Early and late effects of clopidogrel in patients with acute coronary syndromes

Yusuf, S.; Mehta, S.R.; Zhao, F.

doi:10.1016/s1062-1458(03)00194-6

Cited by 50 publications

(73 citation statements)

References 5 publications

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“…1,14,15 Therefore, inhibition of platelet aggregation is believed to be crucial for the strategic management of primary and secondary prevention of thromboembolic events in high-risk patients. 1,[15][16][17] One important finding of the present study was that the CD62p expression was substantially higher pre-procedure in the study patients than in the normal control subjects, which is important information for the management of patients with ACS.…”

Section: Discussionmentioning

confidence: 99%

“…Previous clinical trials showed that early use of potent anti-platelet agents gave most clinical benefit to patients with ACS; 16,17 however, the efficacy of these anti-platelet therapies for secondary prevention following ACS was not based on measuring platelet activity in individual patients, but rather on clinical observation. 1,2,5,16,17 Therefore, the findings of the present study are clinically important because they reinforce the rationale of strategic management based on the finding of the previous studies.…”

Section: Discussionmentioning

confidence: 99%

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Serial Changes in Platelet Activation in Patients With Unstable Angina Following Coronary Stenting Evaluation of the Effect of Clopidogrel Loading Dose in Inhibiting Platelet Activation

Yip

Hang

et al. 2005

Circ J

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revious studies have demonstrated that combined therapy with aspirin and ticlopidine can synergically inhibit platelet reactivity, and thus substantially reduce the incidence of early ischemic events following coronary artery stenting. 1-3 However, acute or subacute stent thrombosis still occurs in up to 1-2% of patients, especially soon after stent implantation, 1,2 and it has been suggested that this phenomenon is caused by the delayed onset of the antiplatelet effect of ticlopidine. 4 Clopidogrel, a new thienopyridine derivative that is chemically related to ticlopidine, blocks platelet activation by selectively and irreversibly inhibiting the binding of adenosine diphosphate (ADP) to its receptor on platelets, and subsequently inhibiting the ADP-dependent activation of the Gp IIb-IIIa complex, the major receptor for fibrinogen binding on platelet surface. 5 Some recent studies have shown that clopidogrel, particularly as a loading dose of 300 mg, can rapidly and significantly inhibit platelet aggregation in both healthy subjects and patients with atherosclerotic disease, even after just 2 h. 6-8 Thus, such a loading dose, followed by daily doses of 75 mg, has become one of the most popular regimens for patients after coronary stenting in our clinical practice. However, a more recent study has demonstrated that the conventional loading dose in patients with unstable angina (UA) undergoing coronary stenting inhibited no more than 40% of ADP (20 g) induced platelet aggregation within the first 4 h, whereas a loading dose of 600 mg of clopidogrel more substantially inhibited ADP (20 g) induced platelet aggregation. 4 These findings 4,6-8 raise suspicions regarding which dose regimen is most suitable for patients, particularly those with acute coronary syndrome (ACS) and platelet hyperreactivity who are undergoing coronary stenting.The ADP stimulation test, a physiologic assay that can provide information regarding platelet aggregation ability, is well established in various clinical settings. 4,[6][7][8] However, the CD62p expression test using flow cytometry, which can provide essential information on platelet activation, has not been fully investigated in patients with UA or other clinical settings. Furthermore, data are not available regarding the serial changes in platelet activation after a loading dose of 300 mg of clopidogrel therapy, followed by daily doses of 75 mg, in the clinical setting of UA. This is very important for physicians in their daily clinical practice, because platelet activation is a hallmark of ACS, 9-11 and formed the basis of the present study. Background Platelet activation is crucial in the development of acute or subacute stent thrombosis following implantation. This study investigated whether a conventional regimen comprising a loading dose of 300 mg of clopidogrel, followed by daily doses of 75 mg, could significantly suppress platelet activation in patients with unstable angina (UA) undergoing coronary stenting. Methods and ResultsPlatelet activation (expressed by CD62p) was ser...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Serial Changes in Platelet Activation in Patients With Unstable Angina Following Coronary Stenting Evaluation of the Effect of Clopidogrel Loading Dose in Inhibiting Platelet Activation

Yip

Hang

et al. 2005

Circ J

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“…Combining our findings with those of the other studies 5,8,10,15 supports the suggestion that early administration of antiplatelet agents and IIb/IIIa receptor inhibitors could provide additional benefit to patients with ACS. 3,6,7,16 Correlation Between Platelet Activity and Myocardial Damage Notably, while the relationship between the thromboembolic risk and platelet activity has been extensively debated, 1,2,[5][6][7][8][9]14 the association between myocardial damage and platelet activation has seldom been studied. 10 Plaque rupture, an index of acute inflammatory stimulus, increases platelet activation 11 and additionally, acute ischemic stroke or AMI, which indicates tissue necrosis, markedly enhances platelet activity.…”

Section: Platelet Activity Is An Index Of a Thromboembolic Eventmentioning

confidence: 99%

Platelet Activity is a Biomarker of Cardiac Necrosis and Predictive of Untoward Clinical Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Stenting

Yip

Chang

Sun

et al. 2006

Circ J

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“…A reduction of recurrent ischemia was already present within 6 h of randomization. 30 The salutary effects were noted across all of the subgroups, including those without ST-segment deviation or troponin release and those with a low TIMI risk score. 14,17 The major benefit was a reduction in MI; although death and stroke trended in favor of clopidogrel, the reduction in these events did not achieve statistical significance.…”

Section: Clopidogrelmentioning

confidence: 92%

Application of Current Guidelines to the Management of Unstable Angina and Non-ST-Elevation Myocardial Infarction

Braunwald

2003

Circulation

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Abstract-Unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI) is a common but heterogeneous disorder with patients exhibiting widely varying risks. Early risk stratification is at the center of the management program and can be achieved using clinical criteria and biomarkers, or a combination. In addition to anti-ischemic therapy and aspirin, the thienopyridine clopidogrel is indicated except in patients who are potential candidates for urgent coronary artery bypass grafting (CABG

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Early and late effects of clopidogrel in patients with acute coronary syndromes

Cited by 50 publications

References 5 publications

Serial Changes in Platelet Activation in Patients With Unstable Angina Following Coronary Stenting Evaluation of the Effect of Clopidogrel Loading Dose in Inhibiting Platelet Activation

Serial Changes in Platelet Activation in Patients With Unstable Angina Following Coronary Stenting Evaluation of the Effect of Clopidogrel Loading Dose in Inhibiting Platelet Activation

Platelet Activity is a Biomarker of Cardiac Necrosis and Predictive of Untoward Clinical Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Stenting

Application of Current Guidelines to the Management of Unstable Angina and Non-ST-Elevation Myocardial Infarction

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