 4.33 ml/day). The two types of aspirin produced equivalent serum concentrations of salicylates. We conclude that enteric-coated aspirin reduces gastrointestinal blood loss.

Adolescent↗
PubMedDate not supplied

Asthma with aspirin intolerance. Clinical entity or coincidence of nonspecific bronchial hyperreactivity and aspirin intolerance.

The study was performed in 52 aspirin - sensitive asthmatics. It was possible to establish aspirin intolerance from the history in 46 persons and after aspirin challenge in 6 persons. All patients underwent allergological and laryngological examination and 41 aspirin oral challenge. A history of intolerance in the family was reported by 3 persons. In 6 persons, i.e. 11.5%, aspirin intolerance perceded the development of asthma. 36 persons, i.e. 70% exhibited at least 2 features of atopy, namely positive history and positive skin tests. Nasal and paranasal polyps were found in 77% of the group examined. The sequence of asthma, polyps and aspirin sensitivity has been analyzed. The authors conclude that aspirin - induced bronchoconstriction is the effect of the coincidence of two different phenomena in one subject, i. e. bronchial hyperreactivity and ASA - intolerance.

Adult↗
PubMed1980

The aspirin myocardial infarction study: final results. The Aspirin Myocardial Infarction Study research group.

The Aspirin Myocardial Infarction Study (AMIS) was a multicenter, randomized, double-blind, placebo-controlled trial of 1.0 g of aspirin daily in men and women who had had a documented myocardial infarction. In the trial 4524 persons, ages 30-69 years, were recruited; 2267 were randomized to aspirin and 2257 to placebo. The major end point, total mortality, was 10.8% in the aspirin group and 9.7% in the placebo group. There was a nonsignificant trend indicating a lower incidence of nonfatal myocardial infarction in the aspirin group (6.3%) compared with the placebo group (8.1%). Symptoms suggestive of gastrointestinal irritation appeared in 23.7% of the aspirin group and in 14.9% of the placebo group. Based on these findings, routine use of aspirin after myocardial infarction is not recommended.

Aspirin↗
PubMedDate not supplied

Effect of aspirin on beta-receptors in lymphocytes from patients with aspirin-induced asthma.

We studied the effect of aspirin on beta-adrenergic receptors in lymphocytes from three groups of subjects: 5 asthmatic patients presenting sensitivity to aspirin, 10 asthmatic patients with tolerance to aspirin and a control group. Lymphocytes were incubated with aspirin-lysine (36 micrograms/ml). The number of beta-receptors/cell and the dissociation constants (Kd) were assessed by means of [125I]-cyanopindolol (ICYP). There was a decrease in the number of beta-receptors after incubation with aspirin in all asthmatic patients with sensitivity. The differences between mean basal (660 +/- 171 receptors/cell) and postincubation (398 +/- 110 receptors/cell) values were significant (p < 0.05). There were also significant differences (p < 0.01) between basal (23.4 +/- 6 pM) and postincubation (15 +/- 5.1 pM) Kd values, which indicates that the affinity of ICYP increased. In the subjects in the other two groups, aspirin both increased and decreased the number of beta-receptors, but the effects were not significant. It is suggested that in patients with sensitivity, aspirin could induce changes in the plasmatic membrane, thus altering beta-receptors or inducing the release of inflammatory mediators that exert their effect upon these receptors.

Adult↗
PubMed2003

Rationale for a trial of low-dose aspirin for the primary prevention of major adverse cardiovascular events and vascular dementia in the elderly: Aspirin in Reducing Events in the Elderly (ASPREE).

Low-dose aspirin (acetylsalicylic acid) therapy has been shown to reduce the risk of vascular events and there is increasing evidence of its potential to reduce the rate of cognitive decline in the elderly. Adverse effects including gastrointestinal and intracranial haemorrhage may offset these benefits. The balance of risks versus benefits of aspirin for the primary prevention of cardiovascular disease and vascular dementia has not been established in the elderly. There is clearly a need to conduct a study in family practice to investigate whether routine use of low-dose aspirin for the primary prevention of cardiovascular disease and vascular dementia in the elderly is beneficial or harmful. Aspirin in reducing events in the elderly (ASPREE) is a placebo-controlled trial of low-dose aspirin for the primary prevention of major adverse cardiovascular events and vascular dementia. It will follow 15,000 subjects aged 70 years or more for an average of 5 years. This sample size has a power of 87% to detect a 15% reduction in primary events in the aspirin group, with an anticipated combined primary event rate of 20 per 1000 patient years.

Aged↗
PubMed2003

Aspirin-angiotensin-converting enzyme inhibitor coadministration and mortality in patients with heart failure: a dose-related adverse effect of aspirin.

BACKGROUND: It is debated whether in patients with chronic heart failure (CHF), aspirin may contrast the clinical benefits of angiotensin-converting enzyme inhibitors (ACEIs). Two major unresolved issues in patients with CHF are whether these agents together can affect mortality and whether the interaction is related with the dose of aspirin. We aimed at exploring these possibilities. METHODS: We evaluated more than 4000 hospitalizations with a principal discharge diagnosis of CHF from January 10, 1990, to December 31, 1999. The final analysis was restricted to 344 patients taking ACEIs who satisfied the selection criteria, in whom reliable information was available concerning drug therapy during follow-up. In these patients, treatment included no aspirin in 235 (group 1), a low dose (< or =160 mg) in 45 (group 2), and a high dose (> or = 325 mg) in 64 (group 3). RESULTS: During a mean follow-up of 37.6 months, there were 84 (36%) deaths in group 1, 15 (33%) in group 2, and 35 (55%) in group 3. By the Kaplan-Meier approach, survival was similar in groups 1 and 2, and significantly (P =.009) worse in group 3 compared with groups 1 and 2. After adjusting for potential confounding factors (including treatment, cause of heart disease, age, smoking, and diabetes mellitus), a time-dependent multivariate Cox proportional hazards regression analysis showed that the combination of high-dose aspirin with an ACEI was independently associated with the risk of death (hazard ratio, 1.03; P =.01) and that the combination of low-dose aspirin with an ACEI was not (hazard ratio, 1.02; P =.18). CONCLUSION: These results support the possibility that in some patients with CHF who are taking an ACEI, a dose-related effect of aspirin may adversely affect survival.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Randomized clinical trial of the antiplatelet effects of aspirin-clopidogrel combination versus aspirin alone after lower limb angioplasty.

BACKGROUND: There is a high risk of reocclusion after successful lower limb angioplasty. Platelets play a central role in this process. The aim of this study was to investigate the antiplatelet effect of a combination of aspirin and clopidogrel compared with aspirin alone in patients with claudication undergoing endovascular revascularization. METHODS: This was a double-blind randomized placebo-controlled trial. Some 132 patients were randomized to clopidogrel and aspirin or placebo and aspirin, with a loading dose 12 h before endovascular intervention. Flow cytometric measurements of platelet fibrinogen binding and P-selectin expression were taken as measures of platelet function at baseline, 12 h after the loading dose, and 1 h, 24 h and 30 days after intervention. RESULTS: Within 12 h of the loading dose, platelet activation in the clopidogrel group had decreased (P-selectin by 27.3 per cent, P = 0.017; fibrinogen binding by 34.7 per cent, P = 0.024; stimulated fibrinogen binding by 49.2 per cent, P < 0.001). No change was observed in the placebo group. Platelet function in the clopidogrel group was significantly suppressed compared with baseline at 1 h, 24 h and 30 days after endovascular intervention (stimulated fibrinogen binding by 53.9, 51.7 and 57.2 per cent respectively; all P < 0.001). CONCLUSION: A combination of clopidogrel and aspirin inhibited platelet function more than aspirin alone in patients with claudication before and after angioplasty.

Adolescent↗
PubMed1980

Aspirin--a national survey I: Semiautomated determination of aspirin in bulk and tablet formulations and salicyclic acid in tablet formulations.

A semiautomated assay to determine aspirin (acetylsalicylic acid) in aspirin tablets, powdered tablet composites, and pure drug substances is presented. The sample was dissolved in alcoholic buffer, diluted, and extracted with chloroform. The absorbance of the chloroform solution was read at 280 nm. Results obtained by the USP XIX and semiautomated methods are compared. The proposed method is accurate and precise, and common excipients do not interfere. Recoveries of 100% were obtained. A semiautomated assay for salicylic acid in aspirin tablets also is presented. The sample was dissolved in alcoholic buffer, ferric nitrate was added, and the absorbance of the resulting purple color was read at 532 nm. The method is suitable as a rapid screening procedure for testing the salicylic acid content of aspirin products. Results obtained by the USP XIX and semiautomated methods are compared, and the accuracy and precision of the proposed method are given. One hundred seventy tablet samples and 34 bulk drug substances were analyzed for aspirin and salicylic acid content. Approximately 5% of the tablet samples failed to meet the USP XIX limits for aspirin content, and 10% failed to meet the limits for salicylic acid.

Aspirin↗
PubMed1994

Safety and anticoagulation effect of a low-dose combination of warfarin and aspirin in clinically stable coronary artery disease. Coumadin Aspirin Reinfarction (CARS) Pilot Study Group.

The hypothesis that the combination of low-dose aspirin and warfarin therapy is more effective than aspirin alone in secondary prophylaxis after myocardial infarction is to be examined in the Coumadin Aspirin Reinfarction Study. This pilot study addressed the safety and anticoagulation effect of a fixed, low-dose combination in 114 patients (aged 64 +/- 8 years, 85% men) with stable coronary artery disease receiving 3 mg of warfarin plus 80 mg of aspirin daily for 8 weeks. The international normalized ratio (INR) was measured within 72 hours of initial therapy, and weekly. Of the 110 patients with evaluable INRs, 87 patients (79%) maintained the 3 + 80 mg combination, 19 (17%) had the dose reduced to 1 mg warfarin + 80 mg aspirin, and 4 (4%) discontinued therapy because of a confirmed INR of > or = 4.5. At steady state, patients had INRs of 1.48 +/- 0.41 (3 + 80 mg group) and 1.21 +/- 0.23 (1 + 80 mg group), and inter- and intra-patient variability (estimated by the mean of the between- and within-patient SDs at steady state) was 0.49 +/- 0.08 and 0.13 +/- 0.14, respectively. There was no apparent effect of age on INR distribution. Microscopic hematuria was the most frequent (20%) adverse clinical event, but was unrelated to the INR. Three patients required discontinuation of therapy because of bleeding events (persistent hematuria and epistaxis). A fixed low-dose combination of warfarin and aspirin results in a predictable and stable increase in the INR in a large proportion of patients with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Two-year follow-up of aspirin responder and aspirin non responder. A pilot-study including 180 post-stroke patients.

Aspirin is proposed to be effective in stroke-prophylaxis because it completely inhibits the platelet prostanoid-pathway. In about 90% of stroke victims, increased platelet reactivity (PR) can be reduced to the normal range by aspirin. Twelve hours later, about one third of them show an enhanced PR again. These patients are called secondary aspirin non responders (SANR). In this study the potential pathogenetic and prognostic impact of this biological feature on stroke recurrence was evaluated. Before discharge from the hospital, PR was determined 12 hours after an oral administration of 500 mg aspirin in 180 patients aged 58 +/- 15 years; 74 were female and 106 male. All had suffered a stroke in the internal carotid artery territory. Patients were treated with 3 x 500 mg aspirin/d and were followed up over a 24-month period. Major endpoints of this study were stroke, myocardial infarction or vascular death. On discharge from the hospital, 120 of the 180 patients showed a normal PR under aspirin treatment. High test values were found in 60 patients (SANR). Six patients were lost for follow-up. Because of side effects 36 (20%) of the 180 patients enrolled discontinued medication. Major endpoints occurred in 4 of these 36 patients (11%) and in 25 of the 138 remaining patients (18.1%); 19 patients died in consequence of a vascular event during the observation period. Major endpoints were seen in only 5 of 114 (4.4%) of the aspirin responders, but in 24 out of 60 SANR (40%, p < 0.0001). It may be assumed that early identification of SANR's is a clinically useful tool to classify patients at high risk for recurrence of vascular events.

Adult↗
PubMed1993

In vitro and ex vivo effects of aspirin in patients on a low-dose aspirin therapy.

In 19 patients on a low-dose aspirin therapy with 100 mg/d, an insufficient effect of aspirin was observed in five patients (aggregations induced by arachidonic acid and collagen, thromboxane B2-formation in serum and after collagen). Aspirin added in vitro increased the inhibition to a degree comparable to that seen in the other 14 patients, i.e. the insufficient effect could be due to a lack of compliance or to a reduced availability of the drug. In another 20 patients there was a good inhibitory effect of aspirin; additional aspirin did not increase the inhibition of arachidonic acid-induced aggregation and serum-thromboxane B2, but slightly increased collagen-induced aggregation and thromboxane B2 formation. The effect was the same, whether the aspirin was given in vivo or added in vitro.

Adult↗
PubMed1976

Refractory period to aspirin in a patient with aspirin-induced asthma.

Oral aspirin challenge was used to detect unrecognized aspirin intolerance in a select group of 50 asthmatic patients who denied aspirin intolerance. A double-blind protocol was used to further study those patients who reacted to initial graded aspirin challenge. In one patient the use of a double-blind protocol led to the serendipitous discovery of a 72-hr refractory period to the adverse effects of aspirin, after initial ingestion of aspirin resulted in respiratory and systemic symptoms.

Adult↗
PubMed1993

Reaction of aspirin with cysteinyl residues of lens gamma-crystallins: a mechanism for the proposed anti-cataract effect of aspirin.

Incubation of lens crystallins with aspirin inhibits the development of opacities caused by cyanate. Cyanate-induced opacities are thought to be due to carbamylation of the lysyl residues which causes a decrease in the protein charge and subsequent conformational changes that permit disulfide bonding. Because aspirin can also react with lysyl residues, it has been proposed that the aspirin inhibition of cataractogenesis is due to acetylation of the lysyl residues which would block their reaction with cyanate. However, acetylation of lysyl residues also lowers the protein charge and would be expected to effect changes in protein conformation similar to those caused by carbamylation. Therefore, acetylation of the lysyl residues is not a satisfactory explanation for the inhibitory effect of aspirin on lens opacification. Our investigations of the reactions of cyanate and aspirin with bovine gamma II-crystallins show that the cysteinyl residues are also carbamylated and acetylated at pH 7.4. At this pH, the carbamylation at the cysteinyl residues is reversible, leading to regeneration of the thiol group and disulfide bonding. In contrast, the acetylation at cysteinyl residues is stable at pH 7.4 and can prevent disulfide bonding. This difference in stability explains how cyanate promotes, and aspirin inhibits, cataractogenesis.

Acetylation↗