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Project

Regulation of the transcriptome by circulating microRNAs in patients with acute coronary syndromes.

The long-term outcome after acute myocardial infarction (MI) remains poor: up to 20% of patients develop heart failure (HF) or recurrent ischemic events. Inflammation plays a pivotal role in the pathogenesis of atherosclerosis and in acute myocardial infarction (MI). Subsets of leukocytes, such as monocytes and neutrophils, play a distinct role in the different phases of MI. High sensitivity CRP (hsCRP) is traditionally measured in clinical practice as a surrogate quantitative marker of inflammation. In patients with acute MI, the admission level of (hs)CRP are an independent predictor of death. Inflammation also appears to be closely related with infarct size. However, several strategies for limiting infarct size by targeting this acute inflammatory response in acute MI (eg. anti-interleukin-1 (IL-1), IL-6 and p38 MAPK), have so far not resulted in improved clinical outcome.

Therefore, the aim of this project to better phenotype the inflammatory response in MI patients. We will determine the RNA expression profile of the inflammatory cells upstream from CRP in patients with acute MI and at follow-up to identify new prognostic markers of HF or recurrent events and identify new possible therapeutic targets.

Date:1 Sep 2013 →  29 May 2019
Keywords:Myocardial infarction, Gene expression, Left ventricular dysfunction
Disciplines:Cardiac and vascular medicine
Project type:PhD project