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Modified USP procedures are described for the simultaneous determination of nonaspirin salicylates and aspirin in aspirin and buffered aspirin tablets. The existing USP procedures are not stability indicating for intact aspirin when significant levels of nonaspirin salicylates are present, as is often the case in short-term, high temperature stability programs. The modified procedures yeld considerably shorter analysis times and stability-indicating assays for intact aspirin without the need for sophisticated equipment other than that presently required by USP XIX.
A quantitative high-pressure liquid chromatographic method, using a reversed-phase column and an aqueous acetic acid-methanol solution as the mobile phase, was employed for the determination of O-acetyl-O-salicylsalicylic acid and O-salicylsalicylic acid in pharmaceutical aspirin preparations. The aspirin was dissolved, filtered, and injected into the chromatograph. The absorbance of the impurities was measured at 254 nm. Acetylsalicylic anhydridge was determined by a spectrophotometric method. The aspirin was dissolved in pH 11.3 buffer and extracted with benzene. An aliquot of the benzene was evaporated, and the residue was dissolved in alpha-benzamidocinnamate-pyridine reagent. The acetylsalicylic anhydride was measured using the difference between the absorbance at 362 and 372 nm. Possible interference of aspirin with the procedure is discussed. Thirty-four bulk aspirin and 172 tablet formulations were examined. Results for O-acetyl-O-salicylsalicylic acid, O-salicylsalicylic acid and acetylsalicylic anhydride are given.
A quantitative high-pressure liquid chromatographic method, using a reversed-phase column coupled to a fluorescence detector, was developed to determine salicylic acid in bulk aspirin and plain and buffered aspirin tablets. The aspirin was dissolved, filtered, and injected into the chromatograph; the fluorescence of the salicylic acid was measured at approximately 425 nm. Excipients and impurities did not interfere, and recoveries of 100% were obtained. The method was used to analyze 84 aspirin samples.
In a group of aspirin-sensitive asthmatics we studied skin weal and flare responses to intradermal injections of compound 48/80 and histamine during oral aspirin (ASA) provocation and after ASA "desensitisation". During provocation (bronchospasm accompanied by naso-ocular symptoms) the mean weal area after compound 48/80 increased to about 42.4% (P less than 0.05). Neither the threshold (provocative) doses of ASA nor 600 mg ASA, when given after ASA-desensitisation, significantly influenced the weal reactions to compound 48/80 (mean changes of area were -1.8% and -16.5% respectively). Aspirin did not change flare reactions to compound 48/80 and weal and flare reactions to histamine on any of the three study occasions. Initial (pre-aspirin) weal reactions to compound 48/80 after desensitisation to the threshold ASA doses were significantly reduced, but after desensitisation to 600 mg ASA were significantly increased as compared with the reactions before. These data suggest that ASA-"desensitisation" may influence the skin reactivity to non-specific mast cell degranulating stimulus in ASA-sensitive asthmatics.
In summary, an incremental dosage of aspirin (660 mg) shortens the bleeding time prolonged by daily low-dosage aspirin (81 mg) in healthy subjects. The "Aspirin Reversal" phenomenon might be useful to control excessive bleeding during surgery in patients taking daily low-dosage aspirin as anti-coagulants.
AIMS: A new formulation, low dose microencapsulated aspirin, permits slow absorption of aspirin and presystemic acetylation of platelet cyclo-oxygenase within the portal circulation, potentially avoiding deleterious effects on gastric and systemic prostaglandin synthesis. The objective of this study was to determine whether the administration of microencapsulated aspirin was as effective as enteric coated (EC) aspirin as an inhibitor of platelet function in patients with atherosclerosis. METHODS: One hundred and four patients were enrolled and randomised after a run in period of at least 14 days on aspirin EC 75 mg (day 0), to receive either microencapsulated aspirin 162.5 mg (n=34), aspirin EC 150 mg (n=36) or continue on aspirin EC 75 mg (n=34) for 28 days. Serum thromboxane B2 and collagen-induced platelet aggregation and release of 5-hydroxytryptamine (EC50 values) were measured on days 0 and 28. Aggregation/release EC50s were then repeated in the presence of a large dose of aspirin added in vitro to determine the EC50 at the maximum level of platelet inhibition. RESULTS: Median thromboxane B2 levels were low after 14 days run-in therapy with aspirin EC 75 mg, but significant further reductions were seen on day 28 in patients randomised to microencapsulated aspirin 162.5 mg (P=0.0368) and aspirin EC 150 mg (P=0.0004) compared with those remaining on aspirin EC 75 mg. Median EC50 s on day 28 showed small but significant increases from baseline (day 0) in aggregation in patients randomised to microencapsulated aspirin 162.5 mg (0.62-0.85, P=0.0482) and in both aggregation and release in patients randomised to aspirin EC 150 mg (0.95-1.20, P=0.0002, 8.4-11.7, P<0. 0001, respectively) signifying enhanced antiplatelet activity. No changes were seen in patients continuing on aspirin EC 75 mg. Results following addition of high dose aspirin in vitro suggest that mechanisms other than thromboxane synthesis may be operative in the long term effects of microencapsulated aspirin 162.5 mg and aspirin EC 150 mg over aspirin EC 75 mg. CONCLUSIONS: The results show good inhibition of thromboxane B2 synthesis and subsequent platelet activity by all preparations of aspirin, although both microencapsulated aspirin 162.5 mg and aspirin EC 150 mg are slightly more effective than aspirin EC 75 mg. A randomised trial is now required to determine whether microencapsulated aspirin is associated with fewer gastric side-effects.
BACKGROUND: Although the mechanisms of aspirin-induced rhinosinusitis-asthma appear to be related to arachidonic acid abnormalities, only recently has a specific aspirin-triggered enhancement of 15-hydroxyeicosatetraenoic acid (15-HETE) generation in nasal polyp epithelial cells from aspirin-sensitive patients been demonstrated. OBJECTIVE: The aim of this study was to assess generation of 15-HETE and other eicosanoids by peripheral blood leukocytes (PBLs) from aspirin-sensitive and aspirin-tolerant asthmatic patients and modulation of 15-HETE generation by a prostaglandin (PG) E(1) analogue (misoprostol). METHODS: Twenty-four aspirin-sensitive patients with asthma-rhinosinusitis and 18 aspirin-tolerant asthmatic patients were studied, and eicosanoids released from PBLs were assessed by means of enzyme immunoassays. RESULTS: Unstimulated PBLs from aspirin-sensitive and aspirin-tolerant patients generated similar amounts of PGE(2), leukotriene C(4), and 15-HETE, but lipoxin A(4) release was significantly less in aspirin-sensitive patients (300 +/- 70 pg/mL) in comparison with that seen in aspirin-tolerant patients (690 +/- 100 pg/mL, P <.05). Cell incubation with 2, 20, or 200 micromol/L aspirin resulted in a dose-dependent increase in 15-HETE generation (mean change of +85%, +189%, and +284% at each aspirin concentration, respectively) only in aspirin-sensitive asthmatic patients. Naproxen stimulated 15-HETE generation in aspirin-sensitive asthmatic patients, but indomethacin or specific COX-2 inhibitors (NS-398 and celecoxib) did not affect 15-HETE release. A synthetic PGE(1) analogue (misoprostol) inhibited aspirin-induced 15-HETE release but enhanced 15-HETE generation by aspirin in leukocytes from aspirin-tolerant patients. After preincubation with misoprostol, aspirin induced a dose-dependent production of lipoxin A(4) in both groups. CONCLUSION: PBLs from patients with aspirin-sensitive rhinosinusitis-asthma might be specifically triggered by aspirin to generate 15-HETE. Metabolism of 15-HETE is differentially regulated by misoprostol in aspirin-tolerant and aspirin-sensitive asthmatic patients.
BACKGROUND: For patients with a diagnosis of vascular dementia there is evidence that aspirin is widely prescribed - in one study, completed by geriatricians and psychiatrists in the UK, 80% of patients with cognitive impairment (with vascular risk factors) were prescribed aspirin. However, a number of queries remain unanswered: Is there convincing evidence that aspirin benefits patients with vascular dementia? Does aspirin affect cognition or improve prognosis? In addition, does the risk of cerebral or gastric haemorrhage outweigh any benefit? The aim of this review is to assess the evidence of effectiveness of aspirin in those with a diagnosis of vascular dementia. OBJECTIVES: To assess the evidence of effectiveness of the use of aspirin for vascular dementia. SEARCH STRATEGY: Computerised databases were searched independently by two reviewers. In addition, relevant websites were searched and some journals were handsearched. Specialists in the field were approached for unpublished material and also any publications found were searched for additional references. SELECTION CRITERIA: All randomised controlled trials investigating the effect of aspirin for vascular dementia are included. Inclusion/exclusion of studies comprised systematic assessment of the quality of study design and the risk of bias. DATA COLLECTION AND ANALYSIS: Data were extracted independently by both reviewers, using a previously tested data extraction form and, where required, authors were contacted for data not provided in the papers. The aim was to evaluate data recorded via tools assessing cognitive and behavioural changes along with mortality, morbidity and institutionalisation data. MAIN RESULTS: One randomised controlled trial ( approximately approximately Meyer 1989 approximately approximately ) was included, and yielded data for analysis on a total of 70 patients. The only relevant outcome assessed in this trial was cognition. Change in cognitive outcome was towards being in favour of treatment. REVIEWER'S CONCLUSIONS: There is very limited evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia. Further research is needed to assess the effect of aspirin on cognition, and also on additional outcomes such as behaviour, and quality of life. At present it is not possible to provide evidence for other queries regarding the use of aspirin for dementia (these are described in the Background section of this review).
The levels of leukotriene C4 (LTC4), leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and histamine were measured in nasal lavage fluids obtained from aspirin-sensitive, desensitized aspirin-sensitive, and aspirin-insensitive asthmatics and normal volunteers before and after ingestion of aspirin. Increased levels of LTC4 and histamine were associated with significant decreases in the FEV1 for 3 of 4 aspirin-sensitive asthmatics who had both naso-ocular and bronchospastic reactions to aspirin. In contrast, no increase in LTC4 or histamine release was detected in aspirin-sensitive asthmatics who had only bronchospastic reactions to aspirin. No significant decreases in PGE2 levels or increases in LTB4 levels were detected during these reactions to relatively low doses of aspirin regardless of the clinical symptoms, nor was any increase in mediator release apparent in lavage fluids from normal donors, aspirin-insensitive asthmatics, and desensitized aspirin-sensitive subjects before or after various doses of aspirin. Levels of PGE2 decreased in nasal secretions from normal volunteers, aspirin-insensitive asthmatics, and desensitized aspirin-sensitive subjects after ingestion of 650 mg of aspirin. These decreases were not associated with increased LTC4 or LTB4 or with histamine release, decreased FEV1, or naso-ocular symptoms. In addition, reductions of PGE2 release were similar for normal and desensitized aspirin-sensitive volunteers (63 +/- 11 versus 61 +/- 10%, respectively). The data demonstrate that LTC4 and histamine are released into nasal secretions of aspirin-sensitive asthmatics with naso-ocular and bronchospastic reactions after ingestion of low doses of aspirin without a decrease in the levels of PGE2 and suggest that LTC4 and histamine contribute to the naso-ocular and bronchospastic symptoms characteristic of reactions to aspirin.
PURPOSE: We sought to investigate the association of aspirin dose and aspirin resistance in stable coronary artery disease patients measured by a point-of-care assay. METHODS: We studied 468 consecutive stable coronary artery disease patients in a referral cardiac center who were taking aspirin 80 to 325 mg daily for > or =4 weeks. The VerifyNow Aspirin (Ultegra RPFA-ASA, Accumetrics Inc, San Diego, Calif) was used to determine aspirin responsiveness. An aspirin reaction unit (ARU) > or =550 indicates the absence of aspirin-induced platelet dysfunction, based on correlation with epinephrine-induced light transmission aggregometry. Demographic and clinical data were collected to analyze the predictors of aspirin resistance. RESULTS: Aspirin resistance was noted in 128 (27.4%) patients. Univariate predictors of aspirin resistance include elderly (P = 0.002), women (P <0.001), anemia (P <0.001), renal insufficiency (P = 0.009) and aspirin dose < or =100 mg (P = 0.004). Multivariate analysis revealed hemoglobin (odds ratio [OR] 0.6; 95% confidence interval [CI] 0.51 to 0.69; P <0.001) and aspirin dose < or =100 mg (OR 2.23; 95% CI 1.12 to 4.44; P = 0.022) to be independent predictors of aspirin resistance. Daily aspirin dose < or = 100 mg was associated with increased prevalence of aspirin resistance compared with 150 mg and 300 mg daily (30.2% vs 16.7% vs 0%, P = 0.0062). CONCLUSION: A 100 mg or less daily dose of aspirin, which may have lower side effects, is associated with a higher incidence of aspirin resistance in patients with coronary artery disease. Prospective randomized studies are warranted to elucidate the optimal aspirin dosage for preventing ischemic complications of atherothrombotic disease.
BACKGROUND: In this study, the efficacy of oral aspirin vs. topical aspirin in moisturizer (Vaseline Intensive Care Lotion) was studied in an open, randomized, parallel trial in patients with acute herpetic neuralgia. METHODS: Thirty patients were evaluated in the trial, with 15 in each group. The patients were randomized to receive either oral aspirin, 375-750 mg three times a day, or 75 mg topical aspirin/mL of moisturizer (5-10 mL, depending on the extent of involvement), three times a day, for 21 days. Pain was assessed daily by means of a self-rating visual analog scale and physician assessment. In addition, the skin and plasma levels of aspirin were measured in both groups. RESULTS: The mean time to onset of pain relief was 44 min with topical aspirin and 110 min with oral aspirin. The mean duration of pain relief after a single application of topical aspirin was 5.4 h, whereas it was 3.5 h with oral aspirin. The mean visual analog scale scores for pain with oral aspirin decreased from 68.2 +/- 6.1 on day zero to 43.1 +/- 8.7 on day 21, which was not significant compared with the baseline score. With topical aspirin, the baseline pain score was 77.5 +/- 3.7 and decreased to 6.8 +/- 3 on day 21 (P < 0.001 compared to the baseline score and compared to oral aspirin). The mean plasma and skin levels of aspirin following oral administration were 16.21 +/- 1.1 microg/mL and 1.97 +/- 0.3 microg/mm2, respectively. After topical administration, the mean plasma level of aspirin was 2.29 +/- 0.5 microg/mL (P < 0.01 vs. oral aspirin) and the skin level was 5.96 +/- 0.4 microg/mm2 (P < 0.05 vs. oral aspirin). Treatment tolerance was excellent in both groups. CONCLUSIONS: This trial has demonstrated that topical aspirin in moisturizer is clearly superior to oral aspirin in relieving the pain of acute herpetic neuralgia, and that the analgesic activity of aspirin is largely due to its local effect.
The Coumadin Aspirin Reinfarction Study demonstrated that combination treatment with fixed dose warfarin (1 or 3 mg) + aspirin 80 mg was not superior to aspirin 160 mg alone after myocardial infarction for reducing nonfatal reinfarction, nonfatal stroke, and cardiovascular death. In this analysis, we examined the importance of aspirin dose in the protection against the secondary end point of ischemic stroke. The comparison arms for this analysis were warfarin 1 mg + aspirin 80 mg versus aspirin 160 mg. In the Coumadin Aspirin Reinfarction Study, 2,028 patients were randomized to aspirin 80 mg plus warfarin 1 mg, and 3,393 were randomized to aspirin 160 mg alone. A predictive model for ischemic stroke was developed using the Cox proportional-hazards model. A reduced Cox proportional-hazards model was developed to test for the effect of aspirin dose on ischemic stroke in predefined subgroups. The incidence of ischemic stroke was lower in patients treated with aspirin 160 mg than in patients treated with aspirin 80 mg + warfarin 1 mg (0.6% vs 1.1%; p = 0.0534). Age, previous stroke or transient ischemic attack, and aspirin dose were independent predictors of ischemic stroke. In addition, the highest risk patients, those with Q-wave myocardial infarction and male patients, appeared to receive greater benefit from aspirin 160 mg than from aspirin 80 mg + warfarin 1 mg. The results of this secondary analysis suggest that aspirin 160 mg is more effective than aspirin 80 mg + warfarin 1 mg in preventing ischemic stroke in post-myocardial infarction patients.
BACKGROUND: Antiplatelet therapy with aspirin and systematic anticoagulation with warfarin reduce cardiovascular morbidity and mortality after myocardial infarction when given alone. In the Coumadin Aspirin Reinfarction Study (CARS), we aimed to find out whether a combination of low-dose warfarin and low-dose aspirin would give superior results to standard aspirin monotherapy without excessive bleeding risk. METHODS: We used a randomised double-blind study design. At 293 sites, we randomly assigned 8803 patients who had had myocardial infarction, treatment with 160 mg aspirin, 3 mg warfarin with 80 mg aspirin, or 1 mg warfarin with 80 mg aspirin. Patients took a single tablet daily, and attended for prothrombin time (PT) measurements at weeks 1, 2, 3, 4, 6, and 12, and then every 3 months. Patients were followed up for a maximum of 33 months (median 14 months). FINDINGS: The primary event was first occurrence of reinfarction, non-fatal ischaemic stroke, or cardiovascular death. 1-year life-table estimates for the primary event were 8.6% (95% CI 7.6-9.6) for 160 mg aspirin, 8.4% (7.4-9.4) for 3 mg warfarin with 80 mg aspirin, and 8.8% (7.6-10) for 1 mg warfarin with 80 mg aspirin. Primary comparisons were done with all follow-up data. The relative risk of the primary event for the 160 mg aspirin group compared with the 3 mg warfarin with 80 mg aspirin group was 0.95 (0.81-1.12, p = 0.57). For spontaneous major haemorrhage (not procedure related), 1-year life-table estimates were 0.74% (0.43-1.1) in the 160 mg aspirin group and 1.4% (0.94-1.8) in the 3 mg warfarin with 80 mg aspirin group (p = 0.014 log rank on follow-up). For the 3382 patients assigned 3 mg warfarin with 80 mg aspirin, the INR results were: at week 1 (n = 2985) median 1.51 (IQR 1.23-2.13); at week 4 (n = 2701) 1.27 (1.13-1.64); at month 6 (n = 2145) 1.19 (1.08-1.44). INTERPRETATION: Low, fixed-dose warfarin (1 mg or 3 mg) combined with low-dose aspirin (80 mg) in patients who have had myocardial infarction does not provide clinical benefit beyond that achievable with 160 mg aspirin monotherapy.
BACKGROUND: A subset of patients with asthma experience adverse nasoocular reactions after ingestion of aspirin or agents that inhibit cyclooxygenase. Recent evidence has implicated the leukotrienes in the nasoocular reaction, but the cellular sources and mechanism of activation are unknown. We used nasal lavage with and without a 5-lipoxygenase inhibitor, zileuton, to define the role of leukotrienes and to profile nasal cellular activation during this reaction. METHODS: A group of eight patients with asthma shown to have adverse reactions to aspirin documented by a 15% or greater decrease in forced expiratory volume in 1 second, accompanied by an elevation in urinary leukotriene E4 after ingestion of aspirin, received aspirin or placebo in a study with a crossover design. Nasal symptoms and nasal tryptase, histamine, leukotriene, and eosinophil cationic protein levels were evaluated. Serum tryptase and urinary histamine levels were also assessed. Subjects were then randomized to receive a week of treatment with zileuton or placebo, according to a double-blind, crossover design followed by aspirin challenge and measurement of the same mediators. RESULTS: Aspirin ingestion produced a marked increase in nasal symptoms from a baseline symptom score of 2.1 +/- 0.7 to a maximum of 8.4 +/- 1.2 (p < 0.0007). Aspirin ingestion produced a mean maximal increase in nasal tryptase of 3.5 +/- 2.6 ng/ml, whereas placebo ingestion produced a mean maximal increase of 0.1 +/- 0.2 ng/ml (p < 0.05, aspirin vs placebo). Mean maximal nasal histamine increased 1.73 +/- 1.16 ng/ml versus 0.08 +/- 0.08 ng/ml from baseline (p < 0.05, aspirin vs placebo). Aspirin produced a mean maximal increase in nasal leukotriene value of 152 pg/ml versus a 16 pg/ml decrease after placebo ingestion (p < 0.05). Zileuton treatment blocked the increase in nasal symptoms after aspirin ingestion (maximum nasal symptom score of 1.6 +/- 0.6 with zileuton vs 5.5 +/- 0.9 with placebo [p < 0.0053]). It also blocked the rise in nasal tryptase (p = 0.011) and nasal leukotriene (p < 0.05) levels after aspirin ingestion. Zileuton treatment had no significant effect on the recovery of nasal histamine. CONCLUSION: The increase in nasal symptoms in aspirin-sensitive patients with asthma after aspirin ingestion is associated with increases in nasal tryptase, histamine, and cysteinyl leukotriene levels. This mediator profile is consistent with mast cell activation during the nasal response to aspirin and suggests that 5-lipoxygenase products are essential for the nasal response to aspirin.
BACKGROUND AND PURPOSE: The widespread use of aspirin requires clarification of the aspirin resistance phenomenon. Most studies on this field are focused on patients which may affect the action of aspirin. METHODS: We evaluated the biological efficacy of aspirin in healthy subjects. RESULTS: Agonist-induced platelet aggregation was fully abrogated by 100 mg of aspirin in all individuals. By contrast, with the platelet function analyzer-100 device, 33.3% of the subjects displayed no response. This failure was overcome by 500 mg or by in vitro treatment of blood with 30 mumol/L acetylsalicylic acid. Intake of 100 mg of aspirin efficiently reduced by 75% the level of 11-dehydro thromboxane B2 (11-dTxB2) in all cases. However, variability on the pre-aspirin level (range 72.4 to 625.9 ng/mmol creatinine) led to substantial differences in the residual amount of the metabolite between subjects treated with aspirin (range 12.9 to 118.0 ng/mmol creatinine). Finally, there was no influence of platelet glycoprotein IIb/IIIa (Pro33Leu), platelet glycoprotein Ia/IIa, (C807T), and FXIII (Val34Leu) polymorphisms on the efficacy of aspirin. However, the cyclooxygenase (Cox)-1 50T allele associated with higher level of 11-dTxB2, both before and after aspirin. Moreover, the Cox-2 -765C variant displayed a slightly higher reduction in 11-dTxB2 level on treatment with aspirin. CONCLUSIONS: Our findings suggest that full resistance of healthy subjects to aspirin is rather unlikely. However, differences in aspirin absorption, or pharmacokinetic, or other unrecognized factors may lead to lack of effect of low dose of aspirin in some subjects when using tests like platelet function analyzer-100. Whether Cox polymorphisms are thrombotic risk factor for patients under aspirin will require further research.
The efficacy of single doses (1.2 g) of soluble aspirin and aspirin tablets was determined in a randomised, placebo-controlled, double-blind, parallel study in 90 patients (45 females) with postoperative pain after removal of impacted lower third molars. Also investigated was the relationship between plasma aspirin esterase activity and overall pain scores after both aspirin preparations. Patients reported significantly less pain (p less than 0.001) after treatment with aspirin than after treatment with placebo. However, patients receiving soluble aspirin reported both an earlier onset and a longer duration of pain relief than those who received aspirin tablets. A significant correlation was observed between plasma aspirin esterase activity and overall pain scores after both soluble aspirin (r = 0.57, p less than 0.01) and aspirin tablets (r = 0.51, p less than 0.02). It is concluded that soluble aspirin is the preferred aspirin formulation for treating postoperative pain after third molar surgery and that plasma aspirin esterase activity is determinant of a patient's analgesic response to aspirin in postoperative dental pain.
OBJECTIVES: This study was designed to determine if non-aspirin non-steroidal anti-inflammatory drugs (NANSAIDs) are associated with lower odds of myocardial infarction (MI) and if NANSAIDs, particularly ibuprofen, interfere with aspirin's cardioprotective effect. BACKGROUND: The NANSAIDs may reduce the risk of MI but may also interfere with aspirin's cardioprotective effect. METHODS: A case-control study was conducted, with cases of first, nonfatal MI identified prospectively and controls identified randomly from the community. RESULTS: The use of NANSAIDs was associated with a significant reduction in MI among those not using aspirin (adjusted odds ratio [OR] 0.53; 95% confidence interval [CI]: 0.42 to 0.67). This was true for both ibuprofen (adjusted OR 0.52; 95% CI: 0.39 to 0.69) and naproxen (adjusted OR 0.48; 95% CI: 0.28 to 0.82). Although aspirin itself was associated with decreased odds of MI in those not also using NANSAIDs (adjusted OR relative to no aspirin use 0.79; 95% CI: 0.63 to 0.98), it was not associated with decreased odds of MI among those who were using NANSAIDs (OR 1.28; 95% CI: 0.85 to 1.94; p value for interaction = 0.026). The association of aspirin and reduced odds of MI diminished with increasing frequency of NANSAID use (test for interaction p = 0.006), particularly for ibuprofen (p = 0.018). Among frequent (4 times/week) NANSAID users, the OR for aspirin versus no aspirin was 2.04 (95% CI: 1.06 to 3.94). Users of prophylactic aspirin plus frequent ibuprofen had an OR relative to aspirin-only users of 2.03 (95% CI: 0.60 to 6.84). CONCLUSIONS: In the absence of aspirin use, NANSAIDs are associated with reduced odds of MI. In those using aspirin, NANSAIDs do not provide additional protection. Additional study is needed to determine the clinical impact of using NANSAIDs along with aspirin for cardioprotection.