Antiplatelet Effect of Aspirin in Patients With Cerebrovascular Disease

Alberts, Mark J.; Bergman, Deborah; Molner, Elise; Jovanovic, Borko; Ushiwata, Issei; Teruya, Jun

doi:10.1161/01.str.0000106763.46123.f6

Cited by 174 publications

(103 citation statements)

References 27 publications

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“…It would be important to repeat this study with assays of platelet inhibition. It should be noted however that studies using urinary or serum thromboxane levels, or the Platelet Function Assay-100 have found a dose response with low vs. higher doses of aspirin, which lend support to our observations [19][20][21][22][23][24] although both these methods, also have significant limitations themselves.…”

Section: Discussionsupporting

confidence: 83%

Aspirin administered to women at 100 mg every other day produces less platelet inhibition than aspirin administered at 81 mg per day: implications for interpreting the women’s health study

Swaim

Hillman

2008

J Thromb Thrombolysis

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We found significantly less inhibition of platelet function with the dose used in the WHS than the usual U.S. dose. We observed that the degree of platelet inhibition was significantly less with aspirin 100 mg every other day compared with aspirin 81 mg daily, suggesting that results of the Women's Health Study may have underestimated both the efficacy and toxicity of aspirin as it is commonly administered. These data need to be considered when developing recommendations about the use of aspirin in the primary prevention of cardiovascular disease in women.

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Section: Discussionsupporting

confidence: 83%

Aspirin administered to women at 100 mg every other day produces less platelet inhibition than aspirin administered at 81 mg per day: implications for interpreting the women’s health study

Swaim

Hillman

2008

J Thromb Thrombolysis

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“…There are some data suggesting an association between severity and frequency of acute vascular events and poor platelet response after ASA in patients with coronary artery disease [5]. A high prevalence of ASA resistance (28.0–65.0%) was also demonstrated among poststroke ASA users [6,7,8]. …”

Section: Introductionmentioning

confidence: 99%

Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Karepov¹,

Tolpina²,

Kuliczkowski

et al. 2008

Cerebrovasc Dis

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Background: Although aspirin (ASA) remains the most popular and accepted agent for secondary stroke prevention, its efficacy does not exceed 25%. Platelet function monitoring in ASA users suggests that some individuals exhibit a reduced or even absent antiplatelet response after ASA. This phenomenon, also known as ‘resistance’, is prevalent in stroke survivors. We sought to evaluate the blood lipid profile in poststroke ASA users dependent on their antiplatelet response to ASA. Methods: Ninety-six consecutive ASA users after first-ever ischemic stroke confirmed by imaging were prospectively enrolled. The platelet function analyzer (PFA-100, Dade Behring, USA) was utilized to assess the response after ASA. The lipid profile (total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides) was measured using the Cardiochek instrument (Polymer Technology, USA) from the autologuos blood samples. Results: The poststroke duration was 3–26 months, and all patients were treated with ASA for at least 3 months. The allowed daily ASA doses were from 75 up to 325 mg, with a mean of 158 mg. The mean age of the patients was 71 years, almost 60% were women, and over 85% of the patients were treated with statins. Thirty-seven patients were identified as low ASA responders, while 59 patients exhibited an adequate response. There were no differences between ASA responders and nonresponders with regard to demographics, clinical characteristics, risk factors and concomitant medications. The lipid profile biomarkers were similar between groups with the exception of triglycerides, which were significantly increased in the patients with ASA resistance, compared with ASA responders. Conclusion: The fact that hypertriglyceridemia affects platelet response to ASA has potential practical implications in light of growing evidence that ASA may exert antiplatelet properties beyond the cyclooxygenase pathway. The mechanism of such an association is unclear but may be related to the diminished platelet membrane fluidity and inability of ASA to downregulate such ‘strong’ protected platelets.

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“…Interestingly, previous studies reported that the antiplatelet effect of ASA is diminished in many patients with cerebrovascular disease, ranging from 5 to 60% [7,8,9,10,11,12,13], a problem colloquially termed ‘aspirin resistance’ [13,14,15]. Such variability in the extent of platelet inhibition by ASA may also reflect the use of various nonstandardized laboratory assays and suggests that one single platelet function test may not allow a general definition of ASA hypo- or nonresponse [16].…”

Section: Introductionmentioning

confidence: 99%

Variable Platelet Response to Aspirin in Patients with Ischemic Stroke

Hohlfeld

Weber²,

Junghans³

et al. 2007

Cerebrovasc Dis

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Background: A large number of patients experience ischemic stroke despite treatment with aspirin (acetylsalicylic acid, ASA). It is not clear whether all of these patients with ischemic stroke respond normally to ASA or are hyporesponsive as assessed by inhibition of aggregation and thromboxane (TX) synthesis. Methods: We studied the effect of ASA given orally and ASA in vitro on collagen- and arachidonic-acid-induced TX formation and aggregation in platelet-rich plasma of 90 patients with ischemic stroke and 25 healthy control subjects. Results: Thirty-seven patients were being treated with ASA at the time of stroke. Arachidonic-acid-induced TX formation was not depressed below a predefined threshold of 25 ng/ml in 9 patients. Eight of these however exhibited a normal platelet sensitivity to ASA in vitro, suggesting poor compliance or a pharmacokinetic mechanism of nonresponse. The addition of ASA in vitro did not inhibit arachidonic-acid-induced TX formation below the above threshold in 6 patients (11%) in the group of 53 stroke patients not receiving oral ASA, indicating an impaired response to ASA at the platelet level. Moreover, platelets from stroke patients showed an increased collagen-induced, TX-independent aggregation as compared with those of healthy individuals. Conclusion: Different categories of ASA nonresponders can be distinguished in patients with ischemic stroke. These include patients with poor bioavailability or noncompliance, an impaired platelet response to ASA in vitro and an increased, TX-independent hyperreactivity to collagen.

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Antiplatelet Effect of Aspirin in Patients With Cerebrovascular Disease

Cited by 174 publications

References 27 publications

Aspirin administered to women at 100 mg every other day produces less platelet inhibition than aspirin administered at 81 mg per day: implications for interpreting the women’s health study

Aspirin administered to women at 100 mg every other day produces less platelet inhibition than aspirin administered at 81 mg per day: implications for interpreting the women’s health study

Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Variable Platelet Response to Aspirin in Patients with Ischemic Stroke

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