Prior Aspirin Use Research Articles

Does prior use of aspirin affect outcome in ischemic stroke?

BACKGROUND: Large intervention studies suggest that aspirin may reduce mortality when given to patients who present with strokes or transient ischemic attacks. We sought to determine whether patients who were already using aspirin at the time of an ischemic stroke had a lower mortality than those who were not. METHODS: A prospective cohort study was undertaken in patients (mean age 76 ± 15 years) with acute ischemic stroke. Detailed information on demography, stroke characteristics, and aspirin use prior to the stroke was collected from patients, medical records, and other sources. Patients were classified by cause and subtype of stroke using standard criteria. Mortality was measured 4 weeks after the initial episode. RESULTS: Of the 1,457 patients, 650 (45%) were using aspirin (median dose 75 mg; range 75 to 300 mg) prior to the stroke. Prior use of aspirin was associated with lower 4-week mortality (14% versus 20%, P <0.01). Beneficial effects of prior aspirin use on mortality were seen in patients with atherosclerotic strokes (15% versus 21%, P <0.05) and with cardioembolic strokes (21% versus 34%, P <0.05), but not among patients with strokes due to small vessel occlusion (10% versus 11%, P = 0.8). Prior aspirin use was also associated with lower mortality in patients in whom the cause of ischemic stroke could not be determined (15% versus 22%, P <0.01). The effect of prior aspirin use on mortality was independent of age, gender, other risk factors, and use of other medication. CONCLUSIONS: Prior use of low-dose aspirin may be associated with a small but significant reduction in stroke mortality.

Factors associated with failure of medical therapy in patients with unstable angina and non-Q wave myocardial infarction. A TIMI-IIIB database study.

Current management of patients with unstable angina and non-Q wave myocardial infarction generally consists of intensive medical therapy, with angiography and revascularization sometimes limited to those who fail such therapy. To determine if certain baseline characteristics are predictive of patients who fail medical therapy, since such patients could then be expeditiously directed to a more invasive strategy in a cost-effective manner. The study cohort consisted of the 733 patients in the Thrombolysis in Myocardial Ischemia (TIMI) IIIB study who were randomized to conservative strategy. Patients were to be treated with bedrest, anti-ischaemic medications, aspirin, and heparin, and were to undergo risk-stratifying tests, consisting of an exercise test with ECG and thallium scintigraphy, scheduled to be performed within 3 days prior to, or 5 days after, hospital discharge and 24 h Holter monitoring scheduled to begin 2-5 days after randomization. Baseline clinical and ECG characteristics were compared between patients who 'failed' medical therapy and those who did not 'fail'. Failure was defined using clinical end-points (death, myocardial infarction, or spontaneous ischaemia by 6 weeks after randomization) or a strongly positive risk-stratifying test. For each test an ordered failure profile of results was calculated and consisted of death, myocardial infarction, or rest ischaemia occurring prior to performance of the test, a markedly abnormal test result, and no abnormality. Clinical end-points occurred in 241 (33%) patients and were more likely to occur in patients who at presentation were older, had ST-segment depression on the qualifying ECG, or were being treated with heparin or aspirin. Characteristics independently predictive of developing a clinical event or an abnormal exercise treadmill test included: ST-segment depression on the qualifying ECG, history of prior angina, family history of premature coronary disease (i.e. onset <55 years of age), prior use of heparin or aspirin, and increasing age. By combining these baseline risk characteristics for each outcome the incidence of developing a clinical event ranged from 8% if none was present to 63% if all six were present, and of developing a markedly abnormal risk stratifying test from 8-21% if none were present to approximately 90% if all six were present. Baseline characteristics associated with developing a clinical event or a markedly abnormal risk stratifying test were similar: rest anginal episode accompanied by ST-segment depression and occurring despite treatment with aspirin and heparin, a history of angina, older age, and family history of coronary disease. Patients with these characteristics are appropriate candidates for expeditious cardiac catheterization and consideration for revascularization, while patients without them may be suitable for medical management alone.

Prior aspirin use predicts worse outcomes in patients with non–ST-elevation acute coronary syndromes

Aspirin is beneficial in the prevention and treatment of cardiovascular events, but patients who have events while taking aspirin may have worse outcomes than those not on aspirin. We investigated the association between prior aspirin use and clinical outcomes in 9,461 patients with non–ST-elevation acute coronary syndromes enrolled in the Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial, before and after adjustment for baseline factors. We also examined whether eptifibatide has a differential treatment effect in prior aspirin users. Prior aspirin users were less likely to have an enrollment myocardial infarction (MI) (vs unstable angina) (43.9% vs 48.8%, p = 0.001) but more likely to have death or MI at 30 days (16.1% vs 13.0%, p = 0.001) and at 6 months (19.9% vs 15.9%, p = 0.001). After adjustment, prior aspirin users remained less likely to have an enrollment MI (odds ratio 0.88, 95% confidence interval 0.79 to 0.97) and more likely to have death or MI at 30 days (odds ratio 1.16, 95% confidence interval 1.00 to 1.33) but not at 6 months (odds ratio 1.14, 95% confidence interval 0.98 to 1.33). In a multivariable model, eptifibatide did not have a different treatment effect in prior aspirin users compared with nonusers (p = 0.534). Prior aspirin users had fewer enrollment MIs but worse long-term outcomes than nonusers. We found no evidence for a different treatment effect of eptifibatide in prior aspirin users.

Prior Aspirin use Potentiates the Effect of GP IIb/IIIa Inhibition in Patients With Non-ST Elevation Acute Coronary Syndromes

Prior Aspirin use Potentiates the Effect of GP IIb/IIIa Inhibition in Patients With Non-ST Elevation Acute Coronary Syndromes

Acute myocardial infarction mortality related to use of calcium antagonists before admission to hospital.

We investigated whether prior use of calcium antagonists in 80 (16.8%) out of 477 patients (64% males) admitted with acute myocardial infarction (MI) had any impact on in-hospital mortality. Patients using calcium antagonists were slightly older (74 years vs. 72 years, 2P = 0.039) than those not taking them and fewer were male patients. Previous MI, diabetes mellitus, and prior use of aspirin, beta-blockers, and long-acting nitrates were more frequent in patients on calcium antagonists. In contrast, fewer patients on calcium antagonists prior to symptoms received thrombolytic treatment (21.3% vs. 34.8%, 2P = 0.018). The study had an observational exposed/nonexposed design, and we looked for both crude and adjusted effects. Of the 83 patients (17.4%) who died during hospitalization, 18 patients were in the calcium antagonist group (22.5%). The odds ratio (OR) for these patients to die in the hospital was 1.48 and the 95% confidence interval (CI) 0.78-2.78; 2P = 0.19. When adjusting for confounders (gender, age, smoking habit, previous MI, and diabetes mellitus, as well as prior use of aspirin, beta-blockers, long-acting nitrates, and thrombolytic treatment at entry) OR was 1.08 and 95% CI 0.57-2.05; 2P = 0.85. Thus, we found no excess in-hospital mortality in patients with acute MI using calcium antagonists prior to the onset of symptoms.

Prior aspirin use potentiates the effect of GP IIb/IIIa inhibition in patients with non-ST elevation acute coronary syndromes

Prior aspirin use potentiates the effect of GP IIb/IIIa inhibition in patients with non-ST elevation acute coronary syndromes

The influence of prior and concurrent use of aspirin and vitamins on cognitive function scores in elderly Japanese-American men : K.H. Masaki, L.R. White, H. Petrovitch, G.W. Ross, J.D. Curb, E. Ardo, J. Grove. The Honolulu Heart Program (347 N. Kuakini Street, Honolulu, HI 96817, USA), University of Hawaii, NIA (NIH) and VA Honolulu

The influence of prior and concurrent use of aspirin and vitamins on cognitive function scores in elderly Japanese-American men : K.H. Masaki, L.R. White, H. Petrovitch, G.W. Ross, J.D. Curb, E. Ardo, J. Grove. The Honolulu Heart Program (347 N. Kuakini Street, Honolulu, HI 96817, USA), University of Hawaii, NIA (NIH) and VA Honolulu

Effects of prior use of non-steroidal anti-inflammatory drugs on renal function and transfusion requirements after upper gastrointestinal haemorrhage.

The possibility has been investigated that, after admission to hospital with acute upper gastrointestinal bleeding, patients who have been users of aspirin and non-aspirin non-steroidal anti-inflammatory drugs have poorer baseline renal function, a greater improvement in renal function during their hospital stay, and a larger transfusion requirement than non-users. Patients over 50 years of age admitted to public hospitals with acute upper gastrointestinal bleeding were studied. Creatinine clearance was estimated from serum creatinine and the transfusion requirement was recorded as the number of units of blood transfused on Day 1 and throughout the entire hospital stay. Data were obtained prospectively from case notes and by structured interview. Users of non-steroidal anti-inflammatory drugs were significantly older than non-users. The estimated creatinine clearance on admission to hospital declined with age. Creatinine clearance was 13.2 (95% CI 6.0 to 20.4) ml.min-1 lower in users than non-users of non-aspirin non-steroidal anti-inflammatory drugs. However, the difference was attributable to the older age of the drug users rather than to the drugs themselves. On average, the increase in creatinine clearance during hospital stay was the same in users and non-users of non-aspirin non-steroidal anti-inflammatory drugs. Prior use of aspirin had no effect on any measure of renal function. The incidence of blood transfusion was higher in older than in younger patients but neither the incidence of transfusion, nor the transfusion requirement, was different between users and non-users of non-aspirin non-steroidal anti-inflammatory drugs and aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)

Stroke and acute Myocardial Infarction in the Thrombolytic era: Clinical correlates and long-term prognosis

Thirteen (1.8%) of 708 patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I, II and III trials developed a stroke. Four strokes were hemorrhagic and nine were nonhemorrhagic. Of five prespecified risk factors for intracranial hemorrhage (age >65 years, history of hypertension, history of prior cerebrovascular disease, aspirin use and acute hypertension), two patients had two risk factors and one patient had one risk factor. However, 80% of patients without intracranial hemorrhage had at least one risk factor and 31% had two risk factors. No patient with a prior stroke or transient ischemic attack (all >6 months previously) had an intracranial hemorrhage.Of three prespecified risk factors for nonhemorrhagic stroke (atrial fibrillation, prior cerebrovascular disease and large anterior wall infarction), only the occurrence of a large anterior myocardial infarction (with ejection fraction <45%) was a predictor (p = 0.0015).The in-hospital death rate was 25% for patients with hemorrhagic stroke versus 11% for patients with a non-hemorrhagic stroke and 6% for those patients without a stroke. Furthermore, the hospital stay was >50% longer in patients who had a stroke than in those who did not.Thus, intracranial hemorrhage remains an unpredictable risk in patients treated with thrombolytic therapy and cerebral infarction is related to anterior myocardial infarction and poor left ventricular function. Both types of stroke are associated with substantial morbidity and mortality.

Fatal peptic ulcer complications and the use of non-steroidal anti-inflammatory drugs, aspirin, and corticosteroids.

Although non-steroidal anti-inflammatory drugs are known to cause peptic ulcer and its complications, controversy exists about the number of deaths from ulcer which are attributable to their use. A case-control study was therefore performed to determine whether prior use of non-steroidal and other anti-inflammatory compounds was associated with an increased case fatality rate from complications of peptic ulcer. Non-steroidal anti-inflammatory drugs were used by 39% of a series of 80 patients who had died from peptic ulcer complications and by 37% of 160 controls who were survivors matched for sex, age, ulcer site, and nature of complication (odds ratio 1.1; 95% confidence interval 0.6 to 2.1). Similarly, the rates of prior use of aspirin by cases and controls were almost identical (odds ratio 1.2; 95% confidence interval 0.5 to 1.9). Thus neither nonsteroidal anti-inflammatory drugs nor aspirin were associated with increased case fatality rates from peptic ulcer complications. In contrast, corticosteroids were associated with an increased mortality (odds ratio 4.2; 95% confidence interval 0.9 to 25.6). Although this increase in the estimated relative risk was not statistically significant, a review of the case records indicated that most deaths in steroid users were due to serious sepsis, indicating that there might be a causal association between use of the drugs and the mode of death.

The aggregation of human platelets by ascitic fluid. a mechanism for the disseminated intravascular coagulation (DIC) complicating leveen shunts

Disseminated intravascular coagulation (DIC) is a common problem in patients with LeVeen shunts. There is little doubt that this is caused by the infusion of ascitic fluid into the systemic circulation since ligation of the shunt is associated with cessation of DIC and patients who do not develop this complication usually have non-functioning shunts. The factor in the ascitic fluid responsible for the precipitation of DIC has not been previously recognized. This study is concerned with the effects of ascitic fluid on human platelets and offers an explanation for the mechanism of DIC post-LeVeen shunts. The addition of ascitic fluid concentrated 5-fold to platelet rich plasma resulted in marked platelet aggregation which was inhibited by EDTA and adenosine. No aggregation was observed when aspirin treated platelets were used. The aggregating activity could be precipitated by high-speed ultracentrifugation at 100,000 g for 60 min. The pre-incubation of the aggregating fluid with collagenase resulted in . complete loss of aggregation. These findings suggested that the aggregating factor was collagen. This was confirmed by a hydroxyproline assay and the finding of a brand corresponding to type I collagen on SDS polyacrylamide gel electrophoresis. Besides its ability to activate platelets, collagen can also activate the contact clotting factors, namely factors XI and XII. This dual activation would result in significant thrombin generation with the development of DIC in vivo . Preliminary experiments in rabbits indicate that the infusion of collagen obtained from ascitic fluid precipitates DIC which is prevented by the prior use of aspirin. The role of aspirin in the prevention or modification of DIC post-LeVeen shunts in man needs to be explored.