24-hour antiplatelet effect of aspirin in patients with previous definite stent thrombosis

Würtz, Morten; Hvas, Anne‐Mette; Jensen, Lisette Okkels; Kaltoft, Anne; Tilsted, Hans‐Henrik; Kristensen, Steen Dalby; Grove, Erik Lerkevang

doi:10.1016/j.ijcard.2014.05.013

Cited by 36 publications

(31 citation statements)

References 33 publications

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“…Previous studies have demonstrated that aspirin does not provide consistent 24‐hour platelet inhibition in a significant proportion of CAD patients and that residual platelet aggregation is 5‐fold more frequent 24 versus 2 hours after aspirin ingestion . Few previous studies have accounted for these pharmacokinetic conditions, which in part may explain the large proportion of patients with reduced antiplatelet effect of aspirin .…”

Section: Discussionmentioning

confidence: 97%

Reduced Antiplatelet Effect of Aspirin Does Not Predict Cardiovascular Events in Patients With Stable Coronary Artery Disease

Larsen

Grove

Neergaard‐Petersen

et al. 2017

JAHA

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BackgroundIncreased platelet aggregation during antiplatelet therapy may predict cardiovascular events in patients with coronary artery disease. The majority of these patients receive aspirin monotherapy. We aimed to investigate whether high platelet‐aggregation levels predict cardiovascular events in stable coronary artery disease patients treated with aspirin.Methods and ResultsWe included 900 stable coronary artery disease patients with either previous myocardial infarction, type 2 diabetes mellitus, or both. All patients received single antithrombotic therapy with 75 mg aspirin daily. Platelet aggregation was evaluated 1 hour after aspirin intake using the VerifyNow Aspirin Assay (Accriva Diagnostics) and Multiplate Analyzer (Roche; agonists: arachidonic acid and collagen). Adherence to aspirin was confirmed by serum thromboxane B2. The primary end point was the composite of nonfatal myocardial infarction, ischemic stroke, and cardiovascular death. At 3‐year follow‐up, 78 primary end points were registered. The primary end point did not occur more frequently in patients with high platelet‐aggregation levels (first versus fourth quartile) assessed by VerifyNow (hazard ratio: 0.5 [95% CI, 0.3–1.1], P=0.08) or Multiplate using arachidonic acid (hazard ratio: 1.0 [95% CI, 0.5–2.1], P=0.92) or collagen (hazard ratio: 1.4 [95% CI, 0.7–2.8], P=0.38). Similar results were found for the composite secondary end point (nonfatal myocardial infarction, ischemic stroke, stent thrombosis, and all‐cause death) and the single end points. Thromboxane B2 levels did not predict any end points. Renal insufficiency was the only clinical risk factor predicting the primary and secondary end points.ConclusionsThis study is the largest to investigate platelet aggregation in stable coronary artery disease patients receiving aspirin as single antithrombotic therapy. We found that high platelet‐aggregation levels did not predict cardiovascular events.

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Section: Discussionmentioning

confidence: 97%

Reduced Antiplatelet Effect of Aspirin Does Not Predict Cardiovascular Events in Patients With Stable Coronary Artery Disease

Larsen

Grove

Neergaard‐Petersen

et al. 2017

JAHA

Self Cite

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“…[19,20] However, the antiplatelet effects [i.e. inhibition of TXA 2 production ( Figure 3B) and of arachidonic acid-induced platelet aggregation] in healthy individuals begin to recover within 24 h, [29,30] as aspirin is metabolized to inactive antiplatelet substances and newly generated platelets with uninhibited COX enzymes enter the circulation. [14,30] This reduction in antiplatelet effects likely occurs even more quickly in patients with rapid platelet turnover, such as patients with diabetes.…”

Section: Aspirin: Antiplatelet Effects and Pharmacokineticsmentioning

confidence: 99%

Aspirin in the prevention of cardiovascular events in patients with diabetes

Bell

2016

Postgraduate Medicine

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Diabetes imparts a substantial increased risk for cardiovascular disease-related mortality and morbidity. Because of this, current medical guidelines recommend prophylactic treatment with once-daily, low-dose aspirin (acetylsalicylic acid) for primary and secondary prevention of cardiovascular (CV) events in high-risk patients. However, only modest reductions in CV events and mortality have been observed with once-daily aspirin treatment in patients with diabetes, including patients with a previous CV event, perhaps because of disparity between aspirin pharmacokinetics and diabetes-related platelet abnormalities. Once-daily aspirin irreversibly inactivates platelets for only a short duration (acetylsalicylic acid half-life, approximately 15-20 minutes), after which time newly generated, active platelets enter the circulation and weaken aspirin's effect. Platelets from patients with diabetes are more reactive and are turned over more rapidly than platelets from normal individuals; the short inhibitory window provided by once-daily aspirin may therefore be insufficient to provide 24-h protection against CV events. Alternative conventional aspirin regimens (e.g. higher daily dose, twice-daily dosing, combination with clopidogrel) and newer formulations (e.g. 24-h, extended-release) have been proposed to overcome the apparent limited efficacy of conventional aspirin in patients with diabetes; however, tolerability concerns and limited clinical efficacy data need to be taken into account when considering the use of such regimens. ARTICLE HISTORY

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“…3 nificant but relatively weak correlation between delay and platelet inhibition, clinical impact remains hypothetical. A correlation between time and antiplatelet efficacy has been proved on aspirin and could be associated with ischemic events [23,24]. Therapy compliance is a major challenge after ACS.…”

Section: Discussionmentioning

confidence: 99%

Is platelet inhibition correlated with time from last intake on P2Y12 blockers after an acute coronary syndrome? A pilot study

et al. 2016

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Delay from the last intake of drug could be an important and unexplored variable in the biological response to antiplatelet agents after acute coronary syndrome (ACS) discharge. The objective was to define the impact of the delay from P2Y12 blocker intake on the platelet inhibition level. We compared ticagrelor-, prasugrel-, and clopidogrel-treated patients. All consecutive patients, who had been addressed between 2013 and 2014 for ACS, treated with aspirin and a P2Y12 blocker as maintenance dose, were eligible. One month after discharge, blood sample and a questionnaire were proposed to the patient by a nurse blinded to the protocol. On this questionnaire, three questions about name of the drug, regularity of the intakes, and hour of the last intake were collected. The response to antiplatelet therapy was assessed using platelet reactivity index vasodilator-stimulated phosphoprotein (PRI VASP) and % of adenosine-5'-diphosphate-induced aggregation (%ADP).The primary objective of this study was to evaluate the correlation between platelet inhibition and delay from drug intake. We enrolled 474 ACS treated with clopidogrel 75 mg in 182 cases (38% patients), prasugrel in 190 cases (40%), or ticagrelor in 102 patients (22%). We observed a significant correlation between delay from intake and PRI VASP and %ADP for ticagrelor (r = 0.25, p = 0.01; r = 0.21, p = 0.03; respectively). On clopidogrel (r = 0.09, p = 0.24; r = 0.02, p = 0.80; respectively) and prasugrel (r = 0.02, p = 0.82; r = 0.11, p = 0.12 respectively), no correlation exists. In conclusion, ticagrelor, unlike thienopyridines, is associated with a significant correlation between delay from the last intake and platelet inhibition.

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24-hour antiplatelet effect of aspirin in patients with previous definite stent thrombosis

Cited by 36 publications

References 33 publications

Reduced Antiplatelet Effect of Aspirin Does Not Predict Cardiovascular Events in Patients With Stable Coronary Artery Disease

Reduced Antiplatelet Effect of Aspirin Does Not Predict Cardiovascular Events in Patients With Stable Coronary Artery Disease

Aspirin in the prevention of cardiovascular events in patients with diabetes

Is platelet inhibition correlated with time from last intake on P2Y12 blockers after an acute coronary syndrome? A pilot study

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