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PubMed1993

Airway responsiveness to leukotriene C4 (LTC4), leukotriene E4 (LTE4) and histamine in aspirin-sensitive asthmatic subjects.

We wanted to determine whether the airway response to inhaled leukotriene C4 (LTC4) is similar to inhaled leukotriene E4 (LTE4) in aspirin-sensitive asthma and, therefore, determined airway responsiveness to histamine, LTC4 and LTE4 in seven aspirin-sensitive subjects and 13 control asthmatic subjects, who were tolerant of aspirin. The concentration of inhaled lysine-aspirin which produced a 15% fall in forced expiratory volume in one second (FEV1) (PC15) was determined in aspirin-sensitive asthmatic subjects. The dose of histamine, LTC4 and LTE4 which produced a 35% fall in specific airways conductance (PD35sGaw) was determined by linear interpolation from the log dose response curve. There was no correlation between the PC15 for lysine-aspirin and the airway reactivity to inhaled LTC4 or LTE4. There was no difference in airway response to histamine and LTC4 between any of the groups of asthmatic subjects. There was a rank order of potency LTC4 > LTE4 > histamine in both groups, with LTC4 approximately 1,000 fold more potent than histamine in both groups. Aspirin-sensitive asthmatic subjects were significantly more responsive to LTE4 (p = 0.02) than aspirin-tolerant asthmatic subjects. The relative responsiveness of LTE4 to histamine (PD35 histamine/PD35 LTE4) was significantly greater in aspirin-sensitive asthmatic subjects compared to aspirin-tolerant asthmatic subjects (p = 0.05). There was no difference in relative responsiveness of LTC4 to histamine between aspirin-sensitive or aspirin-tolerant asthmatic subjects. We conclude that the airways of aspirin-sensitive asthmatic subjects demonstrate a selective hyperresponsiveness to LTE4, which is not observed for LTC4.

Adolescent↗
PubMedDate not supplied

Aspirin in ischemic heart disease--an overview.

Aspirin is one of the oldest and most commonly used nonprescription drugs in the world. Although commonly it is used for relief from common headache and muscular pain, its use in the prevention and treatment of platelet related complications in cardiovascular diseases (CVD) and cerebrovascular disease (CBVD) is quite controversial. A brief review of the major aspirin trials indicated that a full strength aspirin taken daily had no significant beneficial effect in reducing mortality of patients with CVD/CBVD. However, two major trials (ISIS-2, PHS) in which either low dose aspirin (160 mg) or one aspirin administered every other day, have demonstrated significant reduction in fatal and nonfatal cardiovascular events. Even a dose as low as 1 mg aspirin per day significantly lowers platelet thromboxane synthesis. As a result of these studies, low dose aspirin should be the choice of prophylactic therapy aimed at the inhibition of platelet cyclooxygenase activity. Controlled-release low dose aspirin may favorably reduce platelet thromboxane production and spare vascular prostacyclin synthesis. At least 100 mgs of aspirin per day are essential to completely inhibit steady state thromboxane formation. Low dose aspirin (160 mgs) has been shown to be as effective as the full strength aspirin (325 mgs) in reducing clinical complications related to platelet activation. The antithrombotic effect of aspirin is well established and improved formulations, well thought out therapeutic protocols, customized dosage, appropriate timing of delivery, a better understanding of platelet function and pathophysiology of CUD/CBUD will facilitate maximization of the beneficial effects of aspirin.

Arachidonic Acid↗
PubMed1999

Mis-medication and Under-utilization of Aspirin in the Prevention and Treatment of Cardiovascular Disease.

CONTEXT: Aspirin has been clearly established as an important therapy in the secondary prevention of cardiovascular disease (CVD), and also plays a role in primary prevention. OBJECTIVE: To determine the prevalence of use of aspirin or other over-the-counter analgesics to prevent or treat CVD. DESIGN: Representative national survey conducted in 1996. SETTING: National Family Opinion (NFO) Mail Panel. PARTICIPANTS: 23,158 persons aged 40 or older with no prior CVD, and 3818 who reported prior CVD. MAIN OUTCOME MEASURES: Use of aspirin and other over-the-counter (OTC) analgesics to prevent or treat cardiovascular problems. RESULTS: Overall, 10% of survey respondents reported regular use of any analgesic for primary prevention, and 8% specifically reported using aspirin. The prevalence of aspirin use was associated with age and cardiovascular risk factors, including overweight, family history of heart problems, high cholesterol, and high stress. Of those reporting analgesic use, 11% used only non-aspirin analgesics to prevent CVD, and an additional 10% used these with aspirin. Such mis-medication was greater in women than in men, but was not related to age. Among those reporting prior CVD, only 43% used aspirin for secondary prevention. Of those using analgesics, 11% used only non-aspirin products and an additional 14% used these with aspirin. We project that 1.3 million people nationally may be erroneously taking non-aspirin products for CVD prevention, with another 1.4 million taking these along with aspirin. CONCLUSION: Efforts to increase public awareness and advocate the appropriate use of aspirin are needed, and could have an important impact on public health.

Journal Article↗
PubMed2001

Effects of low-dose aspirin on endothelial function in hypertensive patients.

BACKGROUND: It has been reported that administration of low-dose aspirin significantly reduces the frequency of major cardiovascular events in patients with hypertension and coronary artery disease. It is generally considered that the preventative effects of long-term aspirin administration on major cardiovascular events are due to the inhibition of platelet aggregation. HYPOTHESIS: It is not known whether administration of low-dose aspirin restores endothelium-dependent vasodilatation, and this study was undertaken to prove or disprove this question in patients with hypertension. METHODS: Flow-mediated endothelium-dependent dilatation and glyceryl trinitrate-induced endothelium-independent dilatation were investigated in 18 hypertensive patients and 10 normotensive control subjects. In the hypertensive patients, flow-mediated dilatation was investigated and cyclic guanosine monophosphate plasma (cGMP) was measured before and at 8 weeks after the administration of 162 mg of aspirin. RESULTS: Flow-mediated dilatation before aspirin administration was more reduced in the hypertensive patients than in the control subjects (6.4+/-2.0% vs. 11.3+/-2.3%, p <0.0001). Glyceryl trinitrate-induced dilatation before aspirin administration was similar in hypertensive patients and control subjects. Flow-mediated dilatation after aspirin administration was improved compared with that before aspirin administration (10.4+/-3.5% vs. 6.4+/-2.0%, p<0.0004). The cGMP product after aspirin administration was significantly higher than that before aspirin administration. CONCLUSIONS: Administration of low-dose aspirin may restore the endothelium-dependent vasodilatation in hypertensive patients. Furthermore, increased nitric oxide production may play a partial role in the improvement in endothelial function induced by administration of low-dose aspirin.

Aged↗
PubMed1999

Production of prostanoids and nitric oxide by infarcted heart in situ and the effect of aspirin.

The production of prostacyclin (PGI2) and thromboxane A2 (TXA2) in infarcted and noninfarcted portions of the rabbit heart was studied prior to and following administration of acetylsalicylic acid (aspirin). Aspirin was administered intravenously (iv) as water-soluble Aspisol, d-lysinmono (acetylsalicylate) (Bayer, Leverkusen, Germany) into an ear vein. A branch of the left circumflex coronary artery was ligated. The animals were divided into three groups. The first group received 150 mg/kg/day of aspirin (75 mg/kg of aspirin every 12 h, n = 10). The first administration of aspirin was 1 h after ligation of the coronary artery and the last injection was 1 h before euthanasia. The second group received 5 mg/kg/day of aspirin (every 24 h, n = 10). A separate group of rabbits not receiving aspirin served as controls (n = 12). Two days following onset of ischemia, inducible form of nitric oxide synthase (iNOS) was measured in heart muscle and the oxidation products of nitric oxide (nitrite, NO-2 plus nitrate, NO-3: their sum referred to as NOx) were determined in arterial and coronary venous blood. Concentrations of both PGI2 and TXA2 were elevated in the infarcted portions of the heart compared to the noninfarcted regions. Formation of prostanoids was accompanied by increased activation of iNOS. Both doses of aspirin diminished the concentrations of PGI2 and TXA2 in infarcted heart muscle; in contrast, small doses of aspirin failed to influence myocardial iNOS activity. Apparently small doses of aspirin changed the relationship of iNOS to cyclooxygenase (COX). Coronary arterial-venous difference of NOx and myocardial iNOS activity showed parallel increases. Diminution of prostacyclin by aspirin can damage gastric mucosa and interfere with vasodilatation. Since NO counters these deficiencies, a combination of aspirin with a nitric oxide donor may be advantageous.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Low-dose aspirin before spinal surgery: results of a survey among neurosurgeons in Germany.

The main problem faced by the increasing numbers of patients presenting for spinal surgery are receiving concurrent medication with low-dose aspirin, leading to dysfunctional circulating platelets. The contribution of low-dose aspirin to increased peri-operative risk of bleeding and blood loss is a contentious issue with conflicting published results from different surgical groups. Data from neurosurgical spine patients is sparse, but aspirin has been identified as an important risk factor in the development of post-operative hematoma following intracranial surgery. We surveyed the opinions and working practices of the neurosurgical facilities performing spinal operations in Germany regarding patients who present for elective spinal surgery. Identical questionnaires were sent to 210 neurosurgical facilities and proffered five main questions: (1) the adherence of any policy of stopping aspirin pre-operatively, (2) the personal risk assessment for patients with spinal surgery under low-dose aspirin medication, (3) the preferred method of treatment for excessive bleeding in this context, (4) personal knowledge of hemorrhagic complications in this group of patients, and (5) the characteristics of the neurosurgical units concerned. There were 145 (69.1%) responses of which 142 (67.6%) were valid. Of the respondents, 114 (80.3%) had a (written) departmental policy for the discontinuation of pre-operative aspirin treatment, 28 (19.7%) were unaware of such a policy. The mean time suggested for discontinuation of aspirin pre-operatively was 6.9 days (range: 0-21 days), with seven respondents who perform the operations despite the ongoing aspirin medication. Ninety-four respondents (66.2%) considered that patients taking low-dose aspirin were at increased risk for excessive peri-operative hemorrhage or were indetermined (8.6%), and 73 (51.4%) reported having personal experience of such problems. Ninety-two respondents (65.5%) would use special medical therapy, preferably Desmopressin alone or in combination with other blood products or prohemostatic agents (46.1%), if hemorrhagic complications developed intra- or post-operatively. The average number of spinal operations per year in each service was 607.9 (range: 40-1,500). Despite the existence of distinct departmental policies concerning the discontinuation of low-dose aspirin pre-operatively in the majority of neurosurgical facilities performing spinal operations, there is a wide range of the moment of this interruption with an average of 7 days. Two-thirds of the respondents felt that aspirin was a risk factor for hemorrhagic complications associated with spinal procedures, and more than half of the interviewees reported having personal experience of such problems. Finally, various medicamentous methods of counteracting aspirin-induced platelet dysfunction and excessive bleeding in this context are elicited, discussed and evaluated.

Aspirin↗
PubMed2005

The role of exercise on platelet aggregation in patients with stable coronary artery disease: exercise induces aspirin resistant platelet activation.

OBJECTIVES: The aim of our study was to determine the relation between exercise stress test and aspirin resistance in patients with stable coronary artery disease. BACKGROUND: Clinically aspirin resistance is defined as having thrombotic and embolic cardiovascular events despite regular aspirin therapy. METHODS: We studied platelet functions of 62 patients with stable coronary artery disease and 20 subjects with normal coronary arteries by Platelet Function Analyzer (PFA-100, Dade Behring, Germany) at rest and after exertion with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP cartridges. Closure time (CT)<186 seconds was defined as aspirin resistance with Col/Epi cartridges of PFA-100. Symptom limited treadmill stress test (protocol of Bruce) was performed with Oxford Streslink TD-1 system. RESULTS: 8 (12.9%) patients were aspirin resistant by PFA-100 (CT<186s despite regular aspirin therapy) at rest. At the first minute of the recovery period of exercise stress test 14 (22.5%) patients were aspirin resistant by PFA-100. CTs with Col/ADP were respectively 89+/-6 s (83--100s) and 89+/-5 s (82--104s) at rest and after exercise (p=0.107). 20.3% (11/54) of patients known as in vitro aspirin sensitives at rest had shorter CTs and 11.1% (6/54) had aspirin resistance after exercise (p=0.004). There was no statistically significiant difference in platelet functions in the control group after exertion. CONCLUSION: We conclude that 11.1% of in vitro aspirin sensitive subjects at rest had aspirin resistance after exercise by PFA-100. In some individuals, exercise induced platelet activation is aspirin insensitive at usual antiplatelet doses. We need further clinical trials to optimize antiplatelet therapy in patients with coronary artery disease.

Adult↗
PubMed2006

The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events.

BACKGROUND: Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. AIM: The aim of our study was to determine; the prevalence of aspirin resistance in patients with acute coronary syndromes, the role of aspirin resistance on outcome in the follow-up and the effect of clopidogrel therapy in the prevention of MACE in aspirin resistant subjects. MATERIAL AND METHODS: We detected the prevelance of aspirin resistance in 105 patients with acute coronary syndrome. Platelet functions were analyzed in Platelet Function Analyzer (PFA)-100 (Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP (Col/ADP) cartridges. Primary end points of the study were myocardial infarction, unstable angina, cardiac death. RESULTS: 19% (n = 20) of patients were aspirin resistant by PFA-100. In the follow-up, MACE occured in 9 patients (45%) with aspirin resistance and in 10 patients (11.7%) with aspirin sensitive platelet aggregation (p = 0.001). Multivariate analysis showed that aspirin resistance was an independant predictor of MACE. The prevalence of MACE in patients who were on clopidogrel treatment for 12 months were lower compared to those who were on a clopidogrel treatment for the first six months (p = 0.040). CONCLUSIONS: We determined that the MACE risk in patients with acute coronary syndromes having detected aspirin resistance, was higher at statistically significant levels compared to patients having aspirin sensitive platelet aggregation. Our results showed that aspirin resistance, was an independant predictor of MACE in patients with acute coronary syndrome.

Angina, Unstable↗
PubMed1991

Aspirin does not inhibit cholesterol cholelithiasis in two established animal models.

The effect of aspirin on cholesterol cholelithiasis was examined in the hamster and the prairie dog. In the prairie dog, diets were composed of semipurified components of chow, plus cholesterol (1.2%), with and without aspirin. Animals were studied for either 2 weeks or 4 weeks. Cholesterol gallstones were present in all groups at the end of each period; aspirin did not alter the incidence of cholelithiasis. All animals studied had cholesterol crystals in the bile when they were killed. Liver cholesterol levels in prairie dogs with and without aspirin tended to be lower in animals fed chow than in animals fed semipurified diets. There were no significant differences in cholesterol levels in the plasma or bile. The cholesterol saturation index of all biles approached unity when animals were fed chow with aspirin; animals fed the semipurified diets had cholesterol saturation indices of less than 1.0. The prairie dogs fed aspirin plus cholesterol in the semipurified diet showed increased levels of biliary chenodeoxycholic acid amidates and concomitant decreased levels of cholic acid amidates compared with animals fed the same diet without aspirin. Hamsters fed aspirin plus cholesterol in a semipurified diet tended to have a greater incidence of gallstones than animals given no aspirin (80% vs. 55%). Liver and bile cholesterol levels were similar with and without aspirin; plasma cholesterol levels increased significantly with aspirin [14.20 vs. 7.80 mmol/L (549 vs. 301 mg/dL)]. Lithogenic indices in all hamsters were above unity; biliary lipids, total lipid concentration, and biliary bile acid composition were similar. These results show that the addition of aspirin to a lithogenic diet does not reduce the incidence of cholelithiasis.

Animals↗
PubMed1991

Effect of aspirin on local prostaglandin production and serotonin accumulation in a canine model with coronary cyclic flow variations or thrombosis.

We have reported that thromboxane A2 and serotonin are two important mediators of coronary cyclic flow variations (CFVs) caused by recurrent platelet aggregation and dislodgement on a stenosed coronary arterial wall with endothelial injury. To test the hypothesis that blocking the synthesis of thromboxane A2 would not prevent serotonin release, 1.1, 4.6, and 9.2 mg/kg of aspirin were administered through the left atrium to 27 dogs with CFVs. The CFV elimination rate was 70% in the aspirin-treated dogs. Thromboxane B2 and serotonin concentrations were measured in different coronary arterial segments. There were significantly lower thromboxane B2 and 6-keto-PFG1a levels in the stenosed left arterior descending (LAD) segments with increasing dosage of aspirin-208 +/- 36, 24 +/- 31, 50 +/- 6 ng/g (P less than 0.0001) and 125 +/- 27, 58 +/- 38, 25 +/- 5 ng/g (P less than 0.0001), respectively. Serotonin levels were significantly higher in stenosed LAD (265.7 +/- 131.2 ng/g) than in LAD segments proximal or distal to the stenosis and in corresponding circumflex coronary artery segments, 17.1 +/- 3.7, 18.6 +/- 3.7, and 19.2 +/- 5.1 ng/g, respectively (P less than 0.05) following the highest dose of aspirin. In 41 additional dogs, electrical injury was used to initiate thrombosis in the circumflex artery and in those receiving aspirin (15 mg/kg) (n = 5), occlusive thrombus formation was inhibited. However, the local accumulation of serotonin was not significantly different between the control (194 +/- 27 ng/g) (n = 36) and the aspirin-treated group (167 +/- 19 ng/g) (n = 5). In vitro platelet aggregation induced by arachidonic acid was inhibited by the in vivo administration of 1.1 mg/kg of aspirin and abolished by 4.6 + 1.1 and 9.2 + 4.6 + 1.1 mg/kg of aspirin. However, serotonin-induced platelet aggregation was not affected following all doses of aspirin. Thus, aspirin eliminates CFVs in 70% of dogs, and markedly diminishes thromboxane A2 and prostacyclin concentrations in stenosed canine coronary arteries, but it does not prevent local serotonin accumulation. Similarly, aspirin prevents occlusive coronary thrombosis in dogs with electrically-induced endothelial injury, but it did not prevent local assumulation of serotonin. These experimental findings suggest that cyclo-oxygenese inhibition does not prevent serotonin accumulation at sites of coronary artery endothelial injury, and they thereby help provide a potential explanation of the lack of complete protection provided by aspirin in eliminating CFVs in this experimental model.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

The differential inhibition of prostaglandin synthesis in platelets and vascular tissue in response to aspirin.

Since aspirin inhibits the platelet as well as vascular prostaglandin synthesis it may therefore, paradoxically induce a thrombotic tendency when used as an antithrombotic agent. The in vivo effect of therapeutic doses of aspirin on the prostaglandin synthetic capacity of the rat platelets and vascular tissue was therefore studied to determine the significance of this paradoxical aspirin effect. A single aspirin dose of 5 mg/kg or greater was found to significantly decrease the synthesis of prostaglandin E by rat platelets. Even the normal augmentation of PGE synthesis by N-ethyl maleimide was significantly reduced by this single aspirin dose. In contrast, doses as high as 20 mg/kg of aspirin failed to reduce the production of 6-keto PGF1 alpha by aortic slices from rats pretreated with aspirin. These results indicate that the cyclo-oxygenase enzyme (CO) system in the prostaglandin biosynthetic pathway within blood vessel walls has the capacity to recover from this inhibitory effect of aspirin or it is less susceptible to inhibition than the CO in platelets. This relative resistance of CO to the inhibitory effects of aspirin may serve to protect the organism from excessive thrombotic tendencies brought about by the effect of aspirin on the vascular prostaglandin generating system. These results indicate that an aspirin dose of 5-10 mg/kg would be optimal if aspirin were to be used as an antithrombotic agent.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Implications of preoperative administration of aspirin in patients undergoing coronary artery bypass grafting. Department of Veterans Affairs Cooperative Study on Antiplatelet Therapy.

The perioperative consequences of preoperative aspirin administration were assessed in a large prospective cooperative study of 772 patients undergoing coronary artery bypass grafting. The 772 patients were randomized to receive either aspirin (325 mg once a day), aspirin (325 mg three times a day), aspirin plus dipyridamole (325 and 75 mg together three times a day) (aspirin group), sulfinpyrazone (267 mg three times a day) or placebo (nonaspirin group). The therapy, except in the aspirin group, was started 48 h before the operation. In all aspirin subgroups, one 325 mg aspirin dose was given 12 h before surgery and maintained thereafter according to the assigned regimen. Patients in the aspirin group had significantly more postoperative bleeding and received more packed blood cells and blood products than did patients in the nonaspirin group. Although total operative duration and cardiopulmonary bypass duration were not different, the interval between completion of cardiopulmonary bypass and wound closure was significantly longer (p = 0.035) in the aspirin group. Thirty-one (6.6%) of 471 patients in the aspirin group and 5 (1.7%) of 301 patients in the nonaspirin group also required reoperation for control of postoperative bleeding (p = 0.002). The site of bleeding found at reoperation was not different between the two groups. There was no difference in operative mortality rates, incidence of other bleeding complications or occurrence of other post-operative complications between the two groups. Thus, antiplatelet regimens involving preoperative initiation of aspirin therapy, which has been shown to improve graft patency, increase the risk of abnormal postoperative bleeding and the need for reoperation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed2005

The role of platelet glycoprotein IIIa polymorphism in the high prevalence of in vitro aspirin resistance in patients with intracoronary stent restenosis.

OBJECTIVES: The aim of our study was to determine the relation between platelet glycoprotein IIIa (Pl A ) polymorphism and aspirin resistance in patients with intracoronary stent restenosis. BACKGROUND: Clinically, aspirin resistance is defined as having thrombotic and embolic cardiovascular events despite regular aspirin therapy. Platelet glycoprotein IIIa polymorphism is said to be a possible mechanism of aspirin resistance. METHODS: We studied the prevalence of aspirin resistance in 204 previously intracoronary stent-implanted patients with stable coronary artery disease. In 102 of these patients, intracoronary stent restenosis was present. Platelet functions were analyzed in a platelet function analyzer (PFA-100, Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or adenosine diphosphate cartridges. Closure time <186 seconds was defined as aspirin resistance with Col/Epi cartridges of PFA-100. The Pl A polymorphisms of 43 aspirin-resistant and 51 aspirin-sensitive subjects were determined with polymerase chain reaction and restriction fragments length polymorphism. RESULTS: A total of 31.3% (n = 32) of patients with intracoronary stent restenosis and 10.7% (n = 11) of patients with patent intracoronary stents were resistant to aspirin by PFA-100. The Pl A1,A1 allele of glycoprotein IIIa was present in 36 subjects (83.7.%) and the Pl A1,A2 allele was present in 7 subjects (16.2.%) in the aspirin-resistant patients group. The Pl A1,A1 allele of glycoprotein IIIa was present in 37 subjects (72.5%) and the Pl A1,A2 allele was present in 14 subjects (27.5%) in the aspirin-sensitive patients group ( P = .195). CONCLUSION: Our results suggest that platelets of patients with intracoronary stent restenosis with or without Pl A2 heterozygosity of glycoprotein IIIa are more likely to be resistant to low-dose aspirin therapy.

Aged↗
PubMed2006

Risks and benefits of combining aspirin with anticoagulant therapy in patients with atrial fibrillation: an exploratory analysis of stroke prevention using an oral thrombin inhibitor in atrial fibrillation (SPORTIF) trials.

BACKGROUND: Aspirin is used in combination with anticoagulant therapy in patients with atrial fibrillation (AF), but evidence of additional efficacy is not available. METHODS: We compared ischemic events and bleeding in the SPORTIF III and IV randomized trials of anticoagulation with warfarin (international normalized ratio 2-3) or fixed-dose ximelagatran. Low-dose aspirin (<100 mg/d) was allowed based on prevailing guidelines. RESULTS: The 14% of patients receiving aspirin more often had diabetes (27.5% vs 23%, P < .01), coronary artery disease (69% vs 41%, P < .01), previous stroke or transient ischemic attack (26% vs 20%, P < .01), and left ventricular dysfunction (41% vs 36%, P < .01). Addition of aspirin to either warfarin or ximelagatran was associated with no reduction in stroke or systemic embolism. Major bleeding occurred significantly more often with aspirin plus warfarin (3.9% per year) than with warfarin alone (2.3% per year, P < .01), aspirin plus ximelagatran (2.0% per year), or ximelagatran alone (1.9% per year). The rate of myocardial infarction with aspirin and warfarin (0.6% per year) was not significantly different from that with ximelagatran alone (1.0% per year), warfarin alone (1.0% per year), or aspirin and ximelagatran (1.4% per year). CONCLUSIONS: Aspirin combined with anticoagulant therapy was associated with no reduction in stroke, systemic embolism, or myocardial infarction in patients with AF. Aspirin combined with warfarin was associated with an incremental rate of major bleeding of 1.6% per year. No increased major bleeding occurred with aspirin and ximelagatran. These results suggest that the risks associated with addition of aspirin to anticoagulation in patients with AF outweigh the benefit.

Aged↗
PubMed2005

Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary intervention.

Previous studies have shown that more complete platelet inhibition improves the coronary flow reserve (CFR), a measure of microvascular integrity, in patients undergoing percutaneous coronary intervention (PCI). We hypothesized that patients with aspirin resistance would have impaired CFR after elective PCI. We used VerifyNow Aspirin to determine the response to aspirin in 117 consecutive patients who underwent elective single-lesion PCI. The assay results are expressed quantitatively in Aspirin Reaction Units based on the degree of platelet aggregation. All patients received a 300-mg loading dose of clopidogrel >12 hours before and a 75-mg maintenance dose the morning of PCI. CFR was estimated using the Thrombolysis In Myocardial Infarction frame count method. Of the 117 patients, 22 (18.8%) were aspirin resistant. The clinical, angiographic, and procedural characteristics of the aspirin-sensitive and -resistant patients were balanced. All patients underwent successful PCI with <50% residual diameter stenosis and Thrombolysis In Myocardial Infarction grade 3 flow after PCI. Aspirin-resistant patients had a lower CFR than the aspirin-sensitive patients (1.42 +/- 0.35 vs 1.80 +/- 0.64, p = 0.018). Univariate correlates of CFR included the Aspirin Reaction Unit (r = -0.227, p = 0.014) and post-PCI creatine kinase-MB elevation (p = 0.048). Multivariate linear regression analysis revealed the Aspirin Reaction Unit to be the only independent determinant of CFR after PCI (r2 = 0.051, p = 0.014). Thus, aspirin resistance was associated with impaired CFR in patients who underwent elective PCI, implicating insufficient aspirin-induced platelet inhibition as a cause of microvascular dysfunction by distal atherothrombotic embolization and/or spasm.

Aged↗
PubMed2005

Aspirin use for the primary prevention of coronary heart disease in older adults.

PURPOSE: Aspirin for the primary prevention of coronary heart disease (has a more favorable risk/benefit profile among adults with high coronary heart disease risk than among low-risk adults, but there is little information on the current patterns of aspirin use for primary prevention. We determined the prevalence of aspirin use in relation to coronary heart disease risk and changes over time. SUBJECTS AND METHODS: We measured regular aspirin use in 2163 black and white older adults without cardiovascular disease in a population-based cohort from 1997 to 1998 and 2002 to 2003. We determined the 10-year coronary heart disease risk by using the Framingham risk score. RESULTS: In 1997-1998, 17% of the cohort were regular aspirin users. Aspirin use increased with coronary heart disease risk from 13% in persons with a 10-year risk less than 6% (low risk) to 23% in those with a 10-year risk greater than 20% (highest risk) (P for trend < .001). Blacks were less likely to use aspirin (13%) than whites (20%). In multivariate analysis, black race was still associated with lower aspirin use (odds ratio 0.66, 95% confidence interval 0.49-0.89). In 1997-1998 and 2002 to 2003, aspirin use increased from 17% to 32% among those still free of coronary heart disease (P < .001), and the association with coronary heart disease risk continued (P for trend < .001). Despite their high coronary heart disease risk, diabetic persons were not more likely to use aspirin than nondiabetic persons, even in 2002 and 2003 (odds ratio 0.89, 95% confidence interval 0.56-1.40). CONCLUSION: Regular use of aspirin by older adults with no history of cardiovascular disease has increased in recent years. Individuals at higher coronary heart disease risk are more likely to take aspirin, but there is room for considerable improvement in targeting those at high risk, particularly diabetic persons and blacks.

Aged↗
PubMed2005

Coronary syndromes following aspirin withdrawal: a special risk for late stent thrombosis.

OBJECTIVES: We sought to determine whether aspirin withdrawal is an encountered situation in coronary disease patients who relapsed. BACKGROUND: Despite the recognized benefits of aspirin in coronary disease, and because of the threat of bleeding or poor compliance, aspirin intake is sometimes stopped. It is not known whether withdrawal of aspirin can be harmful in coronary-disease patients. METHODS: Between September 1999 and April 2002, a total of 1,236 patients hospitalized for acute coronary syndrome (ACS) were questioned in order to determine whether aspirin intake had been interrupted. RESULTS: Fifty-one of these ACSs occurred within 1 month after aspirin withdrawal. This represents 4.1% of all coronary events but 13.3% of recurrences. Among those patients who relapsed, the incidence of ST-segment elevation ACS was higher in those who stopped aspirin when compared to the 332 patients who did not stop aspirin (39% vs. 18%; p = 0.001). Ten (20%) cases involved a thrombosis of an uncoated stent implanted on average 15.5 +/- 6.5 months previously. Mean delay between aspirin withdrawal and the acute coronary event was 10 +/- 1.9 days. Reasons for aspirin withdrawal included minor surgery in 7 cases, fibroscopy in 8 cases, dental treatment in 13 cases, bleeding in 3 cases, and patient non-compliance in 20 cases. CONCLUSIONS: Our results support the hypothesis that aspirin withdrawal in coronary patients may represent a real risk for the occurrence of a new coronary event. Many cases involved late uncoated-stent thrombosis. Assessment of the exact incidence of coronary recurrences after aspirin withdrawal will need prospective studies.

Aged↗
PubMed2004

Hypersensitivity to aspirin: common eicosanoid alterations in urticaria and asthma.

BACKGROUND: Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can precipitate adverse reactions in two apparently different clinical conditions: bronchial asthma and chronic idiopathic urticaria (CIU). Recent evidence indicates that the reactions are triggered by the drugs that inhibit cyclooxygenase-1 but not cyclooxygenase-2. OBJECTIVE: To assess whether patients with CIU and aspirin sensitivity share common eicosanoid alterations with patients who have aspirin-sensitive asthma. METHODS: Seventy-four patients with CIU and a history of sensitivity to aspirin and NSAIDs underwent placebo-controlled oral aspirin challenge tests. Concentrations of urinary leukotriene E4 (uLTE4) were measured by ELISA and plasma stable prostaglandin D2 metabolite, 9alpha,11beta prostaglandin F(2) by GC/MS. All measurements were carried out at baseline and after aspirin dosing. Patients were genotyped for the leukotriene C4 synthase (LTC4S) promoter single nucleotide polymorphism. RESULTS: In 30 of 74 patients, the aspirin challenge was positive, resulting in urticaria/angioedema. In these 30 patients, baseline uLTE4 levels were higher than in nonresponders and the healthy control subjects and increased further (significantly) after the onset of clinical reaction. No such increase occurred in subjects with negative aspirin challenge. Baseline uLTE4 levels correlated with severity of skin reactions. Plasma 9alpha,11beta prostaglandin F(2) levels rose significantly in both aspirin responders and nonresponders, although in the latter group the increase occurred later than in the former. In patients who reacted to aspirin, frequency of (-444)C allele of LTC4S was significantly higher than in patients who did not react. CONCLUSIONS: CIU with aspirin sensitivity is characterized by the eicosanoid alterations, which are similar to those present in aspirin-induced asthma.

Adult↗