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At least 307 records · Page 17Linked to original sources
PubMed1983

Platelet thromboxane synthetase inhibitors with low doses of aspirin: possible resolution of the "aspirin dilemma".

Selective pharmacological inhibition of thromboxane A2 synthesis did not prevent arachidonate-induced aggregation of human platelets in vitro. Prevention was instead achieved by a combination of thromboxane A2 inhibitors with low concentrations of aspirin. The latter partially reduced the proaggregatory cyclooxygenase products that accumulated when thromboxane A2 synthesis was blocked. The aspirin concentrations did not affect per se either platelet aggregation or prostacyclin synthesis in cultured human endothelial cells. The combination of thromboxane synthetase inhibitors with low doses of aspirin may offer greater antithrombotic potential than either drug alone.

Aspirin↗
PubMed1993

The effect of aspirin on mononuclear cells in aspirin-sensitive asthmatics and control subjects.

Three groups, comprising normal subjects (n = 10), aspirin-sensitive asthmatics (ASA+; n = 10) and aspirin-insensitive asthmatics (ASA-; n = 10) were entered into a blinded, parallel group study to asses the modulating effect of aspirin (ASA; 0.0275, 0.275, 1.385, 2.75, 6.9, 13.8 and 27.5 microM) on lymphocyte proliferation in vitro, either alone or in combination with the mitogen, phytohemagglutinin (PHA; 10, 25, 50, 100, 200 and 500 micrograms/ml). The percentage and absolute numbers of CD4-positive T cells (normals: 51.3%; ASA+: 51.1%; ASA-: 46.1%; p = 0.4038) and CD8-positive T cells (normal: 27.5%; ASA+: 26.4%; ASA-: 28.4%; p = 0.8408) did not differ significantly between the groups. Significant differences in mean PHA responses between ASA+, ASA- and normal subjects were observed when peripheral blood lymphocytes (PBL) were exposed to PHA concentrations over the range 10-50 micrograms/ml; PHA 10 micrograms/ml (p < 0.005), PHA 25 micrograms/ml (p < 0.005) and PHA 50 micrograms/ml (p < 0.01), the lowest and highest proliferative responses being obtained with PBL from ASA+ and ASA-, respectively. However, at higher PHA concentrations (100-500 micrograms/ml), differences between the three groups were not observed. When ASA was added in combination with PHA, augmentation of the PHA response was observed with cells from all three groups but was most marked in the ASA+ group, especially at lower PHA concentrations (10-50 micrograms/ml) in combination with 0.275-13.8 microM ASA.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1996

Incomplete aspirin desensitization in an aspirin-sensitive asthmatic.

Aspirin desensitization is a valuable treatment for aspirin-sensitive sinusitis. We present a case where long-term desensitization failed. While undergoing desensitization, our patient had prolonged severe asthmatic reactions and therefore received high intravenous doses of prednisone. We hypothesize that high steroid doses administered at the time of desensitization may have raised the threshold of intolerance to a point where the administered aspirin doses were tolerated. Consequently, symptoms of intolerance subsided during the procedure. Subsequent tapering down of the daily prednisone dose caused a re-emergence of the symptoms of intolerance, apparently due to a decrease in the intolerance threshold.

Aspirin↗
PubMed2003

Safety of an aspirin-alone regimen after intracoronary stenting with a heparin-coated stent: final results of the HOPE (HEPACOAT and an Antithrombotic Regimen of Aspirin Alone) study.

BACKGROUND: Stent thrombosis is an infrequent complication of intracoronary stenting that often has devastating clinical consequences. This study assesses the additional benefit of heparin coating with the BX VELOCITY Balloon-Expandable Stent with HEPACOAT, Carmeda end-point attached heparin (HEPACOAT) in patients with de novo or restenotic native coronary artery lesions treated with aspirin monotherapy after optimal stenting. METHODS AND RESULTS: This was a multicenter, prospective, nonrandomized, pilot study. Two hundred patients (69% men; mean age, 64.1+/-11.2 years) meeting the eligibility criteria were treated with the HEPACOAT stent and aspirin alone after stenting. Any other antiplatelet or anticoagulation therapy was not permitted. Procedural success was achieved in all patients. There were 3 postprocedural non-Q-wave myocardial infarctions. The primary end point of stent thrombosis at 30 days occurred in 2 of 200 patients (1%): in one after blunt chest trauma and in the other in the setting of essential thrombocytosis. Major adverse cardiac events (death, myocardial infarction, target lesion revascularization, and coronary artery bypass grafting) were observed at 30 days in 5 of 200 (2.5%) patients. CONCLUSIONS: The BX VELOCITY stent with HEPACOAT and aspirin alone after the procedure was safe in select patients with de novo or restenotic lesions in native coronary arteries. Heparin coating provides additional protection against stent thrombosis.

Angioplasty, Balloon, Coronary↗
PubMed1980

Persantine and aspirin in coronary heart disease. The Persantine-Aspirin Reinfarction Study Research Group.

In the Persantine-Aspirin Reinfarction Study (PARIS) trial, 2026 persons who had recovered from myocardial infarction (MI) were randomized into three groups: Persantine plus aspirin (PR/A) (n = 810); aspirin alone (ASA) (n = 810); placebo (PLBO) (n = 406). The average length of follow-up study was 41 months. Results for the three specified primary end points were: total mortality 16% lower in PR/A and 18% lower in ASA compared with PLBO; coronary mortality 24% and 21% lower; incidence of nonfatal MI plus fatal coronary disease 25% and 24% lower. These differences were not satistically significant by the study criterion (Z greater than or equal to 2.6). By life-table analysis, the rates of coronary mortality and coronary incidence were about 50% lower in the PR/A group than in the PLBO group from 8-24 months, and for coronary incidence all Z values were greater than or equal to 2.6; ASA rates were about 30% lower than PLBO rates, and for coronary incidence, Z values were greater than or equal to 2.6 at two points. For these end points, from 8-20 months, PR/A rates were about 30% lower than ASA rates, but all Z values were less than 2.0 PR/A and ASA patients entering within 6 months of last MI showed the largest percentage reductions in mortality; only the difference between PR/A and PLBO groups for 3-year coronary mortality yielded a Z value of 2.6.

Actuarial Analysis↗
PubMed2005

Effects of clopidogrel and aspirin in combination versus aspirin alone on platelet activation and major receptor expression in patients after recent ischemic stroke: for the Plavix Use for Treatment of Stroke (PLUTO-Stroke) trial.

BACKGROUND AND PURPOSE: Clopidogrel is widely used in patients after recent ischemic stroke; however, its ability to yield additional antiplatelet protection on top of aspirin has never been explored in a controlled study. To determine whether clopidogrel with aspirin (C+ASA) will produce more potent platelet inhibition than aspirin alone (ASA) in patients after ischemic stroke, we conducted the Plavix Use for Treatment of Stroke trial. METHODS: Seventy patients after ischemic stroke were randomly assigned to C+ASA or ASA groups. Platelet studies included aggregometry; cartridge-based analyzers; expression of PECAM-1, P-selectin, GP IIb/IIIa (antigen and activity), vitronectin receptor, and formation of platelet-leukocyte microparticles by flow cytometry. Platelet tests were performed at baseline and after 30 days after randomization. RESULTS: There were no deaths, hospitalizations, or serious adverse events. There were no differences in the baseline platelet characteristics between C+ASA and ASA groups, or significant changes in platelet parameters in the ASA group, except diminished collagen-induced aggregation (P=0.001). In contrast, therapy with C+ASA resulted in a significant inhibition of platelet activity assessed by ADP- (P=0.00001) and collagen-induced (P=0.02) aggregation; closure time prolongation (P=0.03), and reduction of platelet activation units with Ultegra (P=0.00001); expression of PECAM-1 (P=0.01), and GP IIb/IIIa activity with PAC-1 (P=0.02) when compared with ASA group. Therapy with C+ASA also resulted in the reduced formation of platelet-leukocyte microparticles (P=0.02). CONCLUSIONS: Treatment with C+ASA for 1 month provides significantly greater inhibition of platelet activity than ASA alone in patients after recent ischemic stroke in the frame of the small randomized trial.

Aged↗
PubMed1996

Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma.

Bronchial overproduction of leukotrienes and inhibition of prostaglandin synthesis are involved in the pathogenesis of aspirin-induced asthma. We investigated whether inhaled prostaglandin E2 (PGE2) attenuates the response to bronchial challenge with lysine acetylsalicylate (LASA) and the associated increase in urinary leukotriene E4 (u-LTE4) in seven aspirin-sensitive subjects with asthma. Each subject performed two challenges with a single dose of LASA that caused a decrease in FEV1 of 20% or more in a preliminary test, immediately after inhaling 100 micrograms PGE2 in 4 ml saline or placebo, according to a randomized double-blind protocol. FEV1 was recorded at 30-min intervals for 4 h. u-LTE4 was measured by combined high-performance liquid chromatography enzyme immunoassay at 2-h intervals. After placebo, LASA caused an obstructive reaction in all patients, with a maximum decrease in FEV1 of 35 +/- 5% with respect to baseline. u-LTE4 rose from 911 +/- 261 picograms (pg)/mg creatinine at baseline to a maximum value of 2249 +/- 748 after challenge. Inhaled PGE2 provided almost complete protection in all patients. Baseline u-LTE4 was 883 +/- 243 pg/mg creatinine and did not change significantly during the test, reaching a maximum value of 864 +/- 290 (p < 0.05 versus placebo). These results confirm that PGE2 is highly effective in preventing aspirin-induced asthma and suggest that this effect is mediated by inhibition of sulfidopeptide leukotriene production.

Administration, Inhalation↗
PubMed1994

Time-limited protective effect of inhaled frusemide against aspirin-induced bronchoconstriction in aspirin-sensitive asthmatics.

Inhaled frusemide effectively prevents the bronchial obstructive response to allergens and to a number of nonallergic stimuli. In most of the experimental models in which it has been tested, the protective effect of frusemide has been evaluated for only a short time after administration. In aspirin-sensitive patients, acetylsalicylic acid causes an asthmatic reaction which typically lasts for 2 h or more after exposure. We investigated the presence and duration of the protective effect of inhaled frusemide against the bronchial response to aspirin in sensitive patients, using a specific inhalation challenge with lysine acetylsalicylate (LASA). In the first study, eight subjects with aspirin-asthma underwent two bronchial challenges with a single dose of lysine acetylsalicylate administered through a jet nebulizer, after treatment with 40 mg inhaled frusemide or placebo, according to a randomized, double-blind protocol. Forced expiratory volume in one second (FEV1) was monitored for 120 min after challenge. In the second study in eight patients, the protocol was modified by the use of a dosimeter for delivery of lysine acetylsalicylate, by reducing the dose of lysine acetylsalicylate to avoid intense reactions, and by extending the follow-up to 4 h. In the first study, after placebo, FEV1 gradually decreased, reaching a maximum decrement of 39 +/- 3% at 120min. Inhaled frusemide exerted a significant protection at all time-points, although this activity appeared to decrease with time. In the second study, after placebo, inhaled lysine acetylsalicylate caused a gradual decrease in FEV1, which reached a maximum decrement at 180 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1981

Clinical response and serum prostaglandin levels in aspirin idiosyncrasy. Effect of aspirin and a new nonsteroidal anti-inflammatory agent.

Clinical measurements and serum prostaglandin concentrations were monitored in three normal subjects, three asthmatic controls and five asthmatic patients with aspirin (ASA) idiosyncrasy before and after oral challenge with small doses of aspirin. Additionally, in the latter group, the effects of ASA were compared with those of piroxicam, a new nonsteroidal anti-inflammatory agent. Challenge with either agent caused bronchospasm in patients with aspirin idiosyncrasy, but was more severe after piroxicam. Nasal stuffiness and/or rhinorrhea preceded or accompanied the changes in pulmonary function with both agents. Serum prostaglandin concentrations, which reflect synthesis by platelets during the clotting of blood, revealed significant decreases in PGE1, PGE2, and PGF2 alpha and thromboxane B2 within two to four hours after drug administration in all subjects with or without ASA idiosyncrasy. The change in serum PG concentration was presented when bronchospasm developed in patients with ASA idiosyncrasy, but persisted for a longer time, reflecting the irreversible effect of these agents on the cyclo-oxygenase enzyme in platelets. The results demonstrate that administration of minute doses of ASA and other nonsteroidal anti-inflammatory drugs alters prostaglandin synthesis in normal and asthmatic subjects with or without ASA idiosyncrasy. Alteration in arachidonate metabolism may be responsible for the induction of bronchospasm, and cautious use of cyclo-oxygenase inhibitors in patients with known or suspected ASA idiosyncrasy is indicated.

Adult↗
PubMedDate not supplied

Bronchial challenge with aspirin lysine in the diagnosis of asthmatics with sensitization to aspirin and its inhibition by aerosolized furosemide.

We performed bronchial challenge with ASA lysine in 9 patients with a history of aspirin-induced asthma, 4 asthmatics with no history of hypersensitization to aspirin and 4 control subjects. The test consisted of successive inhalations of increasing concentrations of ASA lysine (11.25, 22.5, 45, 90, 180 and 360 mg/ml) and was interrupted when FEV1 showed a decrease of at least 20%. In order to determine the degree of bronchial hyperreactivity, we first carried out a bronchial challenge with histamine. All patients in the group sensitive to aspirin had a positive reaction to ASA lysine, while this was negative for patients in the two control groups. There was no significant correlation between PC20 to histamine and ASA lysine in any of the groups. On the other hand, 6 patients with sensitivity to ASA repeated the bronchial challenge with ASA lysine after previously inhaling furosemide, and in this second test, none of the 6 had a positive reaction. The variation of ASA lysine PC20 in both tests was positive for these patients (p < 0.001).

Adolescent↗
PubMed1989

[The late results of aspirin treatment in patients with aspirin-induced bronchial asthma].

The paper treats long-term results of aspirin treatment of patients with aspirin-induced bronchial asthma. The data obtained indicate that in this patients' group, the beneficial effect of aspirin treatment is also preserved after its withdrawal at any rate within up to one year. The authors have every reason to believe that such a treatment is unlikely to be applied for life.

Adult↗
PubMed1980

[Persantin and aspirin in coronary heart disease. The persantin-aspirin reinfarction study group (PARIS)].

In the Persantine-Aspirin Reinfarction Study (PARIS) trial 2026 persons who had recovered from myocardial infarction (MI) were randomized into three groups: Persantine plus Aspirin (PR/A) (n = 810); aspirin alone (ASA) (n = 810); placebo (PLBO) (n = 406). The average length of follow-up study was 41 months. Results for the three specified primary end points were: total mortality 16% lower in PR/A and 18% lower in ASA compared with PLBO; coronary mortality 24% and 21% lower; incidence of nonfatal MI plus fatal coronary disease 25% and 24% lower. These differences were not statistically significant by the study criterion (Z greater than or equal to 2.6). By life-table analysis, the rates of coronary mortality and coronary incidence were about 50% lower in the PR/A group than in the PLBO group from 8--24 months, and for coronary incidence all Z values were greater than or equal to 2.6; ASA rates were about 30% lower than PLBO rates, and for coronary incidence, Z values were greater than or equal to 2.6 at two points. For these end points, from 8--20 months, PR/A rates were about 30% lower than ASA rates, but all Z values were < 2.0. PR/A and ASA patients entering within 6 months of last MI showed the largest percentage reductions in mortality; only the difference between PR/A and PLBO groups for 3-year coronary mortality yielded a Z value of 2.6.

Adult↗
PubMed1980

The Persantine-aspirin reinfarction study. The Persantine-aspirin Reinfarction Study (PARIS) research group.

The efficacy and safety of a combination of Persantine and aspirin, of aspirin alone and of a placebo as a regimen for preventing reinfarction were compared in 2026 patients who had recovered from a documented acute myocardial infarction (MI) that had occurred 8 weeks to 5 years previously. Baseline variables were comparable, and almost all surviving patients were treated for 3 years. There was a trend toward improved survival rates both for the combination and single drug compared with placebo. Coronary incidence was significantly lower in the combination group compared with placebo at each 4-month interval during the first 24 months of treatment, whereas significant reductions in the aspirin group occurred only at 8 and 24 months. Gastric and renal side effects were more common in the treated groups. To confirm the above results and the findings that the group of patients enrolled within 6 months of last MI had the largest reduction in mortality in the combination group, another study has been designed to compare the combination with a placebo in a large group of patients.

Aspirin↗
PubMed1982

[Controlled clinical trial of the effect of aspirin and aspirin + dipyridamole on the development of diabetic retinopathy. I. General protocol. From the DAMAD Study Group (author's transl)].

In diabetic patients platelet abnormalities and hemostatic dysfunction have been reported and may play a role on the development of retinopathy. It has been shown that aspirin and dipyridamole modify platelet functions in vitro and in vivo. The aim of this multicenter controlled clinical trial was to investigate the effect of aspirin and aspirin + dipyridamole on the evolution of background retinopathy. In this paper are described the main clinical characteristics of the 450 patients included in the study, the protocol and the major end-points. Patient recruitment started in 1977 and was completed in 1981. Compliance to the protocol is satisfactory, side effects have been minimal and the number of patients lost to follow up is small.

Adolescent↗
PubMed1982

Improved liquid-chromatography of aspirin, salicylate, and salicyluric acid in plasma, with a modification for determining aspirin metabolites in urine.

Detailed performance specifications are given for a specific and sensitive liquid-chromatographic assay for aspirin, salicylic acid, and salicyluric acid in plasma. The sensitivity of this method for aspirin (50 micrograms/L) is 10-fold that of previous methods, so that concentrations of aspirin in plasma can now be followed for about four or five half-lives after the peak plasma concentration arising from a single 650-mg dose. In addition, this assay is as sensitive for salicylic and salicyluric acid in plasma as any hitherto. A modification permits measurement of gentisic acid, salicylic acid, and salicyluric acid in urine; further modifications allow indirect measurement of conjugated gentisate and salicylate in urine.

Aspirin↗
PubMed1995

[The influence of misoprostol on post-aspirin bronchoconstriction in patients with aspirin sensitive asthma].

It is believed that aspirin (ASA) and other nonsteroidal antiinflammatory drugs elicit dysponea in ASA sensitive asthmatics by blocking the cyclooxygenase. It is unclear whether this bronchospasm is due to shunting of arachidonic acid into the lipooxygenase pathway or removal of cyclooxygenase product which prevent bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE play also modulatory function to mast call decreasing the release of mediators of anaphylaxis. There are some evidences concerning the mast cell degranulation in postaspirin reaction in ASA sensitive asthmatics. The authors investigated the influence of synthetic analogue of PGE1--misoprostol (Cototec, Searle) on the postaspirin bronchoconstriction in seven ASA sensitive asthmatics aged 33-62. Aspirin threshold doses ranged from 10 to 150 mg. Postaspirin bronchoconstriction begun usually within 1-2 hrs after digestion of ASA and 200 micrograms were additionally given 2 h later. Seven days later misoprostol (400 micrograms) was administered together with previously determined dose of ASA. One the other day the bronchodilating effect of misoprostol alone was examined. In all but one patients we observed the protective influence of misoprostol on ASA induced bronchoconstriction. Max. fall in FEV1 in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol, respectively 10, 9, 4, (+8), 10, (+2) and 45. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction reaching statistical significance at 3 and 3.5 h, and also diminished extrapulmonary symptoms. The authors discuss the possible mechanism of protective influence of misoprostol.

Adult↗