Effect of different aspirin doses on platelet aggregation in patients with stable coronary artery disease

Malhotra, Samit; Sharma, Yash Pal; Grover, Anil; Majumdar, S.; Hanif, Sadaf; Bhargava, V.K.; Bhatnagar, Ajay S.; Pandhi, P

doi:10.1046/j.1445-5994.2003.00360.x

Cited by 19 publications

(9 citation statements)

References 33 publications

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“…Recently though, a randomized study of 60 patients with stable coronary artery disease showed that the effect of aspirin was dose-dependent and the conclusion was that doses of less than 100 mg of aspirin was less effective inhibiting platelet aggregation than doses greater than 100 mg [22]. This could indicate that higher doses of aspirin could be necessary to inhibit increased activity in the thromboxane positive feedback system, but for the time being there is no clear evidence saying that higher doses of aspirin improve clinical outcome [1].…”

Section: Discussionmentioning

confidence: 99%

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Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

et al. 2005

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Background: To be fully activated platelets are dependent on two positive feedback loops; the formation of thromboxane A 2 by cyclooxygenase in the platelets and the release of ADP. We wanted to evaluate the effect of aspirin on platelet function in patients with acute coronary syndromes and we hypothesized that increased levels of ADP in patients with acute coronary syndromes could contribute to aspirin resistance.

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Section: Discussionmentioning

confidence: 99%

“…ADP is released by activated platelets, but also in the heart from cardiac myocytes during ischemia, or from endothelial cells, red blood cells and sympathetic nerves [22,23]. Erythrocytes are known to contain large amounts of ADP, which may increase the platelet activity and modulate the effect of aspirin [24].…”

Section: Discussionmentioning

confidence: 99%

Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

et al. 2005

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“…17 However, a number of studies provide evidence for VPR with aspirin, including a markedly reduced response to platelet function tests in some patients. Decreased aspirin responsiveness occurred in 8.3% of healthy volunteers, 18 7.2% to 36% of CVD patients, 19 -22 60% of PAD patients, 23 and 5.5% to 43% of CAD patients 16,24 -28 (Table 1).…”

Section: Aspirinmentioning

confidence: 98%

Variability in Platelet Response to the Antiplatelet Agents Aspirin and Clopidogrel

Jennings¹

2009

Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine

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Platelet reactivity (eg, platelet adhesion, activation, aggregation) is the underlying pathology for atherothrombotic processes and subsequent ischemic complications. Antiplatelet drugs, including aspirin, dipyridamole, thienopyridines (clopidogrel and ticlopidine), and glycoprotein IIb/IIIa antagonists, have proven efficacy in atherothrombotic event prevention. However, variability of platelet response measured in the laboratory has been reported and is a subject of keen interest.It is unclear to what extent variability of platelet response to antiplatelet agents is associated with clinical outcomes. A better understanding of this issue requires a general consensus for a standard, preferably point-of-care, ex vivo or in vitro assay to determine the effects of antiplatelet agents on key platelet functions. Currently, results using various methods have not yielded an obvious answer. Small-scale studies have examined the correlation between ex vivo inhibition of platelet aggregation or residual platelet activity and clinical endpoints, and although evidence shows that such correlations may exist, results have not been consistent or definitive. Data from large-scale prospective trials are needed to expand our current understanding of the benefits and limitations of utilizing platelet function tests to effectively manage the balance between protection and risks associated with the antiplatelet therapies, aspirin, and clopidogrel.

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“…As little as 81mg of aspirin will impede aggregation by this test. 51 Multiple Electrode Aggregometry (MEA) is a newly developed technique for testing platelet function in whole blood based on classic whole-blood impedance aggregometry. MEA does not require a specialized coagulation laboratory and may be useful for point-of-care analysis.…”

Section: Importance Of Laboratory Testsmentioning

confidence: 99%

Is the Practice of Discontinuing Aspirin Therapy Prior to Dental Extraction Correct? A Review

Chouksey¹,

Dugad²,

Bhargava³

et al. 2015

jemds

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Aspirin is routinely used drug in patients with cardiac problems. When a patient on aspirin requires dental treatment that has the risk of bleeding, the physician or dental surgeon often advices the patient to stop aspirin for few days. This however can lead to thromboembolic events to recur that may cause myocardial infarction, stroke or even death. The decision to stop the medicine prior to dental extraction or oral surgical procedure is critical.

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Effect of different aspirin doses on platelet aggregation in patients with stable coronary artery disease

Abstract: Our results demonstrate that doses of aspirin less than 100 mg are not as effective at inhibiting platelet aggregation as doses greater than 100 mg.

Cited by 19 publications

References 33 publications

Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

Variability in Platelet Response to the Antiplatelet Agents Aspirin and Clopidogrel

Is the Practice of Discontinuing Aspirin Therapy Prior to Dental Extraction Correct? A Review

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