Anti-Inflammatory Strategies for Plaque Stabilization after Acute Coronary Syndromes
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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.
KeywordsAcute coronary syndrome Vulnerable plaque Inflammation Therapeutics Plaque stabilization
Conflicts of Interest
Amos Baruch declares no conflicts of interest.
Nicholas van Bruggen declares no conflicts of interest.
Brian Kim declares no conflicts of interest.
Joshua Lehrer-Graiwer has stock options with Genentech.
A. Baruch, N van Bruggen and J Lehrer-Graiwer are employees of Genentech.
No other disclosures are required.
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
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