Anti-inflammatory strategies for plaque stabilization after acute coronary syndromes

Curr Atheroscler Rep. 2013 Jun;15(6):327. doi: 10.1007/s11883-013-0327-7.


Despite dramatic advances in standard of care, the risk of recurrent myocardial infarction early after an acute coronary syndrome (ACS) remains high. This period of elevated risk after a cardiovascular event is associated with an acute inflammatory response. While post-ACS inflammation correlates with the risk for recurrent events and is likely to play a causal role in this period, the precise pathophysiologic mechanisms have been unclear. Recent studies have proposed that the cardiac event itself activates the sympathetic nervous system to directly mobilize hematopoietic stem cells to differentiate into inflammatory monocytes, acutely infiltrate plaque, and lead to recurrent plaque rupture. Here, we summarize the existing and emerging evidence implicating post-ACS activation of systemic inflammation in the progression of atherosclerosis, and identify possible targets for therapeutic intervention. We highlight experimental therapies and ongoing clinical studies that will validate these targets.

Publication types

  • Review

MeSH terms

  • Acute Coronary Syndrome / drug therapy
  • Acute Coronary Syndrome / immunology*
  • Anti-Inflammatory Agents / therapeutic use
  • Coronary Artery Disease / drug therapy
  • Coronary Artery Disease / immunology*
  • Humans
  • Inflammation
  • Myocardial Infarction / immunology*
  • Myocardial Infarction / prevention & control
  • Plaque, Atherosclerotic / drug therapy
  • Plaque, Atherosclerotic / immunology*


  • Anti-Inflammatory Agents