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At least 289 records · Page 16Linked to original sources
PubMed2003

Warfarin plus aspirin more effective than aspirin alone for secondary prevention of MI.

Compared with aspirin alone, aspirin plus warfarin (goal for international normalized ratio, 2-2.5) or warfarin alone (goal for international normalized ratio, 2.8-4.3) results in fewer re-infarctions and thromboembolic events. Treating 1000 patients for 1 year would result in approximately 10 fewer reinfarctions and 3 fewer strokes at a cost of 4 more major bleeding episodes. In addition, many patients will not be able to tolerate warfarin therapy. For highly motivated patients at low risk of bleeding, warfarin or warfarin plus aspirin is more effective than aspirin for secondary prevention of myocardial infarction.

Comment↗
PubMed2006

Expression of cyclooxygenase and lipoxygenase enzymes in nasal polyps of aspirin-sensitive and aspirin-tolerant patients.

OBJECTIVE: To evaluate the expression of cyclooxygenase (COX) and lipoxygenase (LO) enzymes in nasal polyp specimens from aspirin-sensitive (AS) and aspirin-tolerant (AT) patients. DESIGN: Immunohistochemical staining of archived tissue. Subjects Specimens from 26 patients (11 AS and 15 AT) with nasal polyps were analyzed; specimens from 4 patients were used as controls. INTERVENTIONS: Immunohistochemical techniques were used to evaluate the expression of the enzymes COX-1, COX-2, 5-LO, 12-LO, and 15-LO in nasal polyp tissue specimens from AS and AT patients. The results were compared with those of a control group of patients without a history of nasal polyposis or rhinosinusitis. RESULTS: Characteristic staining patterns of epithelium and submucosal glands were noted for each enzyme. Statistically significant (P<.05) differences in staining of columnar epithelium were noted for COX-1 (basal cell layer cytoplasm), COX-2 (apical cell layer cytoplasm), and 12-LO (full-thickness cytoplasm and nucleus). Increased 15-LO (full-thickness cytoplasm) expression in columnar epithelium was noted only in the AT group. Significant differences in the staining of submucosal glands were noted for COX-2 (plasma membrane and cytoplasm), 12-LO (cytoplasm), and 15-LO (cytoplasm) between control and AS patients as well as between control and AT patients (P<.05). The only significant difference noted between the AS and AT groups was cytoplasm staining for 5-LO in submucosal glands, which was greater in the AS group. No epithelial staining differences were noted between AT and AS patients. CONCLUSIONS: There were significant differences in the expression of COX and LO enzymes between patients with nasal polyps and controls, irrespective of aspirin sensitivity. With 1 exception, there were no significant differences between AS and AT groups.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1981

Kinetics of aspirin, salicylic acid, and salicyluric acid following oral administration of aspirin as a tablet and two buffered solutions.

Twelve fasting normal volunteers received three aspirin dosage forms in a single-dose, complete crossover study; the plasma and urine levels of aspirin, salicylic acid, and salicyluric acid were measured for 10 hr. The three dosage forms were an unbuffered tablet, an effervescent solution with 16 mEq of buffer, and an effervescent solution with 34 mEq of buffer. Significant differences in the absorption rate were observed, with the solution having 16 mEQ of buffer being fastest, the solution having 34 mEq of buffer being intermediate, and the tablet being slowest. These differences are attributed to gastric emptying rates and tablet dissolution. Urine pH and renal clearance for all three acid compounds are influenced by the buffer during the first 2 hr following dosing but not later. Area under the curve comparisons suggest that approximately 20% more aspirin reaches the general circulation intact following the tablet but that the total amount of salicylate absorbed is not different. Further studies are required to select the optimal buffer content to provide rapid absorption with minimal sodium dose and urine alkalinization.

Absorption↗
PubMed1982

Aspirin--a national survey V: Determination of aspirin and impurities in enteric coated tablets and suppository formulations and in vitro dissolution of enteric coated tablets.

The results of a national survey on the quality of enteric coated aspirin tablets and aspirin suppositories are presented. The tablets were analyzed for strength, salicylic acid content, in vitro dissolution rate, and related aspirin impurities. The suppositories were analyzed for strength and salicylic acid content. The methods of analysis and validation of data are also presented.

Aspirin↗
PubMed1987

Determination of aspirin by pre-column transacetylation reaction of 3-aminophenol and reversed-phase high-performance liquid chromatography: simultaneous determination of aspirin, acetaminophen, and caffeine.

The accuracy of the measurement of aspirin by high-performance liquid chromatography (HPLC) is reduced by its hydrolysis into salicylic and acetic acids during sample preparation. The ready and quantitative transacetylation of 3-aminophenol by aspirin, giving 3-hydroxyacetanilide (which is stable), has been utilized as a pre-column reaction for the determination of aspirin either alone or in the presence of acetaminophen and caffeine by reversed-phase HPLC.

Acetaminophen↗
PubMed1988

Decomposition of aspirin in the solid state in the presence of limited amounts of moisture II: Kinetics and salting-in of aspirin in aqueous acetic acid solutions.

The solubility of aspirin in saturated solutions of salicylic acid (and vice versa) was studied in 0 to 16 M aqueous solutions of acetic acid. The solubilities, when expressed in molarity, go through a maximum at an acetic acid concentration of approximately 12 M. The temperature dependence of the solubilities is such that the logarithm of the solubility is linear in reciprocal absolute temperature. The calculated enthalpies are of the order of 11 kcal/mol. The kinetics of aspirin decomposition was also studied at the different acetic acid concentrations, and it was found that the second-order hydrolysis rate constant is fairly independent of acetic acid concentration. Aspirin decomposition follows an Arrhenius equation and has an activation energy of 18 kcal/mol.

Acetates↗
PubMed1978

Selective cytotoxic actions of aspirin on parietal cells: a principal factor in the early stages of aspirin-induced gastric damage.

Electronmicroscopic observations are reported on the effects of orally administered aspirin on the rat gastric mucosa to establish the cytotoxic events that occur during the early stages of the development of gastric damage induced by this drug. The results show that aspirin, apart from damaging superficial mucous cells, causes selective damage to the acid-secreting parietal cells located deep in the fundic mucosa. It is suggested that the selective accumulation of salicylates in the parietal cells may account for the specific cytotoxic actions of aspirin on these cells.

Animals↗
PubMed1979

Effect of other drugs and chemicals on the degradation of aspirin in vitro: possible extrapolation to in vivo metabolism of aspirin.

To assess the possible influence of other drugs and chemicals on the metabolic degradation of aspirin in man, their effect on the serum aspirin esterase activity was determined in vitro. The activation or inhibition of the enzyme as observed with these compounds suggest the possibility that simultaneous ingestion of these drugs with aspirin may influence the pharmacology and toxicity of the analgesic.

Anticoagulants↗
PubMed1991

The coronary artery response to implantation of a balloon-expandable flexible stent in the aspirin- and non-aspirin-treated swine model.

Intracoronary stents may potentially alleviate some of the problems associated with coronary angioplasty. Since the anatomy and physiology of swine coronary arteries closely resemble those of humans, the response to implantation of the Glanturco-Roubin, balloon-expandable, flexible stent was studied in this model. Additionally, the effect of aspirin, 1 mg/kg/day orally, on this response was evaluated. Eighteen Hanford minature swine underwent stenting of the left anterior descending coronary artery. Two died within 24 hours of stent implantation. The 16 survivors were put to death at 4 (n = 4), 11 (n = 4), 28 (n = 4), 56 (n = 3), and 180 (n = 1) days. Angiographically, reduction of stent lumen diameter of 0.1 to 1.3 mm was observed and was maximum at 11 days, with gradual improvement at subsequent time periods. Scanning electron microscopy, transmission electron microscopy, and light microscopy showed early disruption of subjacent endothelium, and adherence of platelets to exposed subendothelium and stent wires. Microthrombi were readily apparent. At 11 days, intimal thickening, made up predominantly of smooth muscle cells with abundant extracellular matrix, was observed and covered the stent wires. At 28 days, regression of intimal thickening was apparent and a confluent endothelium with flow-directed orientation was seen. At 56 and 180 days, the luminal surface was smooth; intimal thickening averaged 525 microns over the stent wires and 55 microns away from the wires. Findings in aspirin-treated animals were similar to results in those that did not receive aspirin. Thus in this swine model, stent implantation results in a time-dependent and self-limited vascular response.

Angioplasty, Balloon, Coronary↗
PubMed1977

Serum aspirin esterase activity in women with habitual aspirin intake.

A method for the determination of aspirin esterase activity in serum is described. Sera from 59 pregnant women who were habitual aspirin users were found to have a mean enzyme activity value statistically lower than those of 68 non-pregnant women controls or of 12 pregnant women controls who were either occasional users of the drug or were non-users. The distribution of enzyme activity in the experimental group was also significantly different from that of the control group. It is postulated that the low enzyme activity may further aggravate the injurious effects of high intake of aspirin.

Adult↗
PubMed1985

Aspirin prevents carbamylation of soluble lens proteins and prevents cyanate-induced phase separation opacities in vitro: a possible mechanism by which aspirin could prevent cataract.

The carbamylation of lens proteins by cyanate causes conformational changes, and cyanate causes cataract. There is some evidence that aspirin is beneficial to cataract patients, so its effect on the carbamylation of lens proteins and on opacification produced by cyanate in vitro was studied. Aspirin decreased the phase separation temperature in lenses exposed to cyanate, and was found to reduce the rate of carbamylation of most, if not all, soluble lens proteins. Studies with radiolabelled aspirin lead to the conclusion that the drug achieves this protection by chemically modifying the proteins. The nature of this modification and the relevance of these results to human cataract is discussed.

Animals↗
PubMed1983

The absence of detectable complement activation in aspirin-sensitive asthmatic patients during aspirin challenge.

Activation of complement was sought by two independent assay methods, total hemolytic complement (CH50) and C4 activation by rocket immunoelectrophoresis for C4d and C4 in plasma samples obtained from 16 aspirin-sensitive asthmatic patients and four control subjects during provocative oral aspirin challenges. No consistent evidence of significant complement activation was detected in either the asthmatic or control groups when serial measurements were performed. The measurements of CH50 and C4 activation did not change in either arterial or venous samples. These findings indicate that oral aspirin given in dosages that provoke bronchospasm did not activate C4 or significantly decrease serum complement activity.

Adult↗
PubMed1997

Progression of the culprit lesion in unstable coronary artery disease with warfarin and aspirin versus aspirin alone: preliminary study.

OBJECTIVES: This study assessed whether combination therapy with aspirin and warfarin for 10 weeks reduces the risk of progression or reocclusion of the unstable coronary artery lesion. BACKGROUND: Reocclusion of the culprit coronary artery occurs in up to one third of patients during the 3 months after myocardial infarction (MI) or unstable angina and is associated with increased morbidity and mortality. METHODS: Fifty-seven patients presenting with unstable angina or MI who had an identifiable culprit lesion at coronary angiography were randomized in double-blind manner to receive warfarin (target international normalized ratio [INR] 2.0 to 2.5) or placebo in addition to aspirin (150 mg daily). Changes in the culprit lesion were assessed by quantitative angiography in 50 patients after 10 weeks of therapy or after a clinical event. Progression of the culprit lesion was defined as a decrease in minimal lumen diameter > 0.4 mm or a new total occlusion. Regression was defined as an increase in minimal lumen diameter > 0.4 mm. RESULTS: In subjects randomized to receive warfarin, the culprit lesion was less likely to progress (1 [4%] vs. 8 [33%]) and more likely to regress (5[19%] vs. 2[9%]) than in subjects receiving placebo (p = 0.02). Recurrent MI or a new occlusion at angiography occurred in 2 (7%) of 29 patients receiving warfarin versus 11 (39%) of 28 patients receiving placebo (p = 0.005). CONCLUSIONS: In patients with an acute coronary syndrome, combined therapy with aspirin and warfarin with a target INR of 2.0 to 2.5 for 10 weeks reduces the risk of progression or reocclusion of the culprit coronary lesion.

Angina, Unstable↗
PubMed2000

Lack of effect of the 5-lipoxygenase inhibitor zileuton in blocking oral aspirin challenges in aspirin-sensitive asthmatics.

BACKGROUND: Leukotrienes (LTs) have been implicated as major mediators of aspirin-(ASA)-induced respiratory reactions. It was therefore logical to assume that an inhibitor of 5-lipoxygenase (5-LO), such as zileuton, given before and during oral challenges with ASA, might prevent ASA-induced respiratory reactions. Indeed, in prior studies, pretreatment of ASA-sensitive respiratory disease patients with leukotriene modifiers eliminated or attenuated respiratory reactions upon re-challenge with the previously established provoking dose of ASA. However, doses higher than the provoking doses were not administered during these reported studies. OBJECTIVE: We wished to determine whether zileuton pretreatment could prevent ASA-induced respiratory reactions in our six volunteers with aspirin-sensitive respiratory disease when ASA challenge doses were started below the usual provoking dose of 60 mg and then increased until a respiratory reaction occurred. METHOD: Aspirin sensitivity was established previously in all six patients during a prior ASA oral challenge. In this study, pretreatment with zileuton 600 mg qid was initiated 7 days prior to, and continued during oral ASA challenges. Patients underwent single-blind oral ASA challenges with escalating doses of ASA, every 3 hours, according to our standard protocol. RESULTS: All six patients reacted to doses of ASA between 45 and 325 mg. Four patients experienced bronchospasm (FEV1 declined 19% to 53%) while receiving zileuton. All six had naso-ocular reactions. Concentrations of urine LTE4 also increased significantly (mean 334 pg/mg Cr at baseline, increasing to 1024 pg/mg Cr at respiratory reactions). CONCLUSIONS: During ASA challenges, zileuton, in standard doses of 600 mg qid was associated with increased synthesis of LTs in five of six patients and naso-ocular reactions in all six patients, as well as bronchospasm in four patients.

Administration, Oral↗
PubMed2003

Differences in the effects of extended-release aspirin and plain-formulated aspirin on prostanoids and nitric oxide in healthy volunteers.

This study was designed to evaluate the effects of extended-release aspirin on platelet aggregation and the production of prostanoids and nitric oxide. The participants in this double blind, randomized and crossover study were 20 healthy volunteers. Interventions were 150 mg of plain-formulated aspirin (PFASA) and 150 mg of extended-release aspirin (ERASA). Blood samples were collected before and 10, 20, 60, 120, 240, 480 and 1440 min after the first dose; 3, 7 and 14 days after daily administration and 24 h after the last dose. The main measures were platelet aggregometry, thromboxane B2, 6-keto-prostaglandin (PG) F1alpha and nitric oxide in each control. Platelet aggregation was inhibited by 50% with ERASA, and by 77% with PFASA. No differences were found in chronic treatment. Thromboxane B2 was inhibited more by the latter (51-67%), but 90% inhibition was observed in both groups after 3 days. The levels of 6-keto-PGF1alpha was reduced by 20% with ERASA and by 58% with PFASA. Nitric oxide production increased in both groups, but after 24 h, and 7-14 days, elevated concentrations of nitric oxide were found only in the ERASA. The antiplatelet effects of ERASA provide pharmacological advantages (greater prostacyclin synthesis and prolonged increase in nitric oxide production) over those provided by the plain formulation.

Adult↗
PubMed2005

Detection of aspirin resistance by PFA-100: prevalence and aspirin compliance in patients with chronic stable angina.

Most acute coronary syndromes result from a platelet-rich occlusion of the coronary arteries. Antiplatelet drugs are of proven efficacy in preventing myocardial infarction, unstable angina, and stroke. However, not all patients on aspirin (ASA) benefit. We studied the phenomenon of aspirin resistance with a simple and reliable platelet function analyzer--the PFA-100. Studying 31 patients with unstable angina and 105 controls, we found aspirin resistance in 42% of patients, most of whom were shown to be compliant utilizing concomitant salicylate levels.

Adult↗
PubMed2000

Effects of warfarin, aspirin and the two combined, on mortality and thromboembolic morbidity after myocardial infarction. The WARIS-II (Warfarin-Aspirin Reinfarction Study) design.

The efficacy and safety of warfarin, aspirin, and the two combined are compared in a long-term, randomized, open, multicentre study involving 3606 patients after acute myocardial infarction (1202 in each treatment group). In this trial three groups receive either warfarin, aimed at a therapeutic level of the International Normalized Ratio (INR) 2.8-4.2, or 160 mg aspirin daily, or 75 mg aspirin daily combined with warfarin with INR 2.0-2.5. A placebo group is not included. Patients are screened before randomization and are given major examinations at 4 weeks and at the end of the study. In addition, all patients are given a questionnaire every 6 months. Composite endpoints include death, non-fatal reinfarction and cerebral stroke. All analyses are conducted on the intention-to-treat principle and on on-efficacy basis. The analyses control for recruiting centre, use of beta blockade, use of thrombolytic therapy and use of angiotensin converting enzyme (ACE) inhibitors.

Adult↗
PubMed1984

Aspirin tolerance induced in aspirin-sensitive asthmatics.

Twenty-nine patients with asthma and aspirin-sensitivity were studied in an attempt to induce tolerance to aspirin (ASA). Starting with the smallest ASA doses eliciting bronchial obstruction (threshold doses) we doubled the doses on subsequent days and finally achieved good tolerance of 600 mg ASA per day in 27 patients. It was more difficult to achieve tolerance in patients with low ASA-thresholds than in patients with high ones. Daily ASA administration led to prolongation of the refractory state but when the intervals between consecutive doses were increased, aspirin hypersensitivity recurred. The pause sufficient for a recurrence of sensitivity to ASA was measured in 16 patients and ranged from 24 h to 9 days. Twelve patients challenged with indomethacin after ASA-desensitisation showed good drug tolerance.

Aspirin↗