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PubMed1992

Gastric mucosal damage due to aspirin and copper aspirinate assessed by gastric mucosal potential difference changes.

When the gastric mucosa is damaged by antiinflammatory agents, such as aspirin, gastric mucosal potential difference (GPD) decreases and may or may not return to predamage values after the agent is removed. The magnitude and time course of the gastric potential difference changes have been suggested as a measure of mucosal damage. Male Sprague-Dawley rats were fasted, anesthetized, and surgically prepared for measurement of GPD by placement of electrodes in the gastric lumen and spleen. Test mixtures of aspirin, copper aspirinate, copper sulfate, or mixtures of aspirin and copper sulfate were administered by gavage, and subsequent changes in GPD were recorded. The area between the extrapolated control (baseline) GPD and the damage GPD was determined. The product of this area and the maximum change in GPD, the Reizindex (RI), was calculated. Values for all copper (II)-containing systems, including those with no aspirin, were significantly greater than aspirin alone. It was concluded that factors other than mucosal damage may contribute to a reduction in GPD and, therefore, an increase in Reizindex.

Animals↗
PubMed1996

Comparison of aspirin alone versus aspirin plus ticlopidine after coronary artery stenting.

This prospective nonrandomized study was performed comparing aspirin alone (n = 46) versus aspirin and ticlopidine (p = 338) following native coronary artery stenting. There were significantly more stent thrombosis events in the aspirin-only group than in the aspirin and ticlopidine group (6.5% vs 0.9%, p = 0.02) and significantly more Q-wave myocardial infarctions and cardiac-related deaths in the aspirin-only group than in the aspirin and ticlopidine group (6.5% vs 0%, p = 0.002 and 4.4% vs 0.3% p = 0.02, respectively).

Aged↗
PubMed1986

Persantine-Aspirin Reinfarction Study. Part II. Secondary coronary prevention with persantine and aspirin.

In the Persantine-Aspirin Reinfarction Study, Part II (PARIS II), 3,128 persons who had recovered from myocardial infarction, suffered from 4 weeks to 4 months previously, were randomized into two groups: dipyridamole (Persantine) plus aspirin (n = 1,563) and placebo (n = 1,565). The average length of follow-up was 23.4 months. Prespecified primary end points were coronary incidence (definite nonfatal myocardial infarction plus death due to recent or acute cardiac event), coronary mortality (death due to recent or acute cardiac event) and total mortality, each at 1 year of patient follow-up and at the end of the study. Coronary incidence in the Persantine plus aspirin group was significantly lower than in the placebo group, both at 1 year (30% reduction) and at the end of the study (24% reduction). The statistically significant differences in coronary incidence, at 1 year and at the end of the study, in favor of the combination treatment remained after adjustment for multiple baseline variables and adjustment for multiple testing (three end points for two time periods). Although there were reductions for other end points, these differences were not statistically significant. Coronary mortality was 20% lower in the Persantine plus aspirin group compared with the placebo group at 1 year, and 6% lower overall. Total mortality in the treated group compared with the placebo group was 11% lower at 1 year and 3% lower overall. The reduced rates of coronary incidence largely reflected lower rates of definite nonfatal myocardial infarction in the Persantine plus aspirin group. Several subgroups were defined a priori and at the end of the study. The beneficial effect of Persantine plus aspirin compared with placebo for coronary incidence tended to be greater for the following groups of patients: those who had a non-Q wave infarct; those who were not taking digitalis; those who were receiving beta-receptor blocking drugs at baseline; those who were in New York Heart Association functional class I; those who had had only one myocardial infarction; or those who were enrolled in the study early, that is within 85 days of the qualifying myocardial infarction.

Actuarial Analysis↗
PubMed2004

Reproducibility of response to nasal lysine-aspirin challenge in patients with aspirin-induced asthma.

BACKGROUND: Peak nasal inspiratory flow (PNIF) and acoustic rhinometry objectively measure the effects of nasal provocation testing. Although the latter is conventionally used in nasal lysine-aspirin challenge, use of the former in aspirin-induced asthma (AIA) has never been evaluated. OBJECTIVE: To evaluate the reproducibility of PNIF and acoustic rhinometry following nasal lysine-aspirin challenge in AIA. METHODS: Fourteen patients with a clear-cut history of AIA underwent nasal lysine-aspirin challenge at 2 separate visits 1 week apart. Both PNIF and minimum cross-sectional area (MCA) were measured using acoustic rhinometry for 120 minutes following standard nasal lysine-aspirin challenge (25 mg). RESULTS: Prechallenge values were not significantly different at visit 1 vs visit 2 for mean [SEM] PNIF (128 [13] vs 127 [9] L/min) and MCA (6.89 [0.51] vs 6.94 [0.57] cm2). The mean (SEM) maximum percent PNIF change from baseline for visit 1 and visit 2 was -42 (5) and -42 (6), respectively, and the mean (SEM) average percent PNIF change from baseline was -25 (4) and -25 (6), respectively. The mean (SEM) maximum percent MCA change from baseline for visit 1 and visit 2 was -49 (4) and -48 (3), respectively, and the mean (SEM) average percent MCA change from baseline was -25 (8) and -24 (4), respectively. Coefficients of variation for maximum and average responses were 2.3% and 6.5%, respectively, for PNIF and 7.4% and 16.1% for MCA. CONCLUSIONS: Measurement of PNIF following nasal lysine-aspirin challenge is a simple and reproducible alternative to acoustic rhinometry, with maximum response being a more reproducible outcome measure than average response.

Adrenal Cortex Hormones↗
PubMed1999

Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production.

Electron spin resonance (ESR) was used to investigate the reaction of aspirin toward reactive oxygen species, such as hydroxyl radicals (*OH), superoxide radicals (O2-) and H2O2. The Fenton reaction (Fe(II) + H2O2 ---> FE(III) + *OH + OR) was used as a source of *OH radicals. The results show that aspirin is an efficient *OH radical scavenger with a reaction rate constant of k = 3.6 x 10(10) M(-1) sec(-1), which is faster than several well established antioxidants, such as ascorbate, glutathione and cysteine. However, aspirin is not a good scavenger for O2- or H2O2. Through its antioxidant property, aspirin exhibited a protective effect against silica-induced lipid peroxidation and DNA strand breakage. Aspirin also inhibited the activation of nuclear transcription factor-kappaB induced by silica, lipopolysaccharide or the transition metal, Fe(II), as demonstrated by electrophoretic mobility shift assay. The results show that aspirin functions as an antioxidant via its ability to scavenge *OH radicals. This antioxidant property may explain some of its various physiological and pharmacological actions.

Animals↗
PubMed2000

Aspirin-tolerant asthmatics generate more lipoxins than aspirin-intolerant asthmatics.

Asthma is characterized by chronic airway inflammation resulting from overproduction of pro-inflammatory mediators, such as leukotrienes (LT). The authors questioned the biosynthetic capacity of asthmatic patients for lipoxins (LX) and 15-epimer lipoxins (15-epi-LX), endogenous regulators of inflammatory responses that inhibit pro-inflammatory events. Levels of LXA4, 15-epi-LXA4 and LTC4 were determined in 14 clinically characterized aspirin-intolerant asthmatics (AIA), 11 aspirin-tolerant asthmatics (ATA) and eight healthy volunteers using a stimulated whole blood protocol. Both LXA4 and 15-epi-LXA4 were generated in whole blood activated by the divalent cation ionophore, A23187. Higher levels of LXA4 were produced in ATA than either AIA or healthy volunteers. Exposure of AIA whole blood to interleukin-3 prior to A23187 did not elevate their reduced capacity to generate LXA4. Generation of a bronchoconstrictor, LTC4, was similar in both AIA and ATA. Consequently, the ratio of LXA4:LTC4 quantitatively favoured the bronchoconstrictor for AIA and differed from both ATA and healthy subjects. In addition, the capacity for 15-epi-LXA4 generation was also diminished in AIA, since whole blood stimulated in the presence of aspirin gave increased levels only in samples from ATA. The present results indicate that asthmatics possess the capacity to generate both lipoxins and 15-epimer-lipoxins, but aspirin-intolerant asthmatics display a lower biosynthetic capacity than aspirin-tolerant asthmatics for these potentially protective lipid mediators. This previously unappreciated, diminished capacity for lipoxin formation by aspirin-intolerant asthmatic patients may contribute to their more severe clinical phenotype, and represents a novel paradigm for the development of chronic inflammatory disorders.

Adult↗
PubMed1998

Enhancement of platelet inhibition of ticlopidine plus aspirin vs aspirin alone given prior to elective PTCA.

BACKGROUND: In many patients today, elective percutaneous transluminal coronary angioplasty is followed by implantation of coronary stents to achieve optimal results. The current medical strategy to prevent early reocclusion is the inhibition of platelet aggregation by administration of ticlopidine, in addition to aspirin, immediately after the procedure. In order to inhibit platelet aggregation as early as possible, many centres begin to treat patients with additional ticlopidine the day before elective coronary intervention. The aim of this study was to determine the effect of this strategy on platelet aggregation before angioplasty. METHOD: Fifty-two consecutive patients admitted to hospital for elective balloon angioplasty were prospectively randomized to receive either standard oral aspirin 100 mg per day or standard therapy plus 250 mg ticlopidine at the time of admission and the morning before angioplasty. Adenosine diphosphate-, collagen- and epinephrine-induced platelet aggregation was measured immediately before the procedure by an investigator who was blinded concerning the arm of therapy. RESULTS: The two groups of patients were comparable in terms of age, sex, body mass index, anginal state, time interval between application of study drug and coronary intervention. Patients on aspirin and ticlopidine had a mean maximal platelet aggregation of 36 +/- 12% with adenosine diphosphate as agonist. For the control group, 54 +/- 12% was measured (P < 0.001). Myocardial infarction or emergency coronary bypass grafting did not occur in either group. Local haemorrhagic complications at the arterial access site occurred in five (aspirin) and six (aspirin and ticlopidine) patients (P = ns) none of them requiring blood transfusion. CONCLUSION: The additional application of ticlopidine to chronic aspirin therapy the day before elective coronary balloon angioplasty leads to a significantly higher inhibition of platelet aggregation at the time of the intervention. It seems to be safe compared to the standard procedure.

Adult↗
PubMed2002

[Aspirin sensitivity: long term follow-up after up to 3 years of adaptive desensitization using a maintenance dose of 100 mg of aspirin a day].

BACKGROUND: The full clinical picture of aspirin intolerance, Sampter's triad, is associated with nasal polyposis, clinical sensitivity to most non steroidal antiinflammatory drugs (NSAID) and intrinsic bronchial asthma. But the triad can be incomplete and nasal polyposis can be the first clinical symptom of aspirin sensitivity. Although the exact mechanisms of aspirin intolerance as well as those of desensitization remain obscure, an in vitro assay on eicosanoid metabolism has been proven to be helpful in diagnosis and treatment as it correlates well to the individual severity of clinical symptoms. METHODS: For this investigation 30 patients, who were undergoing adaptive desensitization for aspirin intolerance, were followed-up between 1 and 3 years. They received a maintenance dose of oral aspirin of only 100 mg a day after an initial application of higher doses. Their clinical course as well as their in vitro parameters of eicosanoid release were monitored throughout the individual observation period. RESULTS: Desensitization was successful in 25 of the 30 patients regarding the recurrence rate of nasal polyps, severity of bronchial asthma and sense of smell. There was a clear positive correlation between clinical and in vitro parameters. Discontinuing of aspirin therapy lead to worsening of clinical symptoms, regardless of the prior duration of treatment. CONCLUSIONS: This article reviews the role of the in vitro assay and presents a desensitization protocol that can be maintained as a long term treatment without adverse side effects. Results suggest that the recurrence rate of nasal polyps after surgical therapy can be reduced using this protocol, however, only long term treatment can secure a beneficial outcome over time.

Adolescent↗
PubMed2005

Aspirin plus warfarin compared to aspirin alone after acute coronary syndromes: an updated and comprehensive meta-analysis of 25,307 patients.

AIMS: In patients recovering from acute coronary syndromes (ACS) the role of oral anticoagulation (and its intensity) in addition to aspirin remains controversial. We conducted a specific meta-analysis of randomized trials comparing aspirin plus warfarin (A+W) with aspirin alone in such patients. METHODS AND RESULTS: MEDLINE and Cochrane databases yielded 14 (of 148 potentially relevant) articles enrolling 25 307 patients. Follow-up ranged from 3 months to 5 years. Irrespective of International normalized ratio (INR), A+W did not significantly affect the risk of major adverse events (MAE: all cause death, non-fatal myocardial infarction, and non-fatal thrombo-embolic stroke) when compared with aspirin alone [OR 0.96 (0.90-1.03), P=0.30], but increased the risk of major bleeds (MB): OR 1.77 (1.47-2.13), P<0.00001. However, in studies with INR of 2-3, A+W was associated with a significant reduction of MAE [OR 0.73 (0.63-0.84), P<0.0001, number needed to treat to avoid one MAE=33], albeit at an increased risk of MB [OR 2.32 (1.63-3.29), P<0.00001; number needed to harm by causing one MB=100]. In both analyses, intracranial bleeding was not significantly increased by A+W when compared with aspirin alone. CONCLUSION: For patients recovering from ACS, a combined strategy of A+W at INR values of 2-3 doubles the risk of MB, but is nonetheless superior to aspirin alone in preventing MAE. Whether this combined regimen is also superior to a 'double' anti-platelet strategy or to newer evolving treatments warrants further investigation.

Angina, Unstable↗
PubMed2005

Resistance to aspirin in patients after coronary artery bypass grafting is transient: impact on the monitoring of aspirin antiplatelet therapy.

The aim of the present study was to assess the responsiveness of blood platelets to aspirin in patients following coronary artery bypass grafting (CABG) surgery. Aspirin was administered following CABG in 24 operated patients (aged 63.2 +/- 6.3 years). Platelet function was monitored on the 10th postoperative day (A) and 1 month after CABG (B) with the use of whole-blood aggregometry (WBEA) and PFA-100 closure time (PFA-100 CTCEPI). Normal platelet response to aspirin was defined by 3 criteria: the complete inhibition of WBEA induced by arachidonic acid (0.5 mmol/L), partial inhibition of collagen (1 microg/mL)-induced aggregation (WBEA < 14 Omega), and prolongation of PFA-100 CTCEPI (>150 seconds) ("good responders"). Depending on whether 0, 1, 2, or 3 of these 3 criteria were fulfilled, patients were classified as "nonresponders," "weak responders," "incomplete responders," or "good responders," respectively. On the 10th postoperative day, there were 3 good responders, 6 incomplete responders, 11 weak responders, and 4 nonresponders among 24 patients. In contrast, 1 month after CABG within the same group of 24 patients there were 18 good responders, 5 incomplete responders, and 1 weak responder. Using a new methodology to assess impaired platelet responsiveness to aspirin ex vivo, we describe here the transient nature of "aspirin resistance" following CABG. These results indicate the necessity for the prolonged monitoring of the antiplatelet effectiveness of aspirin in the postoperative period after CABG.

Aged↗
PubMed2004

Urinary 3-bromotyrosine and 3-chlorotyrosine concentrations in asthmatic patients: lack of increase in 3-bromotyrosine concentration in urine and plasma proteins in aspirin-induced asthma after intravenous aspirin challenge.

BACKGROUND: Eosinophil peroxidase and myeloperoxidase halogenate tyrosine residues in plasma proteins and generate 3-bromotyrosine (BY) and 3-chlorotyrosine (CY), respectively. OBJECTIVES: (1) To estimate urinary concentrations of BY and CY in asthmatic patients. (2) To investigate BY concentration in relation to urinary leukotriene E4 (LTE4) concentration in order to evaluate the activation of eosinophils in patients with aspirin-induced asthma (AIA). METHODS: BY and CY were quantified with a gas chromatograph-mass spectrometer using (13)C-labelled compounds as internal standards. RESULTS: (1) Activation of eosinophils and neutrophils by immobilized IgG1 induced preferential formation of BY and CY, respectively. (2) A significantly higher concentration of BY was observed in the urine from asthmatic patients than in that from healthy control subjects (45+/-21.7 vs. 22.6+/-10.8 ng/mg-creatinine, P<0.01). CY concentration was also elevated in the urine from asthmatic patients (4.4+/-3.2 vs. 1.5+/-1.0 ng/mg-creatinine, P<0.01). (3) After intravenous aspirin challenge of aspirin-induced asthmatic patients, the concentration of BY in urine did not significantly change. No significant change was also observed in the ratio of BY concentration to total tyrosine concentration in plasma proteins. In contrast, the concentration of urinary LTE4 significantly increased after the intravenous aspirin challenge. CONCLUSION: Determination of BY and CY concentrations may be useful for monitoring the activation of eosinophils and neutrophils in asthmatic patients, respectively. After aspirin challenge of AIA patients, the increased concentration of urinary LTE4 did not accompany changes in BY concentration in both urine and plasma proteins. These results may preclude the activation of eosinophils after aspirin challenge in patients with AIA.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Histopathologic and coronary angiographic assessment of effectiveness of aspirin or aspirin-and-gammaglobulin in Kawasaki disease.

Coronary angiography and right ventricular endomyocardial biopsy were performed in 36 children during convalescence (days of illness 23-86; mean = 41.5 days) following acute Kawasaki disease. Treatment of the acute stage was not randomized; it consisted of aspirin alone in 14 subjects (during the years 1980-88), and gammaglobulin and aspirin in 22 subjects (1984-91). The dosage of aspirin was 30 mg/kg orally during the acute febrile stage and 5-10 mg/kg orally after lysis of fever. The dosage of gammaglobulin was 200 mg/kg x 5 days in 19 patients, 200 mg/kg x 3 days in one patient, 200 mg/kg x 1 day + 400 mg/kg x 4 days in one patient and 200 mg/kg x 4 days + 400 mg/kg x 4 days in one patient. Among the 14 patients treated with aspirin alone, large coronary aneurysms were noted in four, moderate aneurysms in three and transient aneurysms in one. Among 22 patients treated with gammaglobulin, only five had aneurysms and these were transient. The histopathological (HP) score based on myocardial disarrangement, degeneration and hypertrophy; interstitial edema, large mononuclear cell infiltration and fibrosis; and endocardial abnormalities was higher in the aspirin group than in gammaglobulin group. Moderate to severe HP changes were noted in five subjects in the aspirin group, while moderate HP changes were found in only two subjects in the gammaglobulin group. Gammaglobulin therapy not only reduced the incidence of the coronary arterial lesions but also reduced the severity of myocardial damage from moderate or severe to mild in Kawasaki disease.

Acute Disease↗
PubMed1998

A randomised trial of low dose aspirin for primiparae in pregnancy. The Jamaica Low Dose Aspirin Study Group.

OBJECTIVE: To investigate whether low dose aspirin medication given to primiparous women provides benefit in preventing pre-eclampsia or intrauterine growth retardation. DESIGN: Randomised double-blind controlled trial of low dose aspirin and placebo in pregnancy. POPULATION: Residents of the parishes of Kingston and St Andrew, Jamaica; 6275 primiparae enrolled between 12 and 32 weeks of gestation. MAIN OUTCOME MEASURES: Hypertensive disorders of pregnancy (including pre-eclampsia and eclampsia), preterm delivery, and low birthweight. In addition, to assess whether enrollment early, rather than late had more beneficial effect. Possible adverse effects on the woman and her infant were monitored. RESULTS: Of enrolled primiparae, 97% were followed throughout pregnancy. There were no differences between those on aspirin and those on placebo in the development of hypertensive disorders (e.g. for a rise in diastolic pressure of 25 mmHg the odds ratio [OR] was 1.02 [95% CI 0.86-1.21]; for proteinuric pre-eclampsia OR 1.15 [95% CI 0.92-1.44]; eclampsia OR 0.82 [95% CI 0.44-1.53]); except for oedema which was significantly less prevalent in those on aspirin (OR 0.85 [95% CI 0.75-0.96]). Women on aspirin were no significantly less likely to deliver preterm (OR 0.93 [95% CI 0.79-1.09]) or have a larger fetus (mean birthweight difference 18 g [95% CI -9 to 45]). They were, however, significantly more likely to suffer from bleeding disorders antenatally, intrapartum and postpartum; for postpartum haemorrhage OR 1.40 (95% CI 1.13-1.73). CONCLUSIONS: This trial shows that low dose aspirin has no consistent beneficial effect in primiparae.

Aspirin↗
PubMed2004

Cooperation between aspirin-triggered lipoxin and nitric oxide (NO) mediates antiadhesive properties of 2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) (NO-aspirin) on neutrophil-endothelial cell adherence.

2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) is a nitric oxide (NO)-releasing derivative of aspirin that inhibits cyclooxygenase (COX) activity and releases NO. Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL). Here, we demonstrate that exposure of neutrophil (PMN)/human umbilical vein endothelial cell (HUVEC) cocultures to aspirin and NCX-4016 triggers ATL formation and inhibits cell-to-cell adhesion induced by endotoxin (LPS) and interleukin (IL)-1beta by 70 to 90%. However, although selective and nonselective COX-2 inhibitors (celecoxib, rofecoxib, and naproxen) or N-t-butoxycarbonylmethionine-leucine-phenylalanine (Boc-1), an LXA(4) receptor antagonist, reduced the antiadhesive properties of aspirin by approximately 70%, antiadhesive effects of NCX-4016 were only marginally affected ( approximately 30%) by COX inhibitors and Boc-1, implying that COX-independent mechanisms mediate the antiadhesive properties of NCX-4016. Indeed, NCX-4016 causes a long-lasting (up to 12 h) release of NO and cGMP accumulation in HUVEC. Scavenging NO with 10 mM hemoglobin, in the presence of celecoxib, reduced the antiadhesive properties of NCX-4016 by approximately 80%. Confirming a role for NO, the NO donor diethylenetriamine-NO also inhibited PMN/HUVEC adhesion by approximately 80%. NCX-4016, but not aspirin, decreased DNA binding of nuclear factor-kappaB (NF-kappaB) on gel shift analysis and HUVEC's overexpression of CD54 and CD62E induced by LPS/IL-1beta. Reduction of binding of the two NF-kappaB subunits p50-p50 and p50-p65 was reversed by dithiothreitol, implying S-nitrosylation as mechanism of inhibition. In summary, our results support that ATL and NO are formed at the PMN/HUVEC interface after exposure to NCX-4016 and mediate the antiadhesive properties of this compound.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1984

Effect of aspirin in "aspirin sensitive" patients.

Eighteen patients with a history of urticaria or asthma, or both, induced by aspirin were studied before and after provocation of symptoms with aspirin. The plasma prostaglandin F2 alpha concentration, which was characteristically raised before challenge, fell significantly at the time of adverse reactions. Repeated administration of aspirin up to a dose of 650 mg daily induced tolerance in most of the patients, and several developed bronchodilator responses to aspirin. Although median total IgE concentrations may be raised in patients with aspirin sensitivity, it appears likely that pharmacological rather than immunological mechanisms are chiefly responsible for the phenomena of aspirin sensitivity and desensitisation.

Adolescent↗
PubMed1975

Electronmicroscopic observations on the effects of orally administered aspirin and aspirin-bicarbonate mixtures on the development of gastric mucosal damage in the rat.

The effects of administering a single dose of (200 mg to 50 mg/kg body weight) aspirin or an equimolar mixture of aspirin (200 mg/kg body wt) with sodium bicarbonate on the fine structure of the rat gastric mucosa were investigated in order to establish the role of particles of the drug in the development of gastric damage. The sequence of cellular events involved in the development of a lesion and the influence of short-term starvation were also investigated. Aspirin-bicarbonate solutions produced much less damage in starved rats than aspirin suspensions given at low (50 mg/kg body weight) or high therapeutic doses (200 mg/kg body weight). Also, when non-starved rats were given 200 mg/kg aspirin, only slight damage was observed. The presence of particles of the drug in intimate contact with the mucosa is thus important in the development of gastric damage. A sequence of events with time involving direct physical exfoliation of mucosal cells and selective structural damage to parietal cells followed by structural damage indicative of a disturbance to oxidative and biosynthetic functions in cells near the developing erosion was observed. The implications of these results on the development of aspirin-induced lesions are discussed.

Animals↗
PubMed1999

Aspirin sensitivity: the role for aspirin challenge and desensitization in postmyocardial infarction patients.

Aspirin is one of the world's most commonly used medications and its use benefits many diverse conditions. Adverse reactions, however, are relatively common as well. Hypersensitivity to aspirin can be manifested as acute asthma, urticaria and/or angioedema, or a systemic anaphylactoid reaction. We report 3 cases in whom aspirin was indicated for secondary prophylaxis of myocardial infarction but in whom a remote history of an untoward reaction to it prevented its initial use. These patients all underwent further evaluation of their pulmonary and allergic history and all 3 were challenged with aspirin. Two patients were found not to be sensitive and started on aspirin, the other had a classic asthmatic reaction to the drug and was successfully desensitized to aspirin allowing for its use.

Adult↗
PubMed2006

Comparison of warfarin versus aspirin for the prevention of recurrent stroke or death: subgroup analyses from the Warfarin-Aspirin Recurrent Stroke Study.

BACKGROUND AND PURPOSE: We performed a combination of prespecified and exploratory subgroup analyses to detect any treatment differences among various baseline subgroups in the Warfarin-Aspirin Recurrent Stroke Study (WARSS) cohort. METHODS: The WARSS compared the efficacy of adjusted-dose warfarin (INR 1.4-2.8) to aspirin (325 mg/day) for recurrent ischemic stroke or death within 2 years. The effect of warfarin and aspirin was compared among prespecified and exploratory subgroups with respect to sociodemographic and vascular risk factors, stroke subtype, arterial territory, and infarct topography. Hazard ratios and 95% confidence intervals comparing warfarin to aspirin were calculated using Cox proportional hazards models. Differences in hazard ratios were tested using interaction terms. RESULTS: No treatment differences between warfarin and aspirin were found across multiple prespecified subgroups. In a multivariate model, warfarin was associated with greater hazard among patients with moderate stroke severity (HR 1.63, 95% CI 1.005-2.64, p = 0.047) and a greater benefit among those with posterior circulation location without brainstem infarction (HR 0.54, 95% CI 0.33-0.88, p = 0.013). In post-hoc analyses of the cryptogenic subgroup, warfarin was associated with worse outcomes among patients with moderate stroke severity and better outcomes among those without baseline hypertension or with posterior circulation infarcts sparing the brainstem. CONCLUSIONS: In the WARSS, the majority of subgroup analyses showed no benefit of warfarin over aspirin. Warfarin benefit was limited to brainstem-sparing posterior circulation infarcts and select cryptogenic stroke subgroups. Pending future clinical trial evidence to the contrary, antiplatelets are recommended for survivors of noncardioembolic stroke.

Aged↗