Clopidogrel effect on platelet reactivity in patients with stent thrombosis: Results of the CREST study

Paul A. Gurbel, Kevin P. Bliden, Waiel Samara, Jason A. Yoho, Kevin Hayes, Mulugeta Z. Fissha, Udaya S. Tantry

Research output: Contribution to journalArticle

Abstract

OBJECTIVES: We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment reactivity than those who do not encounter stent thrombosis. BACKGROUND: High post-treatment platelet reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. METHODS: We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment platelet reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. RESULTS: The SAT patients had higher mean platelet reactivity than those without SAT by all measurements (p <0.05): 49 ± 4% versus 33 ± 2% for 5 μmol/l ADP-induced aggregation and 65 ± 3% versus 51 ± 2% for 20 μmol/l ADP-induced aggregation (p <0.001), 69 ± 5% versus 46 ± 9% for P2Y12 reactivity ratio (p = 0.03), and 138 ± 19 mean fluorescence intensity (MFI) versus 42 ± 4 MFI for stimulated GP IIb/IIIa expression (p <0.001). Of patients with SAT, 60% had high platelet reactivity. CONCLUSIONS: High post-treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT. Measures to uniformly determine platelet reactivity after coronary stenting and treatment strategies to improve P2Y 12 receptor inhibition in patients with high post-treatment platelet reactivity should be further investigated.

Original languageEnglish (US)
Pages (from-to)1827-1832
Number of pages6
JournalJournal of the American College of Cardiology
Volume46
Issue number10
DOIs
StatePublished - Nov 15 2005

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clopidogrel
Stents
Thrombosis
Blood Platelets
Adenosine Diphosphate
Platelet Glycoprotein GPIIb-IIIa Complex
Therapeutics
Fluorescence

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Gurbel, P. A., Bliden, K. P., Samara, W., Yoho, J. A., Hayes, K., Fissha, M. Z., & Tantry, U. S. (2005). Clopidogrel effect on platelet reactivity in patients with stent thrombosis: Results of the CREST study. Journal of the American College of Cardiology, 46(10), 1827-1832. https://doi.org/10.1016/j.jacc.2005.07.056

Clopidogrel effect on platelet reactivity in patients with stent thrombosis : Results of the CREST study. / Gurbel, Paul A.; Bliden, Kevin P.; Samara, Waiel; Yoho, Jason A.; Hayes, Kevin; Fissha, Mulugeta Z.; Tantry, Udaya S.

In: Journal of the American College of Cardiology, Vol. 46, No. 10, 15.11.2005, p. 1827-1832.

Research output: Contribution to journalArticle

Gurbel, Paul A. ; Bliden, Kevin P. ; Samara, Waiel ; Yoho, Jason A. ; Hayes, Kevin ; Fissha, Mulugeta Z. ; Tantry, Udaya S. / Clopidogrel effect on platelet reactivity in patients with stent thrombosis : Results of the CREST study. In: Journal of the American College of Cardiology. 2005 ; Vol. 46, No. 10. pp. 1827-1832.
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abstract = "OBJECTIVES: We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment reactivity than those who do not encounter stent thrombosis. BACKGROUND: High post-treatment platelet reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. METHODS: We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment platelet reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. RESULTS: The SAT patients had higher mean platelet reactivity than those without SAT by all measurements (p <0.05): 49 ± 4{\%} versus 33 ± 2{\%} for 5 μmol/l ADP-induced aggregation and 65 ± 3{\%} versus 51 ± 2{\%} for 20 μmol/l ADP-induced aggregation (p <0.001), 69 ± 5{\%} versus 46 ± 9{\%} for P2Y12 reactivity ratio (p = 0.03), and 138 ± 19 mean fluorescence intensity (MFI) versus 42 ± 4 MFI for stimulated GP IIb/IIIa expression (p <0.001). Of patients with SAT, 60{\%} had high platelet reactivity. CONCLUSIONS: High post-treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT. Measures to uniformly determine platelet reactivity after coronary stenting and treatment strategies to improve P2Y 12 receptor inhibition in patients with high post-treatment platelet reactivity should be further investigated.",
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T1 - Clopidogrel effect on platelet reactivity in patients with stent thrombosis

T2 - Results of the CREST study

AU - Gurbel, Paul A.

AU - Bliden, Kevin P.

AU - Samara, Waiel

AU - Yoho, Jason A.

AU - Hayes, Kevin

AU - Fissha, Mulugeta Z.

AU - Tantry, Udaya S.

PY - 2005/11/15

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N2 - OBJECTIVES: We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment reactivity than those who do not encounter stent thrombosis. BACKGROUND: High post-treatment platelet reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. METHODS: We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment platelet reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. RESULTS: The SAT patients had higher mean platelet reactivity than those without SAT by all measurements (p <0.05): 49 ± 4% versus 33 ± 2% for 5 μmol/l ADP-induced aggregation and 65 ± 3% versus 51 ± 2% for 20 μmol/l ADP-induced aggregation (p <0.001), 69 ± 5% versus 46 ± 9% for P2Y12 reactivity ratio (p = 0.03), and 138 ± 19 mean fluorescence intensity (MFI) versus 42 ± 4 MFI for stimulated GP IIb/IIIa expression (p <0.001). Of patients with SAT, 60% had high platelet reactivity. CONCLUSIONS: High post-treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT. Measures to uniformly determine platelet reactivity after coronary stenting and treatment strategies to improve P2Y 12 receptor inhibition in patients with high post-treatment platelet reactivity should be further investigated.

AB - OBJECTIVES: We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment reactivity than those who do not encounter stent thrombosis. BACKGROUND: High post-treatment platelet reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. METHODS: We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment platelet reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. RESULTS: The SAT patients had higher mean platelet reactivity than those without SAT by all measurements (p <0.05): 49 ± 4% versus 33 ± 2% for 5 μmol/l ADP-induced aggregation and 65 ± 3% versus 51 ± 2% for 20 μmol/l ADP-induced aggregation (p <0.001), 69 ± 5% versus 46 ± 9% for P2Y12 reactivity ratio (p = 0.03), and 138 ± 19 mean fluorescence intensity (MFI) versus 42 ± 4 MFI for stimulated GP IIb/IIIa expression (p <0.001). Of patients with SAT, 60% had high platelet reactivity. CONCLUSIONS: High post-treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT. Measures to uniformly determine platelet reactivity after coronary stenting and treatment strategies to improve P2Y 12 receptor inhibition in patients with high post-treatment platelet reactivity should be further investigated.

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