Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASPIRIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2004

Aspirin-mediated COX-2 transcript stabilization via sustained p38 activation in human intestinal myofibroblasts.

Acetylsalicylic acid (aspirin) is a cyclooxygenase (COX) inhibitor, yet some of its therapeutic effects are thought to derive from mechanisms unrelated to prostaglandin synthesis inhibition. In human intestinal myofibroblasts, aspirin, at therapeutic doses, had the unexpected effect of inducing prolonged COX-2 expression. This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. The COX-2 transcriptional rate, measured by nuclear runoff analysis and heterogeneous nuclear RNA reverse transcription-polymerase chain reaction, was only modestly elevated by aspirin treatment. In contrast, aspirin treatment dramatically stabilized the COX-2 message. The COX-2 mRNA half-life in IL-1 treated cells was 1 h and was increased in excess of 5 h in IL-1 + aspirin-treated cells. Phosphorylation of p38 MAPK was enhanced in aspirin-treated cells (but not in cells treated with 5-ASA or indomethacin) for up to 24 h after treatment. Inhibition of p38 activity negated aspirin-mediated COX-2 mRNA stabilization and the resultant increase in COX-2 mRNA and protein levels. The modest transcriptional response seen in aspirin treated cells was also abolished by p38 inhibition. We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate. Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation.

Aspirin↗
PubMed2001

Pre-hospital aspirin for suspected myocardial infarction and acute coronary syndromes: a headache for paramedics?

OBJECTIVE: To ascertain the frequency with which paramedics follow protocols for the administration of aspirin to patients to whom an ambulance is called for chest pain associated with suspected ischaemic heart disease. METHODS: Ambulance services in England and Wales who had conducted a recent aspirin administration audit were identified through the National Clinical Effectiveness Programme for the Ambulance Service Association. Data were requested from each of these services with a 100% return rate. RESULTS: Nine services out of a total of 35 had collected appropriate data. The proportion of patients who were given aspirin by a paramedic varied from 11% to 74%. The range of proportions of patients receiving pre-hospital aspirin increased after adding those patients who had already received aspirin from an alternative health provider, to 19% to 78%. It is estimated that at least 15% to 74% of patients who should have been given aspirin by the various ambulance services did not receive it. The proportion of patients for whom aspirin was judged to be inappropriate ranged from 4% to 35%. The reason for these widely varying and generally poor levels of compliance is not known. However, the range of indications and contraindications to the administration of aspirin varied considerably by ambulance service. This also made the comparison of data from different sources difficult. CONCLUSIONS: Aspirin has been shown to be beneficial after a myocardial infarction and for other acute coronary syndromes. However, variances in the proportion of patients with suspected ischaemic heart disease given aspirin in different ambulance services indicates the need for a re-emphasis on the importance of this treatment. A standard protocol for all UK ambulance services should be devised that minimises the number of contraindications to aspirin and otherwise requires its administration to all patients with acute coronary syndromes or suspected myocardial infarction. Regular, standardised audits of compliance should also be conducted and their results widely disseminated.

Acute Disease↗
PubMed1994

Role of gastric blood flow, neutrophil infiltration, and mucosal cell proliferation in gastric adaptation to aspirin in the rat.

Gastric mucosa exhibits the ability to adapt to ulcerogenic action of aspirin but the mechanism of this phenomenon is unknown. In this study, acute gastric lesions were produced by single or repeated doses of acidified aspirin in rats with intact or resected salivary glands and with intact or suppressed synthase of nitric oxide. A single oral dose of aspirin produced a dose dependent increase in gastric lesions accompanied by considerable blood neutrophilia and mucosal neutrophil infiltration, significant reduction in gastric blood flow, and almost complete suppression of biosynthesis of prostaglandins. After rechallenge with aspirin, the mucosal damage became smaller and progressively declined with repeated aspirin insults. Gastric adaptation to aspirin was accompanied by a significant rise in gastric blood flow, reduction in both blood neutrophilia and mucosal neutrophil infiltration, and a remarkable increase in mucosal cell regeneration and mucosal content of epidermal growth factor. Salivectomy, which reduced the mucosal content of epidermal growth factor, aggravated the initial mucosal damage induced by the first exposure to acidified aspirin but did not prevent the adaptation of this mucosa to repeated aspirin insults. Pretreatment with NG-nitro-L-arginine (L-NNA), a specific inhibitor of nitric oxide synthase, eliminated the hyperaemic response to repeated aspirin but did not abolish the development of adaptation to aspirin showing that the maintenance of the gastric blood flow plays little part in this adaptation. In conclusion, the stomach adapts readily to repeated aspirin insults and this is accompanied by a considerable reduction in blood neutrophilia and the severity of neutrophil infiltration and by an extensive proliferation of mucosal cells possibly involving epidermal growth factor.

Adaptation, Physiological↗
PubMed2003

Aspirin inhibits the growth of Helicobacter pylori and enhances its susceptibility to antimicrobial agents.

BACKGROUND AND AIM: The role of Helicobacter pylori and aspirin in peptic ulcer formation and recurrence remains an important clinical topic. The interaction between aspirin and H pylori in vitro is also not clear. We investigated the effect of aspirin on the growth of H pylori and on the susceptibility of H pylori to antimicrobials. METHODS: Time killing studies of H pylori were performed with different concentrations of aspirin and salicylate. Growth of bacteria was assessed spectrophotometrically and by viable colony count. The effects of aspirin on the efficiency of colony formation and on metronidazole induced mutation to rifampicin resistance in H pylori were determined. Minimal inhibitory concentrations (MICs) of aspirin and metronidazole were tested by the standard agar dilution method. MICs of amoxycillin and clarithromycin were determined by the E test method. RESULTS: Aspirin and salicylate inhibited the growth of H pylori in a dose dependent manner and bactericidal activity was due to cell lysis. Aspirin 400 micro g/ml caused a 2 logs decrease in colony forming units/ml at 48 hours, and suppressed the normal ability of metronidazole to induce new mutations to rifampicin. The IC(90) of aspirin was 512 micro g/ml. Increased susceptibility of amoxycillin, clarithromycin, and metronidazole to H pylori was observed at 1 mM (180 micro g/ml) aspirin. CONCLUSIONS: Aspirin inhibited the growth of H pylori, suppressed the mutagenic effect of metronidazole, and enhanced the susceptibility of H pylori to antimicrobial agents. This mechanism is important in future drug development for effective clearing and overcoming resistance.

Amoxicillin↗
PubMed2001

Aspirin for primary prevention of coronary heart disease: safety and absolute benefit related to coronary risk derived from meta-analysis of randomised trials.

OBJECTIVE: To determine the cardiovascular and coronary risk thresholds at which aspirin for primary prevention of coronary heart disease is safe and worthwhile. DESIGN: Meta-analysis of four randomised controlled trials of aspirin for primary prevention. The benefit and harm from aspirin treatment were examined to determine: (1) the cardiovascular and coronary risk threshold at which benefit in prevention of myocardial infarction exceeds harm from significant bleeding; and (2) the absolute benefit expressed as number needed to treat (NNT) for aspirin net of cerebral haemorrhage and other bleeding complications at different levels of coronary risk. MAIN OUTCOME MEASURES: Benefit from aspirin, expressed as reduction in cardiovascular events, myocardial infarctions, strokes, and total mortality; harm caused by aspirin in relation to significant bleeds and major haemorrhages. RESULTS: Aspirin for primary prevention significantly reduced all cardiovascular events by 15% (95% confidence interval (CI) 6% to 22%) and myocardial infarctions by 30% (95% CI 21% to 38%), and non-significantly reduced all deaths by 6% (95% CI -4% to 15%). Aspirin non-significantly increased strokes by 6% (95% CI -24% to 9%) and significantly increased bleeding complications by 69% (95% CI 38% to 107%). The risk of major bleeding balanced the reduction in cardiovascular events when cardiovascular event risk was 0.22%/year. The upper 95% CI for this estimate suggests that harm from aspirin is unlikely to outweigh benefit provided the cardiovascular event risk is 0.8%/year, equivalent to a coronary risk of 0.6%/year. At coronary event risk 1.5%/year, the five year NNT was 44 to prevent a myocardial infarction, and 77 to prevent a myocardial infarction net of any important bleeding complication. At coronary event risk 1%/year the NNT was 67 to prevent a myocardial infarction, and 182 to prevent a myocardial infarction net of important bleeding. CONCLUSIONS: Aspirin treatment for primary prevention is safe and worthwhile at coronary event risk >/= 1.5%/year; safe but of limited value at coronary risk 1%/year; and unsafe at coronary event risk 0.5%/year. Advice on aspirin for primary prevention requires formal accurate estimation of absolute coronary event risk.

Aspirin↗
PubMed2002

Outcome of myocardial infarction in patients treated with aspirin is enhanced by pre-hospital administration.

OBJECTIVE: Reducing time to reperfusion therapy is one of the goals in the management of acute myocardial infarction (AMI). We assessed the association between timing of aspirin administration and outcome of patients with AMI. PATIENTS: We studied 922 consecutive AMI patients with ST-segment elevation in Killip class I-III on admission. Patients were divided into two groups based upon the timing of emergency aspirin administration: before (early aspirin users) or after (late aspirin users) hospital admission. RESULTS: Early aspirin users (n = 338; 37%) were younger, less likely to be women, and more likely to smoke (p < 0.006) than late users (n = 584; 63%). Other baseline and clinical characteristics were similar. Early aspirin users were more likely to be treated with thrombolysis or primary percutaneous transluminal coronary angioplasty. Compared with late users, early aspirin users had significantly lower in-hospital complications and lower mortality rates at 7 (2.4 vs. 7.3%, p = 0.002) and 30 days (4.9 vs. 11.1%, p = 0.001). By multivariate adjustment, pre-hospital aspirin was an independent determinant of survival at 7 (odds ratio 0.43; 95% confidence interval 0.18-0.92) and at 30 days (odds ratio, 0.60; 95% confidence interval 0.32-1.08). Survival benefit associated with aspirin persisted for subgroups treated or not with reperfusion therapy. CONCLUSIONS: Outcome of AMI patients treated with aspirin is improved by pre-hospital administration. Our findings suggest that emergency pre-hospital aspirin might facilitate early reperfusion.

Aged↗
PubMed2006

Biological efficacy of low against medium dose aspirin regimen after coronary surgery: analysis of platelet function.

The failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of "aspirin-resistance" remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days. Platelet function was tested the day before surgery and on day +1 and day +5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine. In all patients, baseline platelet aggregation was significantly inhibited by pre-incubation with in vitro aspirin (150 micromol/l), with a mean reduction in TxA2-release of >or=95.5% (82.3,99.1). After 5-days of oral aspirin, platelet aggregation was significantly inhibited, and was not further inhibited by in vitro aspirin. Oral aspirin was also associated with a >or=99.5% (97.8, 99.7) reduction in TxA2-release, and with the reversal of the second-phase of ADP-induced aggregation which is TxA2-dependent. In addition a single-dose of 325 mg aspirin on the first post-operative morning may have a greater inhibitory effect on collagen-induced aggregation than 100 mg aspirin. Western blot analysis provided no evidence for the presence of COX-2 in platelets, while the up-regulation of p38-MAPK following platelet-stimulation and surgery was seen. The inhibition of COX-2 (NS398) or p38-MAPK (SB203580) activity did not affect platelet aggregation and TxA2-release on day +5. In summary, there was no evidence for inherent or acquired aspirin-resistance in this surgical population, or for the involvement of either COX-2 or p38-MAPK.

Adenosine Diphosphate↗
PubMed2000

Aspirin use is low among United States outpatients with coronary artery disease.

BACKGROUND: The goal of the present study was to assess national trends and patterns of aspirin use among outpatients with coronary artery disease. Although there is strong evidence that the use of aspirin reduces the risk of death and recurrent events in patients with coronary artery disease, current national patterns of aspirin use are unknown. METHODS AND RESULTS: We used data from the 1980 to 1996 National Ambulatory Medical Care Surveys. These surveys provide a nationally representative sample of physician activities during patient visits to physician offices. We evaluated the report of aspirin as a new or continuing medication in 10 942 visits to cardiologists and primary care physicians by patients with coronary artery disease. We evaluated trends in the use of aspirin for 1980 to 1996 and used logistic regression to identify independent predictors of aspirin use for 1993 to 1996. Aspirin use in outpatient visits by persons with coronary artery disease without reported contraindications increased from 5.0% in 1980 to 26.2% in 1996. Large increases occurred in the early 1990s. Independent predictors of aspirin use in 1993 to 1996 were male patient gender (29% versus 21% for females), patient age of <80 years (28% versus 17% for age of >/=80 years), and presence of hyperlipidemia (45% versus 24% for patients without hyperlipidemia; all comparisons P<0. 001). Cardiologists (37%) were more likely to report aspirin use than were internists (20%), family physicians (18%), or general practitioners (11%; P<0.001). These effects persisted after we controlled for potential confounders with the use of logistic regression. CONCLUSIONS: Although aspirin use in patients with coronary artery disease has increased dramatically, it remains suboptimum. Low rates of aspirin use and variations in use suggest a need to better translate clinical recommendations into practice.

Adult↗
PubMed1990

Prevention of early aortocoronary bypass occlusion by low-dose aspirin and dipyridamole. Grupo Español para el Seguimiento del Injerto Coronario (GESIC)

To analyze the efficacy of low-dose aspirin in preventing early aortocoronary vein graft occlusion, 1,112 consecutive patients were enrolled in a multicenter, randomized, double-blind, placebo-controlled trial comparing 50 mg t.i.d. aspirin, 50 mg aspirin plus 75 mg t.i.d. dipyridamole, and placebo. All patients received 100 mg q.i.d. dipyridamole for 48 hours before surgery, and assigned treatment was started 7 hours after surgery. Vein graft angiography was performed in 927 patients (83%) within 28 days of surgery (mean, 10 days). Aspirin plus dipyridamole significantly (p = 0.017) reduced the occlusion rate of distal anastomoses from 18% (placebo) to 12.9%. Occlusion rate in the aspirin group was 14%, which approached statistical significance (p = 0.058). Furthermore, only aspirin plus dipyridamole reduced (p = 0.01) the number of patients with occluded grafts (placebo, 33%; aspirin, 27.1%; aspirin plus dipyridamole, 24.3%). Mediastinal drainage was slightly higher (p = 0.04) in the aspirin plus dipyridamole group (713 +/- 456 ml) than in the other two groups (placebo, 670 +/- 437 ml; aspirin, 629 +/- 337 ml), but hospital mortality (average, 4.6%) and early reoperation (average, 3.9%) rates were similar among the three groups. Thus, low-dose aspirin plus dipyridamole safely improves early saphenous vein aortocoronary graft patency; this effect is an added benefit to a preoperative regimen of dipyridamole.

Aged↗
PubMed1991

Immediate postoperative aspirin improves vein graft patency early and late after coronary artery bypass graft surgery. A placebo-controlled, randomized study.

BACKGROUND: The efficacy of aspirin for prevention of thrombotic graft occlusion after coronary artery bypass grafting (CABG) depends both on the dosage and time window of administration. Early and late graft patency were therefore assessed in a prospective, double-blind, randomized, placebo-controlled trial of aspirin, 324 mg daily, given within 1 hour of CABG. METHODS AND RESULTS: Angiographic graft patency was determined at 1 week (231 patients) and 1 year (219 patients) after CABG. The early vein graft occlusion rate was 1.6% on aspirin and 6.2% on placebo (p = 0.004), and late graft occlusion rate was 5.8% on continued aspirin and 11.6% on placebo (p = 0.01). New graft occlusion between 1 week and 1 year was less common in patients on aspirin than on placebo (4.3% versus 7.4%, p = 0.013). The protective effect of aspirin against occlusion persisted in most subgroups of graft type, graft flow, diameter of recipient artery, location of grafted artery, and endarterectomy. Mean chest tube blood loss for the first 24 hours was 571 ml for the aspirin group and 563 ml for the placebo group. Red cell transfusion requirements were 902 ml in the aspirin group and 934 ml in the placebo group (p = NS). The reoperation rate was 4.8% in the aspirin group and 1% in the placebo group (p = 0.1). CONCLUSIONS: Immediate postoperative administration of aspirin (324 mg) improves early graft patency and, with continued usage, protects against further occlusion up to 1 year after CABG. Postoperative blood loss was similar in the two groups; however, aspirin was associated with a nonsignificant higher rate of reoperation.

Angiography↗
PubMed1994

Combination antithrombotic therapy in unstable rest angina and non-Q-wave infarction in nonprior aspirin users. Primary end points analysis from the ATACS trial. Antithrombotic Therapy in Acute Coronary Syndromes Research Group.

BACKGROUND: The purpose of this study was to compare combination antithrombotic therapy with aspirin plus anticoagulation versus aspirin alone, when added to conventional antianginal therapy in patients with unstable rest angina or non-Q-wave myocardial infarction who were nonprior aspirin users. METHODS AND RESULTS: Two hundred fourteen patients were randomized; 109 were randomized to receive aspirin alone (162.5 mg daily) and 105 to receive a combination of aspirin plus anticoagulation, ie, aspirin 162.5 mg daily plus heparin (activated partial thromboplastin time, two times control) followed by aspirin 162.5 mg daily plus warfarin (international normalized ratio, 2 to 3). Trial therapy was begun by 9.5 +/- 8.8 hours of qualifying pain and was continued for 12 weeks. Primary end points were recurrent angina with ECG changes, myocardial infarction, and/or death. Analysis by intention to treat of primary events at 12 weeks was performed. At 14 days, there was a significant reduction in total ischemic events in the combination group versus aspirin alone (10.5% versus 27%, P = .004). An efficacy analysis of primary events at 12 weeks also revealed a large reduction in total ischemic events in the combination group versus aspirin alone (13% versus 25%, P = .06). Bleeding complications were slightly more common with combination therapy. CONCLUSIONS: In nonprior aspirin users, combination antithrombotic therapy with aspirin plus anticoagulation significantly reduces recurrent ischemic events in the early phase of unstable angina.

Angina, Unstable↗
PubMed1995

Comparison of effects of high-dose and low-dose aspirin on restenosis after femoropopliteal percutaneous transluminal angioplasty.

BACKGROUND: Long-term treatment with aspirin is recommended in patients with large-vessel peripheral arterial disease since these patients have a high risk of death from cardiovascular causes. Recent studies have demonstrated the prophylactic effect of low-dose aspirin in reducing the risk of cardiovascular events. Since aspirin is also recommended for prevention of late recurrence after peripheral angioplasty, the present study was undertaken to compare the effects of high-dose (1000 mg/d) and low-dose (100 mg/d) aspirin on long-term patency after femoropopliteal angioplasty. METHODS AND RESULTS: Two hundred sixteen patients treated successfully by percutaneous transluminal angioplasty for femoropopliteal lesions were randomly allocated to therapy with either 1000 or 100 mg aspirin daily. The follow-up was 24 months. The long-term results were analyzed using the Kaplan-Meier method, and differences between curves of cumulative patency were determined with the Wilcoxon and log-rank statistics. Complete follow-up information (patency after 24 months, restenosis, and death) was obtained in 207 patients. During the 2-year follow-up period, 72 patients--36 in the high-dose and 36 in the low-dose aspirin group, respectively--developed angiographically verified reobstruction within the recanalized segment. By intention-to-treat analysis, the cumulative patency rates at 24 months were 62.5% in the high-dose and 62.6% in the low-dose aspirin group (Wilcoxon, P = .97; log-rank, P = .97). The cumulative survival at 24 months of follow-up was 86.6% in the high-dose and 87.7% in the low-dose aspirin group. The number of patients discontinuing therapy was 30 in the high-dose and 11 in the low-dose aspirin group (P < .01). Fewer patients receiving 100 mg of aspirin discontinued therapy because of gastrointestinal symptoms (4 versus 20). CONCLUSIONS: The data indicate that 100 mg aspirin is no less effective in the prevention of restenosis after femoropopliteal PTA than a 1000-mg dose and has fewer side effects.

Aged↗
PubMed1996

Comparison of high-dose with low-dose aspirin in patients with mechanical heart valve replacement treated with oral anticoagulant.

BACKGROUND: There are no reported studies on the safety and efficacy of low-dose aspirin with low-intensity oral anticoagulation in patients with heart valve replacement. In this study, we compared the use of 100 mg/d aspirin with 650 mg/d aspirin in the prevention of systemic embolism and vascular death in patients with heart valve replacement who were being treated with oral anticoagulants with a target international normalized ratio (INR) of 2.0 to 3.0. METHODS AND RESULTS: Four hundred nine of 416 consecutive patients who had cardiac valve replacement were randomized in open allocation into one of two groups; both groups were treated with oral anticoagulant therapy with a target INR of 2.0 to 3.0. Two hundred seven patients who received 100 mg/d aspirin for an average of 24.1 months were compared with 202 patients who received 650 mg/d aspirin for an average of 21.7 months in a randomized-treatment, open-allocation study. There were no significant differences in systemic embolism, vascular death, or total death rates between the low- and high-dose aspirin treatment groups (0.5 and 1.1, 1.2 and 0.5, and 4.6 and 2.5 per 100 patients/y, respectively). The total number of hemorrhagic events was 13.4 per 100 patients/y in the high-dose aspirin group and 7.9 per 100 patients/y in the low-dose aspirin group (P = .035), but the rate of bleeding was influenced by dipyridamole in the 650-mg aspirin group. CONCLUSIONS: In patients with mechanical heart valve replacements, low-dose aspirin (100 mg/d) in conjunction with oral anticoagulants at an INR of 2.0 to 3.0 is as effective as the use of high-dose aspirin (650 mg/d) in the prevention of systemic embolism.

Administration, Oral↗
PubMed1998

Acute hemodynamic interaction of aspirin and ticlopidine with enalapril: results of a double-blind, randomized comparative trial.

BACKGROUND: Coprescription of aspirin and ACE inhibitors is frequent in heart failure caused by coronary artery disease. Negative interaction between aspirin and enalapril has been reported, presumably through inhibition by aspirin of ACE inhibitor-induced prostaglandin synthesis. Ticlopidine is a potent antiplatelet agent without interaction with prostaglandin synthesis. METHODS AND RESULTS: The objective of this study was to compare the influence of a coadministration of ticlopidine or aspirin on the hemodynamic effects of an ACE inhibitor (enalapril) in patients with chronic heart failure. Twenty patients with severe heart failure were enrolled in a double-blind comparative trial and allocated to ticlopidine (500 mg daily, 12 patients) or aspirin (325 mg daily, 8 patients). Hemodynamic evaluation was performed after 7 days of treatment, every hour for 4 hours after an oral administration of 10 mg of enalapril. Significant reductions in systemic vascular resistance were observed in the ticlopidine group, in contrast to no significant decrease in the aspirin group. A significant (P=0.03) time-by-treatment interaction indicated significant aspirin-enalapril drug interaction. Total pulmonary resistance decreased significantly in both groups, with no difference between patients assigned to aspirin or ticlopidine. CONCLUSIONS: Enalapril reduced systemic vascular resistance more effectively when given in combination with ticlopidine than with aspirin. In contrast, the reduction in total pulmonary resistance is similar when enalapril is administered in combination with aspirin or ticlopidine. Negative aspirin-enalapril interaction on prostaglandin synthesis presumably alters vasodilatation in systemic vessels, whereas prostaglandin-independent actions of ACE inhibition such as pulmonary arterial vasodilatation are maintained.

Adult↗
PubMedDate not supplied

Effects of low dose aspirin on platelet function in patients with recent cerebral ischemia.

We tested the antiplatelet effects of low-dose aspirin in patients with occlusive cerebrovascular disease, because conventional dosage aspirin inhibits vascular synthesis of prostacyclin at the same time that it inhibits platelets. The effects on platelet function and thromboxane A2 synthesis of 40 mg of aspirin daily or 40 mg aspirin plus dipyridamole were measured in 23 patients starting within a week after the onset of cerebral ischemia. All patients had normal baseline platelet aggregation responses to four stimuli: arachidonate, epinephrine, adenosine diphosphate and collagen. The generation of thromboxane A2 by platelets, measured as serum thromboxane B2, was also normal. After 3 to 7 days of low dose aspirin therapy, platelet aggregation responses were suppressed to the extent observed with higher dosage aspirin. Serotonin release during platelet aggregation was inhibited by more than 95% and thromboxane B2 levels in clotted blood fell by more than 95%. Responses to aspirin treatment were similar in patients with transient ischemic attacks and in those with stroke and were also similar in both sexes. No differences in platelet responses were observed between patients receiving aspirin alone and aspirin plus dipyridamole. Thus 40 mg aspirin daily inhibited platelet responses as effectively as higher doses of aspirin in patients who had recent cerebral ischemia and showed a cumulative antiplatelet effect.

Aged↗
PubMed2002

Aspirin and urinary 11-dehydrothromboxane B(2) in African American stroke patients.

BACKGROUND AND PURPOSE: The aim of the study was to evaluate the relationship between daily aspirin use and urinary excretion of a stable thromboxane metabolite, 11-dehydrothromboxane B(2) (11-DTB2), in African American stroke patients. METHODS: Subjects were a subgroup of those screened for the African American Antiplatelet Stroke Prevention Study. Subjects were within 4 months of noncardioembolic ischemic stroke and were not being treated with anticoagulants. Antithrombotic therapy at the time of urine collection varied according to the practice patterns of various attending physicians who treated the patients during their acute strokes. 11-DTB2 was measured by enzyme immunoassay in random urine samples 1 to 4 months after the stroke. RESULTS: Eighty-seven of 92 patients enrolled were able to give a urine sample at the time of enrollment. There were 51 men and 36 women aged 36 to 87 (mean 62) years. On the basis of antithrombotic treatment before the sample collection, we divided patients into 4 groups: (1) 16 patients treated with no aspirin (no antithrombotic drugs [n=4] or ticlopidine [n=12]), (2) 21 patients treated with 81 to 325 mg aspirin per day (81 mg/d [n=2], 325 mg/d [n=19]), (3) 20 patients treated with 650 mg aspirin per day, and (4) 30 patients treated with 975 to 1300 mg aspirin per day (975 mg/d [n=2] and 1300 mg/d [n=28]). In patients taking daily aspirin at any dose, the median urinary 11-DTB2 was 783 pg/mg creatinine compared with 1386 pg/mg creatinine in patients not taking daily aspirin (P=0.01 by Wilcoxon rank sum test). In multivariate regression analysis, aspirin use remained significantly associated with lower urinary 11-DTB2 (P=0.008). There was no dose-response effect between the 3 aspirin dose groups and urinary 11-DTB2 (P=0.70). CONCLUSIONS: In African American stroke patients, aspirin use is associated with significantly lower urinary 11-DTB2 independent of other vascular factors, and there does not appear to be a dose-response effect for aspirin doses of 325 to 1300 mg daily. The clinical significance of these finding remains to be determined.

Adult↗
PubMed2001

A comparison of every-third-day versus daily low-dose aspirin therapy on serum thromboxane concentrations in healthy men and women.

Aspirin's antithrombotic effect is mediated predominately by inhibition of platelet cyclooxygenase-1, leading to a decline in serum thromboxane A2 concentrations. We performed a placebo-controlled, randomized, double-blind trial to determine whether aspirin could be given at 3-day intervals and still achieve potent serum thromboxane inhibition. One hundred nine healthy men and women with no recent exposure to aspirin and no contraindications to its use participated. Subjects received 325 mg, 81 mg, or 40 mg of plain aspirin every third day, with placebo on other days; 81 mg of aspirin every day; or placebo every day. Serum concentrations of thromboxane B2 (the metabolite of thromboxane A2) were measured at 3-day intervals during a 31-day treatment period, as well as 4, 7, and 14 days after treatment ended. Serum thromboxane B2 concentrations were nearly identical during treatment with 325 mg of aspirin every third day or 81 mg of aspirin per day (86% inhibition [84%, 89%] and 85% inhibition [73%, 96%], respectively). An aspirin dose of 81 mg every third day was nearly as potent (74% inhibition [70%, 79%]), whereas 40 mg of aspirin every third day achieved only 50% inhibition (40%, 60%). Every-third-day low-dose aspirin regimens (325 and 81 mg) deserve comparison with daily low-dose aspirin regimens in controlled clinical trials because the former regimens could prove to have equal efficacy with reduced toxicity.

Adolescent↗
PubMed2006

The management of aspirin in transurethral prostatectomy: current practice in the UK.

INTRODUCTION: Stopping aspirin prior to transurethral prostatectomy (TURP) may minimise peri-operative blood loss, but it may also increase the risk of a significant cardiovascular event. There are no guidelines on the management of aspirin in TURP. This study sought to determine the variation in the peri-operative management of transurethral prostatectomy (TURP) patients that are taking aspirin. MATERIALS AND METHODS: A questionnaire was sent to 444 consultant urologists in the UK from a list obtained from the British Association of Urologists. This resulted in 290 anonymous replies (65%), of which 287 were suitable for analysis. RESULTS: Of these 287 urologists, 178 (62%) ask patients to stop aspirin prior to TURP. Aspirin is stopped 9.8 days (median, 10 days; range, 2-30 days) prior to surgery, and recommenced 8.8 days (median, 7 days; range, 1-42 days) after surgery. In those that stop aspirin, 62% will stop aspirin in all patients, regardless of the indication, and 40% will cancel a TURP if aspirin use has inadvertently continued. Of the 287 urologists, 109 (38%) do not stop aspirin. CONCLUSIONS: There is a wide variation in the management of aspirin in TURP patients in the UK. Aspirin is being stopped in patients at high risk of serious cardiovascular disease, often for longer than necessary. There is a need for multidisciplinary guidelines to reduce variation in practice.

Aspirin↗