Randomized Trial of High Loading Dose of Clopidogrel for Reduction of Periprocedural Myocardial Infarction in Patients Undergoing Coronary Intervention: Results From the ARMYDA-2 (Antiplatelet therapy for Reduction of Myocardial Damage during Angioplasty) Study

Patti, Giuseppe; Colonna, Giovanni; Pasceri, Vincenzo; Pepe, Leonardo Lassandro; A, Montinaro; Sciascio, Germano Di

doi:10.1016/j.accreview.2005.08.052

Cited by 228 publications

(288 citation statements)

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“…Thus, some [5,8,9], but not other [25], very small studies suggest that patients with higher residual platelet reactivity after the initiation of clopidogrel therapy have more subsequent major adverse clinical outcomes. Higher doses of clopidogrel [26][27][28][29], or other antiplatelet therapy, may therefore be beneficial, especially in those patients with greater platelet reactivity to ADP, measured either before or after clopidogrel therapy. However, definitive evidence for the benefit of guided antiplatelet therapy based on the degree of platelet reactivity will have to await the results of prospective clinical outcome studies [3].…”

Section: Discussionmentioning

confidence: 99%

Evidence that pre‐existent variability in platelet response to ADP accounts for ‘clopidogrel resistance’

Michelson

Linden

Furman

et al. 2007

Journal of Thrombosis and Haemostasis

103

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Summary. Background: Clopidogrel is a widely used antithrombotic agent that inhibits the platelet P2Y 12 adenosine diphosphate (ADP) receptor. There is increasing interest in Ôclopidogrel resistanceÕ. Objectives: To determine whether Ôclopidogrel resistanceÕ is accounted for by a pre-existent variability in platelet response to ADP. Methods: Platelet response to 20 lM ADP was analyzed by four independent whole blood flow cytometric assays: platelet surface activated GPIIb-IIIa, platelet surface P-selectin, monocyte-platelet aggregates and neutrophil-platelet aggregates. In 25 consecutive, non-aspirin-treated healthy subjects, we studied platelet response before and after clopidogrel administration. In addition, we studied the platelet response in 613 consecutive aspirinated patients with or without coronary artery disease (CAD, as determined by angiography) who had or had not been treated with clopidogrel. In these patients, we tested for homogeneity of variance across all durations of clopidogrel exposure and severity of CAD by estimating the Ôgoodness of fitÕ of two independent models. Results: In the healthy subjects, pre-clopidogrel response to ADP predicted post-clopidogrel response to ADP. In the patients, clopidogrel, as expected, inhibited the platelet response to ADP. However, irrespective of the duration of clopidogrel administration, the severity of CAD, and the dose of aspirin, clopidogrel did not increase the variance in the platelet response to ADP in any of the four assays of platelet response. Conclusions: These studies provide evidence that Ôclopidogrel resistanceÕ is accounted for by a pre-existent variability in platelet response to ADP and this variability is not increased by clopidogrel administration.

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Section: Discussionmentioning

confidence: 99%

Evidence that pre‐existent variability in platelet response to ADP accounts for ‘clopidogrel resistance’

Michelson

Linden

Furman

et al. 2007

Journal of Thrombosis and Haemostasis

103

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“…[23][24][25] Many studies have demonstrated that early statin therapy among PCI patients is associated with significant advantages for decreased mortality and morbidity in different patient subsets. 10,[26][27][28] Although the mechanism is not entirely clear, the anti-inflammatory effects of statins might contribute to the reduced myocardial injury during PCI.…”

Section: Discussionmentioning

confidence: 99%

Changes of C-reactive Protein are Associated With Myocardial Injury After Successful Percutaneous Coronary Intervention

Rhee

Yun

et al. 2008

Korean Circ J

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Background and Objectives: Myocardial injury after percutaneous coronary intervention (PCI) occurs frequently and it is associated with an adverse clinical outcome. Mechanical factors have been implicated in this complication and the role of inflammation has not yet been clearly determined. We evaluated the effect of an inflammatory response during PCI on periprocedural myocardial injury. Subjects and Methods: We prospectively studied 231 patients (mean age: 62.8±10.6 years, males: 60.6%) who underwent elective coronary stenting. For the exclusion of mechanical injury to the myocardium, we excluded those patients who developed complications during PCI. Blood samples for measuring the high sensitivity C-reactive protein (hsCRP) and troponin T (TnT) were obtained before the procedure and at 6 hours and 24 hours after PCI. The inflammatory response to PCI was calculated as the difference between the peak postprocedural hsCRP level and the preprocedural hsCRP level (delta CRP). We divided the patients according to the median value of delta CRP: Group I <2.2 mg/dL and Group II ≥2.2 mg/dL. Results: Postprocedural TnT elevation was were observed in 72 (31.2%) patients. The baseline clinical and angiographic characteristics were not difference between the two groups. The incidence of any TnT elevations was higher in the Group II than that in Group I (19.8% vs 42.6%, respectively, p<0.001). The incidences of TnT levels over 3 times the upper normal limit and 5 times the upper normal limit were also higher in Group II than in Group I (11.2% vs 21.7%, respectively, p=0.031, for a TnT level 3 times the upper normal limit, and 6.0% vs 13.9%, respectively, for a TnT level 5 times the upper normal limit). Multivariate analysis revealed that postprocedural hsCRP elevation and complex lesion were the significant independent predictors of postprocedural TnT elevation. Conclusion: Elevated hsCRP levels were associated with a higher risk of postprocedural troponin elevation in patients undergoing uncomplicated PCI. These results emphasized the role of inflammation in the pathogenesis of periprocedural myocardial injury.

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“…The authors have previously reported favorable outcomes with a 600-versus a 300-mg loading dose in patients undergoing PCI [13]. Other studies have confirmed these findings that are in line with the more rapid and potent effects of this dosing regimen, and which now represents the loading dose of choice by most interventionalists.…”

mentioning

confidence: 65%

Contemporary issues on clopidogrel therapy: a critical appraisal

Capodanno

Angiolillo

2009

Intern Emerg Med

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Randomized Trial of High Loading Dose of Clopidogrel for Reduction of Periprocedural Myocardial Infarction in Patients Undergoing Coronary Intervention: Results From the ARMYDA-2 (Antiplatelet therapy for Reduction of Myocardial Damage during Angioplasty) Study

Cited by 228 publications

References 0 publications

Evidence that pre‐existent variability in platelet response to ADP accounts for ‘clopidogrel resistance’

Evidence that pre‐existent variability in platelet response to ADP accounts for ‘clopidogrel resistance’

Changes of C-reactive Protein are Associated With Myocardial Injury After Successful Percutaneous Coronary Intervention

Contemporary issues on clopidogrel therapy: a critical appraisal

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