4.4 Article

Rosuvastatin May Reduce the Incidence of Cardiovascular Events in Patients with Acute Coronary Syndromes Receiving Percutaneous Coronary Intervention by Suppressing miR-155/SHIP-1 Signaling Pathway

Journal

CARDIOVASCULAR THERAPEUTICS
Volume 32, Issue 6, Pages 276-282

Publisher

WILEY-HINDAWI
DOI: 10.1111/1755-5922.12098

Keywords

Acute coronary syndromes; miR-155; SHIP-1; Percutaneous coronary intervention; Rosuvastatin

Funding

  1. Science and Technology Development Plan of Yulin [Yu Ke Ji 20141002]

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PurposeThe beneficial effect of rosuvastatin against percutaneous coronary intervention (PCI) related procedural myocardial injury has been determined mostly in patients with acute coronary syndromes (ACS). However, the detailed therapeutic mechanism has not been well studied. MethodsPatients with ACS receiving PCI (n=159) were randomized to control group (placebo treatment) or to rosuvastatin group (20mg 12h before PCI, and a further 20mg 2h preprocedure dose). Levels of INF-, TNF-, IL-6, miR-155/SHIP-1, and CD4(+)FoxP3(+)Treg in peripheral blood were detected before PCI and 24h after PCI. Clinical data of these patients were also collected in this prospective study. ResultsCompared with placebo, rosuvastatin treatment significantly reduced the incidence of periprocedural myocardial infarction (PMI) and levels of cardiac troponin I (cTnI) associated with decreased relative expression of serum miR-155, levels of inflammatory cytokines (INF-, TNF-, and IL-6), increased SHIP-1 expression and CD4(+)FoxP3(+)Treg percentage values (P<0.05). In addition, patients with rosuvastatin pretreatment also reduced incidence of 30days major adverse cardiac events (MACE) compared to the patients with placebo treatment (16 patients vs. 28 patients, P=0.038). ConclusionsOur study suggests that high loading dose rosuvastatin pretreatment may reduce the incidence of cardiovascular events and levels of inflammatory markers in patients with ACS receiving PCI, which may be explained at least in part, by mechanism involving suppression of miR-155/SHIP-1 signaling pathway.

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