High post-treatment platelet reactivity is associated with a high incidence of myonecrosis after stenting for non-ST elevation acute coronary syndromes

2007 ◽  
Vol 97 (02) ◽  
pp. 282-287 ◽  
Author(s):  
Corinne Frere ◽  
Jacques Quilici ◽  
Pierre-Emmanuel Morange ◽  
Lyassine Nait-Saidi ◽  
Christopher Mielot ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Acute Coronary Syndromes ◽  
Troponin I ◽  
Dual Antiplatelet Therapy ◽  
Platelet Reactivity ◽  
Post Treatment ◽  
Increased Risk ◽  
Coronary Syndromes ◽  
St Elevation

SummaryHigh post-treatment platelet reactivity (HPPR= adenosine diphosphate [ADP] 10 µM-induced platelet aggregation > 70%) identifies low responders to dual antiplatelet therapy with increased risk of recurrent cardiovascular (CV) events after stenting for non-ST elevation acute coronary syndromes (NSTEACS). This study was designed to compare the incidence of periprocedural myocardial infarction (MI) after stenting for NSTEACS patients between non-responders to dual antiplatelet therapy defined by HPPR and normo-responders. One hundred ninety NSTE-ACS consecutive patients undergoing coronary stenting were included in this prospective study. They received 250 mg aspirin and a 600 mg loading dose of clopidogrel at least 12 hours (h) before percutaneous coronary intervention (PCI). A single post-treatment blood sample was obtained before PCI to analyze maximal intensity of ADP-induced platelet aggregation, and troponin levels were analyzed before PCI, and 12 and 24 h after PCI. Troponin I was considered elevated if > 0.4 ng/ ml. HPPR was present in 22% of patients (n=42). Periprocedural MI occurred significantly more frequently in patients with HPPR than in the normo-responders (43% vs. 24%, p=0.014). After being correlated with recurrent ischemic events after stenting for NSTE-ACS, the HPPR seems to be also a marker of increased risk of periprocedural MI for NSTE-ACS patients.

Response to Dual Antiplatelet Therapy Does Not Impact Bleeding Risks in Patients Undergoing Oral Surgery after Acute Coronary Syndromes

Cardiology ◽  
2015 ◽  
Vol 132 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Damian Dudek ◽  
Wiktor Kuliczkowski ◽  
Jacek Kaczmarski ◽  
Joanna Wiechec ◽  
Edyta Reichman-Warmusz ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Acute Coronary Syndromes ◽  
Dual Antiplatelet Therapy ◽  
Oral Surgery ◽  
Antiplatelet Agent ◽  
Real Life ◽  
Control Group ◽  
Platelet Activity ◽  
Coronary Syndromes

Introduction: Oral surgery (OS) in patients on antecedent dual antiplatelet therapy (DAPT) may be associated with extra bleeding risks. Monitoring platelet activity in such patients may be beneficial for safety when performing OS. Objectives: The aim of this study was to assess whether platelet function during DAPT impacted the risk of bleeding following OS in patients with acute coronary syndromes (ACS). Patients and Methods: Patients who required OS on top of DAPT with aspirin and clopidogrel (n = 55) for invasively treated ACS were included. The control group (n = 33) consisted of patients who underwent OS with no antiplatelet agent. Platelet aggregation before OS was assessed with a Multiplate® analyzer. Bleeding during OS and at days 1, 3, 7 and 10 after surgery was serially evaluated. Results: All 88 patients completed the study. An incomplete response to aspirin or clopidogrel was observed in 43.6% of the patients. In 11% of the cases, an excessive response to clopidogrel was demonstrated. No excessive bleeding upon OS was exhibited in either group during the entire follow-up. Platelet aggregation values and the use of DAPT did not impact the performance of OS. Conclusion: Therapy with clopidogrel and aspirin after ACS does not seem to increase the risk of real-life bleeding following OS, regardless of the platelet activity response to DAPT.

Dual antiplatelet therapy in non-ST elevation acute coronary syndromes at Veterans Affairs Hospitals

Heart ◽  
2019 ◽  
Vol 105 (20) ◽  
pp. 1575-1582
Author(s):  
Javier Alfonso Valle ◽  
Kevin Josey ◽  
Andrew F Prouse ◽  
Jeffrey Zimmet ◽  
Stephen W Waldo
Keyword(s):  
Antiplatelet Therapy ◽  
Acute Coronary Syndromes ◽  
Dual Antiplatelet Therapy ◽  
Patient Characteristics ◽  
Coronary Intervention ◽  
Veterans Affairs ◽  
Veterans Affairs Hospitals ◽  
Surgical Revascularisation ◽  
Coronary Syndromes ◽  
St Elevation

ObjectiveCurrent guidelines recommend that patients with non-ST elevation acute coronary syndromes (NSTEACS) receive dual antiplatelet therapy (DAPT) early in hospitalisations. However, observational studies suggest that this rarely occurs. We evaluated site-specific variation and clinical outcomes associated with early DAPT among patients undergoing angiography for NSTEACS.MethodsIn this observational analysis, we identified patients undergoing angiography for NSTEACS in Veterans Affairs hospitals from 2008 to 2016 and assessed characteristics and site variation associated with early DAPT (administration <24 hours of admission). Using propensity matching, we compared time to revascularisation, recurrent myocardial infarction (MI) and mortality between those receiving early DAPT and those not receiving early DAPT (administration ≥24 hours).ResultsOf 45 569 patients undergoing angiography for NSTEACS, 15 084 (33%) received early DAPT. Early DAPT was more frequent in patients with non-ST elevation MI, prior surgical revascularisation and among patients undergoing revascularisation. There was a greater than twofold difference in early DAPT across sites, independent of patient characteristics (median OR 2.43, 95% CI 2.28 to 2.55). There was no difference in time topercutaneous coronary intervention (PCI) between groups, but a significant delay to surgical revascularisation with early DAPT (median 4 vs 3 days, p<0.001) without reduction in hazard of death or MI (HR 1.08, 95% CI 1.00 to 1.16) and similar results demonstrated in the subgroup of patients undergoing revascularisation (HR 1.02, 95% CI 0.91 to 1.13).ConclusionAmong NSTEACS patients undergoing coronary angiography, early DAPT was not associated with improvement of outcomes but was associated with delays in surgical revascularisation.

scholarly journals Clinical Efficacy of Three Assays for Cardiac Troponin I for Risk Stratification in Acute Coronary Syndromes: A Thrombolysis In Myocardial Infarction (TIMI) 11B Substudy

2000 ◽  
Vol 46 (4) ◽  
pp. 453-460 ◽  
Author(s):  
David A Morrow ◽  
Nader Rifai ◽  
Milenko J Tanasijevic ◽  
Donald R Wybenga ◽  
James A de Lemos ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Acute Coronary Syndromes ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Serum Samples ◽  
Increased Risk ◽  
Creatine Kinase Mb ◽  
Coronary Syndromes ◽  
St Elevation

Abstract Background: Significant analytic variability exists between the multiple assays for cardiac troponin I (cTnI) approved for clinical use. Until adequate cTnI standardization is possible, an evidence-based approach evaluating each assay at specific thresholds appears warranted. Methods: We examined the efficacy of three cTnI assays for predicting death, myocardial infarction (MI), or the composite of death, MI, or urgent revascularization at 43 days among patients with non-ST-elevation acute coronary syndromes enrolled in the Thrombolysis In Myocardial Infarction (TIMI) 11B study. Results: Six hundred eighty-one patients with serum samples obtained at baseline and/or 12–24 h had cTnI determined using all three assays. Baseline cTnI was ≥0.1 μg/L for 368, 395, and 418 patients with the Bayer Immuno 1TM, ACS:180®, and Dimension® RxL assays, respectively. Correlation coefficients for the RxL with the ACS:180 and Bayer Immuno 1 results were 0.89 (P = 0.0001) and 0.87 (P = 0.0001), with a coefficient of 0.92 (P = 0.0001) for the ACS:180 and Bayer Immuno 1 assays. Patients with cTnI ≥0.1 μg/L were at increased risk for death or MI by 43 days (relative risk, 2.2–3.0; P &lt;0.0006), regardless of the assay used. This prognostic capacity persisted among those with creatine kinase MB isoenzyme concentrations within the reference interval. Moreover, cTnI was the strongest multivariate predictor of death, MI, or urgent revascularization with adjusted odds ratios of 2.1–2.9 (P &lt;0.0006). Conclusion: This study demonstrates the prognostic efficacy of three independently developed cTnI assays at a threshold of 0.1 μg/L for the prediction of adverse clinical outcomes among patients with non-ST-elevation acute coronary syndromes.

Antiplatelet Therapy in Acute Coronary Syndromes. Lights and Shadows of Platelet Function Tests to Guide the Best Therapeutic Approach

2020 ◽  
Vol 18 (3) ◽  
pp. 262-272 ◽  
Author(s):  
Giovanni Cimmino ◽  
Emanuele Gallinoro ◽  
Luigi Di Serafino ◽  
Nicola De Luca ◽  
Plinio Cirillo
Keyword(s):  
Antiplatelet Therapy ◽  
Platelet Activation ◽  
Platelet Function ◽  
Acute Coronary Syndromes ◽  
Clinical Decision Making ◽  
Platelet Reactivity ◽  
Platelet Function Tests ◽  
Function Tests ◽  
Increased Risk ◽  
Coronary Syndromes

The key role of platelets in pathophysiology of Acute Coronary Syndromes (ACS) has been well recognized. Platelet activation and aggregation, together with tissue factor-pathway activation, lead to acute thrombus formation in the coronary vessels at sites of plaque rupture. Thus, antiplatelet therapy with drugs able to interfere with platelet activation/aggregation represents a cornerstone of ACS treatment in intensive care units and catheterisation labs. Several observational studies have described that residual high platelet reactivity, despite antiplatelet therapy, is associated with increased risk of nonfatal Myocardial Infarction (MI), definite/probable stent thrombosis and cardiovascular mortality. Thus, assessment of platelet function with reliable and reproducible platelet function tests might be crucial to identify patients at high risk of thrombosis or not responding to ongoing antiplatelet strategies. However, despite this promising background, some randomized clinical trials have failed to demonstrate improvement in outcomes when using platelet function tests for clinical decision-making. This review, after describing platelet biology and pathophysiology of ACS, briefly considers the drugs currently approved for use in patients with ACS or treated by the percutaneous coronary intervention (PCI). Finally, we provide an updated overview of the current methods to evaluate platelet reactivity in the clinical setting of ACS illustrating their potential advantages/limitations in current clinical practice.

scholarly journals Direct factor IXa inhibition with the RNA-aptamer pegnivacogin reduces platelet reactivity in vitro and residual platelet aggregation in patients with acute coronary syndromes

2017 ◽  
Vol 8 (6) ◽  
pp. 520-526 ◽  
Author(s):  
Dawid L Staudacher ◽  
Vera Putz ◽  
Lukas Heger ◽  
Jochen Reinöhl ◽  
Marcus Hortmann ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Acute Coronary Syndromes ◽  
Platelet Reactivity ◽  
Coagulation Cascade ◽  
Rna Aptamer ◽  
Reversal Agent ◽  
Blood Samples ◽  
Factor Ixa ◽  
Coronary Syndromes

Background:Residual platelet reactivity is a predictor of poor prognosis in patients with acute coronary syndromes (ACSs) undergoing percutaneous coronary intervention. Thrombin is a major platelet activator and upon initiation of the coagulation cascade, it is subsequently produced downstream of factor IXa, which itself is known to be increased in ACS. Pegnivacogin is a novel RNA-aptamer based factor IXa inhibitor featuring a reversal agent, anivamersen. We hypothesized that pegnivacogin could reduce platelet reactivity.Methods:Whole blood samples from healthy volunteers were incubated in vitro in the presence and absence of pegnivacogin and platelet reactivity was analysed. In addition, platelet aggregometry was performed in blood samples from ACS patients in the RADAR trial featuring the intravenous administration of pegnivacogin as well as reversal by anivamersen.Results:In vitro, pegnivacogin significantly reduced adenosine diphosphate-induced CD62P-expression (100% vs. 89.79±4.04%, p=0.027, n=9) and PAC-1 binding (100% vs. 83.02±4.08%, p=0.010, n=11). Platelet aggregation was reduced (97.71±5.30% vs. 66.53±9.92%, p=0.013, n=10) as evaluated by light transmission aggregometry. In the presence of the RNA-aptamer reversal agent anivamersen, neither CD62P-expression nor platelet aggregation was attenuated. In patients with ACS treated with aspirin and clopidogrel, residual platelet aggregation was significantly reduced 20 min after intravenous bolus of 1 mg/kg pegnivacogin (100% versus 43.21±8.23%, p=0.020).Conclusion:Inhibition of factor IXa by pegnivacogin decreases platelet activation and aggregation in vitro. This effect was negated by anivamersen. In ACS patients, platelet aggregation was significantly reduced after intravenous pegnivacogin. An aptamer-based anticoagulant inhibiting factor IXa therefore might be a promising antithrombotic strategy in ACS patients.

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