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 595 records · Page 33Linked to original sources
PubMed2001

Aspirin use and risk of cataract in posttrial follow-up of Physicians' Health Study I.

BACKGROUND: In Physicians' Health Study I, randomized trial results indicated no major beneficial effect of 5 years of low-dose aspirin treatment on total cataract (relative risk [RR], 0.94; 95% confidence interval [CI], 0.79-1.13) or cataract extraction (RR, 0.81; 95% CI, 0.65-1.01) during the period of treatment. OBJECTIVE: To examine the effect of assigned aspirin treatment and posttrial, self-selected aspirin use on the risk of age-related cataract over the 15 years of follow-up of Physicians' Health Study I. METHODS: Participants were 20 968 US male physicians enrolled in Physicians' Health Study I who did not report cataract at baseline. At 7 years, after termination of the randomized aspirin component of the trial, self-selected aspirin use was computed from annual questionnaires. The main outcome measures were age-related cataract and extraction of age-related cataract, defined as an incident, age-related lens opacity responsible for a reduction in best-corrected visual acuity to 20/30 or worse based on self-report confirmed by medical record review. RESULTS: During a median of 14.9 years of follow-up, there were 2081 cataracts and 1198 cataract extractions. Overall, the age- and beta carotene-adjusted RR of cataract in men assigned to aspirin compared with those assigned to placebo was 1.09 (95% CI, 1.00-1.18). For cataract extraction, the RR was 1.09 (95% CI, 0.98-1.22). During a median posttrial follow-up of 7.9 years, a total of 1225 incident cataracts and 635 cataract extractions were documented. The multivariate RR of cataract in men who reported using aspirin frequently (>/=180 days per year) at 7 years compared with nonusers (0-13 days per year) was 1.20 (95% CI, 1.03-1.40). For cataract extraction, the multivariate RR was 1.22 (95% CI, 0.98-1.51). Results for diagnosis and extraction of cataract subtypes were similar. CONCLUSIONS: Analyses based on randomized aspirin assignment indicated no long-term benefit of 5 years of low-dose aspirin treatment on total cataract or cataract extraction. Posttrial, observational data also indicated no decreased risk of cataract in aspirin users and suggested a small increased risk of cataract in aspirin users. Further randomized trial data to investigate the effect of longer term treatment with low-dose aspirin are being collected as part of the ongoing Women's Health Study, a randomized trial of low-dose aspirin and vitamin E among 39 876 apparently healthy, postmenopausal US female health professionals.

Adult↗
PubMed1997

Low-dose aspirin therapy is associated with few side effects but does not prevent hepatic artery thrombosis in liver transplant recipients.

Hepatic artery thrombosis occurs in 4% to 10% of adult patients and in up to 26% of children undergoing liver transplantation. Aspirin has been used to prevent this complication but may increase procedure-related and gastrointestinal bleeding. The aim of this study was to assess the efficacy and safety of low-dose aspirin in the prophylaxis of hepatic artery thrombosis. The histories of 529 patients who survived liver transplantation between September 1988 and December 1993 were reviewed retrospectively. The routine clinical practice followed until 1992 was to initiate oral aspirin therapy on the first postoperative day (81 mg daily in adults and 40 mg daily in children) as prophylaxis for vascular thrombosis. This was done in 354 patients. Aspirin was not administered to the remaining 175 patients. Hepatic artery thrombosis occurred in 13 patients treated with aspirin (3.7%) and in 7 patients not treated with aspirin (4.0%) (P = .85). Recipient age of younger than 2 years and low donor liver weight were the only factors that predisposed the patients to hepatic artery thrombosis. A total of 1,651 percutaneous liver biopsies were performed in this series, with 1,111 performed in patients treated with aspirin. Significant bleeding after liver biopsy occurred in 12 patients treated with aspirin (1.1%) and in 3 patients not treated with aspirin (0.6%) (P = .29). Gastrointestinal bleeding occurred in 66 patients treated with aspirin (18.9%) and in 23 patients not treated with aspirin (12.8%) (P = .08). Low-dose aspirin therapy is not shown to be effective in preventing hepatic artery thrombosis after liver transplantation. Although aspirin does not produce a statistically significant increase in the risk of bleeding after liver biopsy, there is a trend toward an increased incidence of gastrointestinal bleeding.

Adolescent↗
PubMed2006

A review of aspirin resistance; definition, possible mechanisms, detection with platelet function tests, and its clinical outcomes.

Aspirin (acetylsalicylic acid) is one of the main therapeutics in prevention of thrombo-embolic vascular events. Its efficiency is proved in the prevention of cardiovascular events. However, antiplatelet effect of aspirin is not absolute in all patients and some patients experience thrombo-embolic events despite aspirin. These patients are clinically called as aspirin resistant or aspirin non-responders. Globally, a lot of people are affected by aspirin resistance according to the high prevalence of athero-thrombotic vascular diseases. A prevalence of 5.5-45% in patients with various cardiovascular disease by different laboratory methods has been reported for aspirin resistance. Clinical outcome of aspirin resistance has been demonstrated in patients with different vascular diseases. Detection of platelet function in patients treated with aspirin may be necessary in the prediction of clinical outcome. Point of care methods, which have correlated results with the standard light transmittance aggregometry may be appropriate choices in the detection of platelets' response to antiplatelet therapy. Adequate additional therapies may reduce atherothrombotic risks and major cardiovascular events rate in aspirin resistant subjects. None of the current researches advised the cessation of aspirin therapy. There is need to investigate the efficacy of additional adenosine diphosphate receptor antagonists or newer antiplatelet agents in aspirin resistant subjects. The intent of this paper is to review the literature discussing possible mechanisms, determination techniques, and clinical effects of aspirin resistance.

Aspirin↗
PubMed2004

Too little aspirin for secondary prevention after acute myocardial infarction in patients at high risk for cardiovascular events: Results from the MITRA study.

BACKGROUND: A meta-analysis of randomized trials has shown a significant reduction of mortality rate in patients receiving aspirin for secondary prevention after acute myocardial infarction (AMI). However, a significant number of patients do not receive aspirin after AMI. Little is known about why aspirin is withheld or the long-term outcome of these patients today. METHODS: The Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) registry is a multicenter registry of patients with AMI in Germany. RESULTS: Of 4902 patients, 509 (10%) did not receive aspirin at the time of discharge from the hospital. The mean follow-up period for these patients was 17 months. Relative contraindications to aspirin were significantly associated with the withholding of aspirin (in-hospital bleeding: odds ratio [OR], 3.56; 95% CI, 1.86-6.80; history of peptic ulcer: OR, 2.49; 95% CI, 1.62-3.83). Absolute contraindications to aspirin were rare (2.2%). Other medications of proven benefit were also given less often in these patients (beta-blockers: 49.0% vs 61.9%, P <.001; angiotensin-converting enzyme inhibitors: 65.6% vs 70.2%, P =.06; statins: 12.2% vs 15.1%, P =.10). Patients who were not given aspirin were at high risk for vascular events. They were more likely to have a history of prior AMI (OR, 1.34; 95% CI, 1.02-1.79), were in critical clinical condition at admission more often (cardiogenic shock: OR, 1.98; 95% CI, 1.09-3.56; overt heart failure: OR, 1.6; 95% CI, 1.05-2.3), and received acute revascularization less often (OR, 1.32; 95% CI, 1.05-1.67). The 1-year mortality was 2-times higher in patients who did not receive aspirin than in patients who did receive aspirin (16.5% vs 8.3%, P <.001). A significant association of withheld aspirin at discharge with a higher long-term mortality rate was confirmed with multivariate analysis (OR, 1.62; 95% CI, 1.15-2.29). CONCLUSIONS: Ten percent of patients who sustained an AMI did not receive aspirin at the time of hospital discharge. Most of these patients were at high risk for cardiovascular events. Withheld aspirin was significantly associated with higher mortality rate during follow up.

Aged↗
PubMed2006

Aspirin use among U.S. adults: Behavioral Risk Factor Surveillance System.

BACKGROUND: The role of aspirin in prevention of cardiovascular disease (CVD) and cardiovascular complications among people with diabetes has been examined. A Healthy People 2010 objective calls for increasing the proportion of people with diabetes aged>or=40 years who take aspirin>or=15 times per month. METHODS: Data from 2003 Behavioral Risk Factor Surveillance System were used to examine (1) the prevalence of aspirin intake, (2) aspirin use among those with CVD, (3) aspirin use among those with diabetes, (4) current status with respect to Healthy People objective 5-16, and (5) changes in aspirin intake from 1999. RESULTS: Daily or every-other-day aspirin use was reported by 36.2% of participants in 2003. Aspirin intake among those with CVD and diabetes was 82.8% and 62.6%, respectively. The Healthy People 2010 objective of increasing the proportion of adults with diabetes aged>or=40 years who take aspirin to 30% was achieved. The prevalence of aspirin intake was higher in 2003 compared to 1999 among all participants, those with CVD, and those with diabetes (relative increase of about 20%, 12%, and 36%, respectively). Most participants (74%) reported cardiovascular reasons for aspirin use. Among those without CVD or diabetes, the prevalence of aspirin intake increased with the increasing number of CVD risk factors. CONCLUSIONS: Regular aspirin use increased over a 4-year period. Greater use of inexpensive and easily accessible interventions to prevent cardiovascular events is encouraging. Increased efforts to continue preventive uses of available treatment and reduction in risk by modifying other risk factors will help lower future disease burden.

Adult↗
PubMed2006

Effect of ranitidine on the antiplatelet effects of aspirin in healthy human subjects.

Aspirin is often taken with H2-receptor antagonists. In vitro data suggest that certain antagonists, such as ranitidine, have inhibitory effects on platelet function. There are no reports on the combined effect of aspirin and H2-receptor antagonists on platelet function in humans. Therefore, this study's aim was to evaluate the effects of aspirin, ranitidine, and their combination on platelet function in humans. Ten healthy men aged 34.7 +/- 2 years received aspirin 325 mg/day for 4 days followed by a 9-day washout period, 3 days of ranitidine treatment (150 mg twice daily), and 4 days of dual-drug treatment. Blood samples were drawn at baseline and on the last days of aspirin monotherapy, the washout period, ranitidine monotherapy, and dual-drug treatment. Platelet aggregation was measured in response to 0.5 mg/ml arachidonic acid, 5 and 10 mumol/L adenosine diphosphate, and 1 micro g/ml collagen. The Platelet Function Analyzer 100 test was performed, and blood salicylate levels were measured in 6 subjects. Aspirin caused a marked reduction in platelet aggregation and prolongation of Platelet Function Analyzer 100 closure time. Ranitidine caused a modest decrease in platelet aggregation. Unexpectedly, the combination of aspirin and ranitidine caused less inhibition of platelet aggregation and prolongation of Platelet Function Analyzer 100 time than aspirin alone (p = 0.02 to 0.07 compared with aspirin alone). Blood salicylate levels were lower when subjects took aspirin with ranitidine than when they took aspirin alone (1 +/- 0.8 vs 1.6 +/- 0.7 mg/dl, p = 0.005). In conclusion, ranitidine appears to attenuate the antiplatelet effects of aspirin in healthy volunteers. The most likely mechanism for these findings is a change in the absorption conditions of aspirin in the presence of ranitidine.

Adult↗
PubMed2006

Systematic review and meta-analysis of adverse events of low-dose aspirin and clopidogrel in randomized controlled trials.

PURPOSE: We performed a systematic review to define the relative and absolute risk of clinically relevant adverse events with the antiplatelet agents, aspirin and clopidogrel. MATERIALS AND METHODS: Databases were searched for randomized controlled trials of low-dose aspirin (75-325 mg/day) or clopidogrel administered for cardiovascular prophylaxis. Relative risks (RR) were determined by meta-analysis of 22 trials for aspirin versus placebo and from single studies for aspirin versus clopidogrel, aspirin versus aspirin/clopidogrel, and clopidogrel versus aspirin/clopidogrel. Absolute risk increase was calculated by multiplying RR increase by the pooled weighted incidence of the control. RESULTS: Aspirin increased the risk of major bleeding (RR=1.71; 95% confidence interval [CI], 1.41-2.08), major gastrointestinal (GI) bleeding (RR=2.07; 95% CI, 1.61-2.66), and intracranial bleeding (RR=1.65; 95% CI, 1.06-5.99) versus placebo. No difference between 75-162.5 mg/day and >162.5-325 mg/day aspirin versus placebo was seen. The absolute annual increases attributable to aspirin were major bleeding: 0.13% (95% CI, 0.08-0.20); major GI bleeding: 0.12% (95% CI, 0.07-0.19), intracranial bleeding: 0.03% (95% CI, 0.01-0.08). No study compared clopidogrel with placebo. One study showed increased major GI bleeding (but not non-GI bleeding endpoints) with aspirin versus clopidogrel (RR=1.45; 95% CI, 1.00-2.10). The absolute annual increase was 0.12% (95% CI, 0.00-0.28). CONCLUSIONS: Low-dose aspirin increases the risk of major bleeding by approximately 70%, but the absolute increase is modest: 769 patients (95% CI, 500-1250) need to be treated with aspirin to cause one additional major bleeding episode annually. Compared with clopidogrel, aspirin increases the risk of GI bleeding but not other bleeding; however, 883 patients (95% CI, 357-infinity) would need to be treated with clopidogrel versus aspirin to prevent one major GI bleeding episode annually at a cost of over 1 million dollars.

Aspirin↗
PubMed2004

Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment.

OBJECTIVES: We sought to investigate the effect of aspirin resistance on the incidence of myonecrosis after non-urgent percutaneous coronary intervention (PCI) among patients pretreated with clopidogrel. BACKGROUND: Oral antiplatelet therapy using aspirin and a thienopyridine is the standard of care for preventing thrombotic complications of PCI. The effect of aspirin resistance on the outcomes of patients undergoing PCI is unknown. METHODS: We used the Ultegra Rapid Platelet Function Assay-ASA (Accumetrics Inc., San Diego, California) to determine aspirin responsiveness of 151 patients scheduled for non-urgent PCI. All patients received a 300-mg loading dose of clopidogrel >12 h before and a 75-mg maintenance dose in the morning of the PCI. The incidence of myonecrosis was measured by creatine kinase-myocardial band (CK-MB) and by troponin I (TnI) elevations after PCI. RESULTS: A total of 29 (19.2%) patients were noted to be aspirin-resistant. There was a significantly higher incidence of female subjects in the aspirin-resistant versus aspirin-sensitive groups. The incidence of any CK-MB elevation was 51.7% in aspirin-resistant patients and 24.6% in aspirin-sensitive patients (p = 0.006). Elevation of TnI was observed in 65.5% of aspirin-resistant patients and 38.5% of aspirin-sensitive patients (p = 0.012). Multivariate analysis revealed aspirin resistance (odds ratio [OR] 2.9; 95% confidence interval [CI] 1.2 to 6.9; p = 0.015) and bifurcation lesion (OR 2.8; 95% CI 1.3 to 6.0; p = 0.007) to be independent predictors of CK-MB elevation after PCI. CONCLUSIONS: Despite adequate pretreatment with clopidogrel, patients with aspirin resistance as measured by a point-of-care assay have an increased risk of myonecrosis following non-urgent PCI.

Aged↗
PubMed2005

Aspirin use in older patients with heart failure and coronary artery disease: national prescription patterns and relationship with outcomes.

OBJECTIVES: We sought to determine patterns of aspirin use and the relationship between aspirin prescription and outcomes in patients with coronary artery disease (CAD) and heart failure (HF). BACKGROUND: Because of the potential for exacerbating hypertension or renal insufficiency and possible interactions with angiotensin-converting enzyme (ACE) inhibitors, the use of aspirin for secondary prevention of coronary events is controversial in patients with HF. METHODS: We studied a national sample of Medicare beneficiaries > or =65 years old after hospitalization for HF with CAD and without aspirin contraindications between April 1998 and June 2001. We assessed factors associated with aspirin prescription and the relationship between aspirin and outcomes in regression models accounting for differences in patient, physician, and hospital characteristics and for clustering of patients by hospital. RESULTS: Of the 24,012 patients, 54% received aspirin. Treated patients had lower unadjusted rates of death (31% vs. 39% for those not receiving aspirin, p < 0.001). In multivariable analyses, aspirin remained associated with a lower risk of death (risk ratio [RR] 0.94; 95% confidence interval [CI] 0.90 to 0.99). This association was similar regardless of hypertension, renal insufficiency, or treatment with ACE inhibitors (p for all interactions > 0.2). Aspirin also was associated with lower risks of death or all-cause readmission (RR 0.98; 95% CI 0.97 to 0.99) and of death or readmission for HF (RR 0.98; 95% CI 0.96 to 0.99). CONCLUSIONS: Almost one-half of patients with CAD hospitalized for HF in the U.S. are not treated with aspirin. This study found no evidence of harm from aspirin in this population and suggests a treatment benefit. Withholding aspirin based upon theoretical concerns about adverse effects appears to be unjustified.

Age Factors↗
PubMed2005

Effect of increasing doses of aspirin on platelet function as measured by PFA-100 in patients with diabetes.

INTRODUCTION: Platelets of diabetic patients have been reported to be less sensitive to aspirin. The aim of this study is to compare a medium (300 mg) and low (100 mg) dose of aspirin on platelet function in diabetic patients. METHODS: We have included one hundred and two patients with type 2 diabetes mellitus. Platelet function was measured as closure time (CT) with the Platelet Function Analyzer (PFA)-100 before the administration of aspirin. Initially the patients were given 100 mg aspirin once daily for seven days, and then the measurements were repeated. If the CT exceeded the upper limit of 300 s, the study was terminated. If not, the patients continued the aspirin therapy with a dose of 300 mg daily for another seven days, and the CTs were measured again. RESULTS: After taking 100 mg aspirin, the CT significantly increased from 126+/-29 s to 256+/-66 s (p<0.001). In 68 of 102 (67%) patients, the CT increased to 300 s. In the remaining 34 patients, the baseline CT was 113+/-29, and increased to 170+/-45 s after 100 mg aspirin (p<0.001). In these patients, there was a further increase in the CT from 170+/-45 to 229+/-75 s following 300 mg aspirin (p<0.001). On average, the CT was increased by 60% and 39% following ingestion of 100 and 300 mg aspirin, respectively. CT>300 s were obtained in 15 (44%) of 34 patients after 300 mg aspirin. CONCLUSIONS: Although, a daily dose of 100 mg aspirin effectively inhibited platelet function in a majority of diabetics, a considerable proportion of patients showed a greater platelet inhibition with the use of 300 mg aspirin. The PFA-100 closure time may be used to separate those patients who require a higher dose of aspirin to achieve desired antiplatelet effect.

Adult↗
PubMed2005

Effects of different aspirin formulations on platelet aggregation times and on plasma salicylate concentrations.

BACKGROUND: Early aspirin treatment is widely used to inhibit platelet activity and to reduce morbidity and mortality in patients presenting with an acute myocardial infarction or a stroke. A number of different aspirin formulations have been used for this purpose; however, a comparison of their effectiveness in inhibiting early platelet aggregation has not been determined. METHODS: In this study, we determined plasma salicylate concentrations and platelet inhibitory activities at various times after ingestion of three commonly used aspirin formulations: soluble aspirin (Alka-Seltzer), 325 mg, chewed baby aspirin, 324 mg, and whole compressed non-enteric coated aspirin, 324 mg. Twenty-four healthy volunteers, 18-39 years of age, participated in the prospective single-blinded triple-crossover study. Plasma salicylate concentrations and inhibition of arachidonic acid-induced platelet aggregation were determined on post-dose blood samples collected at 2.5, 5.0, 7.5, 10, 15, 20, 25, 30, and 40 min. All subjects crossed over to the other two formulations with at least 2 weeks between ingestions. RESULTS: The median platelet inhibition times for the chewed, soluble, and whole aspirin formulations were 7.5, 7.5, and 10.0 min, respectively. Soluble and chewed aspirin were found to inhibit platelet aggregation faster than whole aspirin (p<0.001); however, there were no significant differences in platelet aggregation times between the soluble and chewed formulations (p<0.163). Inhibition of platelet aggregation was found to occur at an average plasma salicylate concentration of 2.46 microg/mL, regardless of method of ingestion. CONCLUSION: The results indicate that soluble and chewed aspirin inhibit platelet aggregation in a shorter period of time than does whole aspirin. The results suggest that chewing baby aspirin or taking soluble buffered aspirin may be the preferred route of administration for early platelet inhibition.

Administration, Oral↗
PubMed2002

Underuse of aspirin in a referral population with documented coronary artery disease.

Despite substantial evidence that antiplatelet therapy saves lives and reduces adverse events in patients with coronary artery disease (CAD), use of the most widely available and lowest cost antiplatelet agent, aspirin, continues to be disappointingly low. In a large database of patients with known CAD, we (1) explored trends in the use of aspirin over time, (2) characterized patients most likely to take aspirin regularly, and (3) estimated the effectiveness of aspirin use by examining long-term outcomes. Using patients entered in the Duke Databank for Cardiovascular Diseases, we explored the use of aspirin from 1969 to 1999. More than 25,000 patients were sent a questionnaire that included several questions about medication use, including 1 question specifically about aspirin. Patients who failed to respond to the questionnaire received a follow-up telephone call. Aspirin use increased substantially over the most recent 4 years in the study, from 59% in 1995 to 81% in 1999. Predictors of aspirin use included younger age, male sex, being a nonsmoker, and having had a myocardial infarction or revascularization procedure. Patients who never took aspirin had a risk ratio for death of 1.85 compared with patients who regularly took aspirin. Despite the well-known beneficial effects of aspirin, too many patients without contraindications to aspirin fail to take it regularly. The health care system currently lacks effective methods to ensure that patients who have CAD have adequate follow-up concerning aspirin use.

Adult↗
PubMed1999

The effect of aspirin administration and parity on plasma salicylate concentrations and postpartum reproductive parameters in Brahman cows.

Forty pluriparous (M) and 20 primiparous (P) suckled Brahman cows were used to evaluate the effect of aspirin and parity on plasma 13,14-dihydro-15-keto-prostaglandin F2alpha (PGFM) and progesterone (P4) concentrations and some reproductive parameters. On Day 7 after calving (PP), the cows were allocated within parity into 2 groups: the aspirin group received concentrate containing aspirin at a rate of 100 mg/kg of body weight every 12 h until Day 13 PP; and the control received concentrate every 12 h for the same interval. Blood samples were collected after first and last aspirin feeding and daily from Day 1 PP to Day 6 PP and from Day 14 PP to Day 21 PP, twice daily from Day 7 PP to Day 13 PP, and weekly until first non-return to estrus. Plasma salicylate concentrations in the aspirin group cows were affected by parity (P < 0.01) and time after feeding (P < 0.0001). P cows showed higher plasma salicylate concentrations with a later peak and slower decrease than M cows. Aspirin-treated P cows had longer PP intervals than either control P, control M, or aspirin-treated M cows. Cows receiving aspirin had a lower pregnancy rate, an increased incidence of abnormal estrous cycles, and a decline in the presence of corpora lutea after estrus. Cows that formed a corpora lutea and had received aspirin had higher P4 release between Day 6 and 14 after estrus. Aspirin-treated cows that did not form corpora lutea had lower P4 release between Days 9 and 14 after estrus. A treatment by parity interaction affected mean PGFM proportions (P < 0.01) during the treatment period. Aspirin-fed P cows increased PGFM release as measured by mean proportion of Day 6 PP values. Aspirin-fed M cows showed a decrease in mean PGFM proportions. Aspirin feeding during the early PP showed different effects on some reproductive parameters in P and M Brahman cows, indicating differences in PP physiology between parities.

Animals↗
PubMed1999

Aspirin and mortality in patients treated with angiotensin-converting enzyme inhibitors: a cohort study of 11,575 patients with coronary artery disease.

OBJECTIVES: The purpose of this study was to investigate the significance of the possible negative interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors. BACKGROUND: Several provocative reports have recently suggested that aspirin is unsafe in patients with heart failure and has negative interaction with ACE inhibitors that might attenuate their beneficial effects upon survival. METHODS: We analyzed mortality data of 11,575 patients with coronary artery disease screened for the Bezafibrate Infarction Prevention trial. A total of 1,247 patients (11%) were treated with ACE inhibitors. Of them, 618 patients (50%) used aspirin. RESULTS: Five-year mortality was lower among patients on ACE inhibitors and aspirin than patients on ACE inhibitors without aspirin (19% vs. 27%; p < 0.001). After adjusting for confounders, treatment with aspirin and ACE inhibitors remained associated with lower mortality risk than using ACE inhibitors only (relative risk [RR] = 0.71; 95% confidence interval [CI] = 0.56 to 0.91). Subgroup analysis of 464 patients with congestive heart failure treated with ACE inhibitors revealed 221 patients (48%) on aspirin and 243 patients not on aspirin. Although clinical characteristics and therapy were similar, patients taking aspirin experienced lower mortality than patients who did not (24% vs. 34%; p = 0.001). After adjustment, treatment with aspirin was still associated with lower mortality (RR = 0.70; 95% CI = 0.49 to 0.99). CONCLUSIONS: Among coronary artery disease patients with and without heart failure who are treated with ACE inhibitors, the use of aspirin was associated with lower mortality than treatment without aspirin. Our findings contradict the claim that aspirin attenuates the beneficial effect of ACE inhibitors and supports its use in patients with coronary artery disease treated with ACE inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Effect of leukotriene modifier drugs on the safety of oral aspirin challenges.

BACKGROUND: Aspirin-exacerbated respiratory disease can be diagnosed with oral aspirin challenges and treated with aspirin desensitization. OBJECTIVE: To evaluate whether controller medications, particularly leukotriene modifier drugs, taken during oral aspirin challenges can reduce the risk of severe asthmatic responses. METHODS: The medical records of 676 patients who had undergone oral aspirin challenges, followed by aspirin desensitization, were reviewed. Asthmatic responses were stratified based on severity of bronchospastic response or lack of response. The effect of pretreatment with controller medications on the outcome of oral aspirin challenges was measured. RESULTS: Leukotriene modifier drugs had the most significant effect in protecting the lower airways from severe reactions (P = .004). The protective effect of leukotriene modifier drugs was observed in patients already taking systemic corticosteroids, where the addition of leukotriene modifier drugs significantly shifted the response toward a milder asthmatic response (P < .001). CONCLUSION: Protection from significant aspirin-induced bronchospasm during oral aspirin challenge can be accomplished with leukotriene modifier drugs. The use of a combination of inhaled corticosteroids, long-acting beta-agonists, systemic corticosteroids, and leukotriene modifier drugs stabilized underlying airways in preparation for a reasonably safe and accurate oral aspirin challenge. However, only pretreatment with leukotriene modifier drugs enhanced the safety of oral aspirin challenge in patients with aspirin-exacerbated respiratory disease by significantly decreasing the degree of asthmatic responses. Therefore, outpatient oral aspirin challenges in most well-selected patients appear to be a reasonable decision.

Acetates↗
PubMed2002

Clinical evidence of dose-dependent interaction between aspirin and angiotensin-converting enzyme inhibitors.

Since coronary artery and cerebrovascular diseases are the most common serious complications of long standing hypertension, there is a great potential for combining treatment with aspirin and angiotensin-converting enzyme inhibitors (ACE-I). However, the data regarding interaction of aspirin and ACE-I in relation to blood pressure control and survival benefits are controversial and inconclusive. We presumed that the appearance of dry cough in some of the patients following initiation of ACE-I treatment could be used as a marker for the presence of their influence, whereas ACE-I cough attenuation after addition of aspirin to treatment could be a sign of aspirin and ACE-I interaction on clinical level. The present study was aimed to use ACE-I induced cough as a clinical marker of ACE-I activity to determine whether dose-dependent aspirin and ACE-I interaction does exist. In a cohort of 750 consecutive ACE-I treated hypertensive and postinfarction outpatients we identified 78 (10.4%) non-smoking ACE-I related coughers. Out of them, 31 (21 men, 10 women; mean age 61 +/- 0.9 years) agreed to take part in the study, which was aimed to compare two regimens of combined ACE-I and aspirin treatment (self-matched control data): intermediate (500 mg daily) vs low-dose aspirin (100 mg daily). On each visit the life quality, cough severity (CS, 0-4) and frequency (CF, 0-10) scores were registered. Low doses of aspirin demonstrated an excellent safety profile and did not influence any life quality score and ACE-I induced cough. In contrast, intermediate doses completely abolished cough in 17 patients and reduced coughing in other 11 patients. Cough severity and cough frequency scores decreased, respectively, from 2.7 +/- 1.1 to 0.7 +/- 1.2 (P < 0.001) and from 7.1 +/- 2.3 to 2.0 +/- 2.2 (P < 0.0001). Overall, the cough frequency score method alone could identify a clear modification of cough in 26 (84%) patients, and cough severity score method alone in 24 (77%). Using the combined frequency/severity score method a modification of cough could be identified in 28 (90%) of the patients receiving intermediate dose of aspirin. Aspirin did not influence heart rate and blood pressure control either in hypertensives or in postinfarction patients. We conclude that using ACE-I induced cough as a clinical marker of ACE-I activity demonstrates that an interaction between ACE-I and aspirin at 500 mg/day does exist. We did not find any evidence supporting the presence of a clinically significant interaction between ACE-I and aspirin at 100 mg/day. Thus, combined treatment by low dose aspirin and ACE-I seems to be both safe and useful.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Protection against aspirin-induced human gastric mucosal injury by bosentan, a new endothelin-1 receptor antagonist.

BACKGROUND: Gastric ulceration induced by aspirin and by non-steroidal anti-inflammatory drugs (NSAIDs) is a major clinical problem. The mechanism of injury is unclear. There is evidence that NSAID-induced injury may cause endothelin activation. Endothelin-induced vasoconstriction has been shown to be capable of causing gastric ulceration. AIM: To investigate whether acute gastroduodenal injury induced in humans by aspirin can be prevented by the endothelin-1 antagonist, bosentan. METHODS: Eighteen healthy volunteers each received 5 x 900 mg aspirin every 12 h on three separate occasions (with either placebo, bosentan 700 mg or misoprostol 400 mg). Treatment order was randomized by Latin square design. Subjects were endoscoped and erosions counted before and 90 min after the first and last dose of aspirin. Plasma concentrations of bosentan were measured up to 5 h post-dose. RESULTS: There was a significant reduction in the mean number of erosions in the aspirin plus bosentan and aspirin plus misoprostol groups after the first dose of aspirin, compared with controls (aspirin plus placebo) (P<0.05). This was not sustained after the fifth dose of aspirin in the aspirin plus placebo and aspirin plus bosentan groups, but was still present in the aspirin plus misoprostol group. The mean plasma concentration of bosentan measured 3.5 h post-dose fell from 4510 (95% CI: 2791-6230) ng/mL after the 1st dose to 2508 (95% CI: 1733-3283) ng/mL after the 5th dose (P = 0.02). CONCLUSION: Endothelin receptor antagonism by bosentan can protect the gastric mucosa against aspirin damage. After five doses, bosentan levels fell, possibly because of enzyme induction, and protection was no longer evident. Further investigation is needed to assess whether higher doses would be effective.

Adult↗
PubMed1998

Aspirin for primary prevention of cardiovascular events.

OBJECTIVE: The use of aspirin for primary prevention of cardiovascular events in the general population is controversial. The purpose of this study was to create a versatile model to evaluate the effects of aspirin in the primary prevention of cardiovascular events in patients with different risk profiles. DESIGN: A Markov decision-analytic model evaluated the expected length and quality of life for the cohort's next 10 years as measured by quality-adjusted survival for the options of taking or not taking aspirin. SETTING: Hypothetical model of patients in a primary care setting. PATIENTS: Several cohorts of patients with a range of risk profiles typically seen in a primary care setting were considered. Risk factors considered included gender, age, cholesterol levels, systolic blood pressure, smoking status, diabetes, and presence of left ventricular hypertrophy. The cohorts were followed for 10 years. Outcomes were myocardial infarction, stroke, gastrointestinal bleed, ulcer, and death. MAIN RESULTS: For the cases considered, the effects of aspirin varied according to the cohort's risk profile. By taking aspirin, the lowest-risk cohort would be the most harmed with a loss of 1.8 quality-adjusted life days by taking aspirin; the highest risk cohort would achieve the most benefit with a gain of 11.3 quality-adjusted life days. Results without quality adjustment favored taking aspirin in all the cohorts, with a gain of 0.73 to 8.04 days. The decision was extremely sensitive to variations in the utility of taking aspirin and to aspirin's effects on cardiovascular mortality. The model was robust to other probability and utility changes within reasonable parameters. CONCLUSIONS: The decision of whether to take aspirin as primary prevention for cardiovascular events depends on patient risk. It is a harmful intervention for patients with no risk factors, and it is beneficial in moderate and high-risk patients. The benefits of aspirin in this population are comparable to those of other widely accepted preventive strategies. It is especially dependent on the patient's risk profile, patient preferences for the adverse effects of aspirin, and on the level of beneficial effects of aspirin on cardiovascular-related mortality.

Aspirin↗