Protecting against ischemia-reperfusion injury: Antiplatelet drugs, statins, and their potential interactions

Yumei Ye, Jose R. Perez-Polo, Yochai Birnbaum

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

Statins and antiplatelet agents are currently used as therapeutic agents for patients with acute myocardial infarction. Statins limit myocardial infarct size by activating phosphatidylinositol-3-kinase (PI3K), ecto-5'-nucleotidase, Akt/endothelial nitric oxide synthase (eNOS), and the downstream effectors inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Inhibition of PI3K, adenosine receptors, eNOS, iNOS, or COX-2 abrogates the protective effects of statins. At >5 mg/kg, aspirin attenuates the myocardial infarct-size-limiting effect of statins. In contrast, the combination of low-dose atoravastatin with either the phosphodiesterase-III inhibitor cilostazol or the adenosine reuptake inhibitor dipyridamole synergistically limits infarct size. Low-dose aspirin with dipyridamole started during ischemia augmented the infarct-size-limiting effects of simvastatin. In contrast, high-dose aspirin blocked the protective effect of simvastatin. The combination of dipyridamole with low-dose aspirin and simvastatin resulted in the smallest infarct size. According to themost current data available, we believe that antiplatelet regimens may require modification for patients who are receiving statins.

Original languageEnglish (US)
Pages (from-to)76-82
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1207
DOIs
StatePublished - Jan 1 2010

Keywords

  • Antiplatelet agents
  • Aspirin
  • Cilostazol
  • Dipyridamole
  • Infarct size
  • Ischemia-reperfusion injury
  • Statins

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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