PP-239: Coronary Thrombus Aspiration Beyond the “Golden Hours”: Is It a Valid Option? (original) (raw)
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The American Journal of Cardiology, 2011
Aspirin has been shown to decrease cardiovascular (CV) events by ϳ25%. Despite aspirin therapy 10% to 20% of patients with arterial vascular disease develop atherothrombotic events. A meta-analysis of antiplatelet therapy showed a progressive decrease in clinical efficacy of aspirin after 2 years. Whether this is due to a decreased sensitivity to aspirin during long-term therapy remains unclear. A prospective randomized clinical trial with serial monitoring over 5 years was conducted in 100 patients with documented coronary heart disease. We investigated whether long-term treatment with aspirin 50 and 100 mg affects platelet response similarly. Occurrence of CV events was documented. Platelet sensitivity to aspirin, prostacyclin, and adenosine diphosphate-, collagen-, and epinephrine-induced platelet aggregation were evaluated over time. In addition, -thromboglobulin and inflammatory markers were measured. Four patients were lost to follow-up and 10 patients died. Eleven patients developed nonfatal CV events. In the 2 groups platelet response to aspirin and the referenced variables remained unchanged over 5 years. In patients who developed CV events, the last monitoring interval revealed no difference in platelet response to aspirin. However, patients with nonfatal and fatal CV events showed increased inflammatory markers versus patients without CV events independent of aspirin 50 or 100 mg intake. In conclusion, our study revealed no difference in antiplatelet response to aspirin 50 versus 100 mg or CV events over 5 years in patients with coronary heart disease.
Aspirin Resistance and Adverse Clinical Events in Patients with Coronary Artery Disease
The American Journal of Medicine, 2007
PURPOSE: We sought to determine the clinical significance of aspirin resistance measured by a point-of-care assay in stable patients with coronary artery disease (CAD). METHODS: We used the VerifyNow Aspirin (Accumetrics Inc, San Diego, Calif) to determine aspirin responsiveness of 468 stable CAD patients on aspirin 80 to 325 mg daily for Ն4 weeks. Aspirin resistance was defined as an Aspirin Reaction Unit Ն550. The primary outcome was the composite of cardiovascular death, myocardial infarction (MI), unstable angina requiring hospitalization, stroke, and transient ischemic attack. RESULTS: Aspirin resistance was noted in 128 (27.4%) patients. After a mean follow-up of 379 Ϯ 200 days, patients with aspirin resistance were at increased risk of the composite outcome compared to patients who were aspirin-sensitive (15.6% vs 5.3%, hazard ratio [HR] 3.12, 95% confidence intervals [CI], 1.65-5.91, P Ͻ .001). Cox proportional hazard regression modeling identified aspirin resistance, diabetes, prior MI, and a low hemoglobin to be independently associated with major adverse long-term outcomes (HR for aspirin resistance 2.46, 95% CI, 1.27-4.76, P ϭ .007). CONCLUSIONS: Aspirin resistance, defined by an aggregation-based rapid platelet function assay, is associated with an increased risk of adverse clinical outcomes in stable patients with CAD.
Frequency of Aspirin Resistance in Patients with Cardiovascular Diseases
Journal of Postgraduate Medical Institute, 2012
P l a t e l e t a d h e s i o n , a c t i v a t i o n a n d Its use reduces the risk of major vascular aggregation is the main underlying mechanism of events by approximately 25% in high risk thromboembolic vascular events; like myocardial 2 cardiovascular patiens. infarction and stroke. Inhibiting platelets is the primary strategy for preventing vascular events. Aspirin inhibits platelet aggregation by acetylation of platelet cyclo-oxygenase (COX) enzyme, thus blocking the transformation of 3 arachidonic acid (AA) into thormboxane (TX)A. 2 Aspirin's antiplatelet effect may not be uniform in all patients because many patients taking aspirin still suffer from vascular events. The term aspirin resistance is used to describe clinical and laboratory (biochemical) phenomena. Clinical aspirin resistance include patients who, despite aspirin use, experience vascular 4,5 events. Biochemical aspirin resistance can be defined as incomplete suppression of platelet
Aspirin Resistance: Focus on Clinical Endpoints
Journal of Cardiovascular Pharmacology, 2008
Introduction: Via its antiplatelet effect, aspirin reduces the odds of an arterial thrombotic event in high-risk patients by approximately 25%. However, 10% to 20% of patients with an arterial thrombotic event who are treated with aspirin have a recurrent arterial thrombotic event during long-term follow-up. Nevertheless, the effectiveness of aspirin has been questioned by the emergence of the concept of aspirin resistance, which has been introduced as an explanation of the fact that a considerable proportion of patients treated with aspirin exhibit normal platelet function. Objectives and Methods: We systematically reviewed all available evidence till March 2008 on prevalence of aspirin resistance and its association with clinical outcome. We also collected articles showing the possible way of treatment. Conclusion: Analyzing the data of different laboratory methods aspirin resistance seems to be associated with poor clinical outcome, although currently no standardized or widely accepted definition of aspirin resistance exists. The widely used laboratory methods might not be comparable with each other; therefore, specific treatment recommendations for patients who exhibit high platelet reactivity during aspirin therapy or who have poor platelet inhibition by aspirin are not established.
European Heart Journal, 2007
Aims We sought to compare the results obtained from six major platelet function tests in the assessment of the prevalence of aspirin resistance in patients with stable coronary artery disease. Methods and results 201 patients with stable coronary artery disease receiving daily aspirin therapy (!80 mg) were recruited. Platelet aggregation was measured by: (i) light transmission aggregometry (LTA) after stimulation with 1.6 mM of arachidonic acid (AA), (ii) LTA after adenosine diphosphate (ADP) (5, 10, and 20 mM) stimulation, (iii) whole blood aggregometry, (iv) PFA-100 w , (v) VerifyNow Aspirin w ; urinary 11-dehydro-thromboxane B 2 concentrations were also measured. Eight patients (4%, 95% CI 0.01-0.07) were deemed resistant to aspirin by LTA and AA. The prevalence of aspirin resistance varied according to the assay used: 10.3-51.7% for LTA using ADP as the agonist, 18.0% for whole blood aggregometry, 59.5% for PFA-100 w , 6.7% for VerifyNow Aspirin w , and finally, 22.9% by measuring urinary 11-dehydro-thromboxane B 2 concentrations. Results from these tests showed poor correlation and agreement between themselves. Conclusion Platelet function tests are not equally effective in measuring aspirin's antiplatelet effect and correlate poorly amongst themselves. The clinical usefulness of the different assays to classify correctly patients as aspirin resistant remains undetermined.
Aspirin "resistance" and risk of cardiovascular morbidity: systematic review and meta-analysis
BMJ, 2008
Objective To determine if there is a relation between aspirin "resistance" and clinical outcomes in patients with cardiovascular disease. Design Systematic review and meta-analysis. Data source Electronic literature search without language restrictions of four databases and hand search of bibliographies for other relevant articles. Review methods Inclusion criteria included a test for platelet responsiveness and clinical outcomes. Aspirin resistance was assessed, using a variety of platelet function assays. Results 20 studies totalling 2930 patients with cardiovascular disease were identified. Most studies used aspirin regimens, ranging from 75-325 mg daily, and six studies included adjunct antiplatelet therapy. Compliance was confirmed directly in 14 studies and by telephone or interviews in three. Information was insufficient to assess compliance in three studies. Overall, 810 patients (28%) were classified as aspirin resistant. A cardiovascular related event occurred in 41% of patients (odds ratio 3.85, 95% confidence interval 3.08 to 4.80), death in 5. 7% (5.99, 2.28 to 15.72), and an acute coronary syndrome in 39.4% (4.06, 2.96 to 5.56). Aspirin resistant patients did not benefit from other antiplatelet treatment. Conclusion Patients who are resistant to aspirin are at a greater risk of clinically important cardiovascular morbidity long term than patients who are sensitive to aspirin.
The lack of aspirin resistance in patients with coronary artery disease
Journal of translational medicine, 2016
Aspirin resistance established by different laboratory methods is still a debated problem. Using COX1 specific methods no aspirin resistance was detected among healthy volunteers. Here we tested the effect of chronic aspirin treatment on platelets from patients with stable coronary artery disease. The expression of COX2 mRNA in platelets and its influences on the effect of aspirin was also investigated. One hundred and forty four patients were enrolled in the study. The direct measurement of COX1 acetylation was carried out by monoclonal antibodies specific to acetylated and non-acetylated COX1 (acCOX1 and nacCOX1) using Western blotting technique. Arachidonic acid (AA) induced TXB2 production by platelets was measured by competitive immunoassay. AA induced platelet aggregation, ATP secretion and VerifyNow Aspirin Assay were also performed. COX2 and COX1 mRNA expression in platelets were measured in 56 patients by RT-qPCR. In 138 patients only acCOX1 was detected, in the remaining s...
Journal of Thrombosis and Thrombolysis, 2006
Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. 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. 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. 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). 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.
Annals of Pharmacotherapy, 2007
A spirin therapy is a cornerstone in the management of acute coronary syndromes and in the prevention of atherothrombotic events due to its ability to block arachidonic acid metabolism by irreversibly inhibiting cyclooxygenase-1 and reducing the production of thromboxane A 2 , a platelet activator and vasoconstrictor. Aspirin reduces the risk of nonfatal myocardial infarction (MI), nonfatal stroke, and vascular death in a broad range of high-risk patients by approximately 23%.