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Protecting against ischemia‐reperfusion injury: antiplatelet drugs, statins, and their potential interactions
Author(s) -
Ye Yumei,
PerezPolo Jose R.,
Birnbaum Yochai
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05725.x
Subject(s) - medicine , reperfusion injury , ischemia , pharmacology , cardiology
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 the most current data available, we believe that antiplatelet regimens may require modification for patients who are receiving statins.