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Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity?

Publication ,  Journal Article
Malinin, AI; Oshrine, BR; Sane, DC; O'Connor, CM; Serebruany, VL
Published in: Blood Coagul Fibrinolysis
March 2007

The ability of clopidogrel to inhibit platelet function in patients with congestive heart failure (CHF) was proved by the PLUTO-CHF trial. We retrospectively analyzed platelet characteristics with respect to CHF etiology, class, and ejection fraction in patients enrolled in the PLUTO-CHF study. Twenty-five patients were divided by CHF etiology, severity, and ejection fraction. All patients received aspirin 325 mg for at least 1 month prior to screening. Platelet function studies were performed at baseline and after 30 days of therapy. There were no differences in platelet parameters dependent on clinical characteristics of CHF, except for a significant (P = 0.023) decrease in platelet/endothelial cell adhesion molecule 1 (PECAM-1) expression in the New York Heart Association class III-IV due to the higher baseline values. Therapy with clopidogrel resulted in a significant inhibition of platelet activity assessed by ADP-induced and epinephrine-induced aggregation, closure time, expression of PECAM-1, glycoprotein Ib, glycoprotein IIb/IIIa antigen, glycoprotein IIb/IIIa activity with PAC-1, CD151, and reduced formation of platelet-leukocyte conjugates when compared with baseline. Clopidogrel provides antiplatelet protection in the broad spectrum of patients with CHF independently of its etiology, severity, or myocardial contractility. This uniform platelet inhibition with clopidogrel may be an important consideration in designing future large-scale clinical trials.

Duke Scholars

Published In

Blood Coagul Fibrinolysis

DOI

ISSN

0957-5235

Publication Date

March 2007

Volume

18

Issue

2

Start / End Page

91 / 96

Location

England

Related Subject Headings

  • Ticlopidine
  • Stroke Volume
  • Retrospective Studies
  • Platelet Function Tests
  • Platelet Aggregation Inhibitors
  • Platelet Activation
  • Myocardial Contraction
  • Middle Aged
  • Male
  • Humans
 

Citation

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Chicago
ICMJE
MLA
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Malinin, A. I., Oshrine, B. R., Sane, D. C., O’Connor, C. M., & Serebruany, V. L. (2007). Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity? Blood Coagul Fibrinolysis, 18(2), 91–96. https://doi.org/10.1097/MBC.0b013e32801455db
Malinin, Alex I., Benjamin R. Oshrine, David C. Sane, Christopher M. O’Connor, and Victor L. Serebruany. “Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity?Blood Coagul Fibrinolysis 18, no. 2 (March 2007): 91–96. https://doi.org/10.1097/MBC.0b013e32801455db.
Malinin AI, Oshrine BR, Sane DC, O’Connor CM, Serebruany VL. Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity? Blood Coagul Fibrinolysis. 2007 Mar;18(2):91–6.
Malinin, Alex I., et al. “Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity?Blood Coagul Fibrinolysis, vol. 18, no. 2, Mar. 2007, pp. 91–96. Pubmed, doi:10.1097/MBC.0b013e32801455db.
Malinin AI, Oshrine BR, Sane DC, O’Connor CM, Serebruany VL. Does heart failure etiology, New York Heart Association class, or ejection fraction affect the ability of clopidogrel to inhibit heightened platelet activity? Blood Coagul Fibrinolysis. 2007 Mar;18(2):91–96.

Published In

Blood Coagul Fibrinolysis

DOI

ISSN

0957-5235

Publication Date

March 2007

Volume

18

Issue

2

Start / End Page

91 / 96

Location

England

Related Subject Headings

  • Ticlopidine
  • Stroke Volume
  • Retrospective Studies
  • Platelet Function Tests
  • Platelet Aggregation Inhibitors
  • Platelet Activation
  • Myocardial Contraction
  • Middle Aged
  • Male
  • Humans