Related Experiment Video
Updated: May 11, 2026
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Anti-inflammatory strategies for plaque stabilization after acute coronary syndromes
Amos Baruch1, Nicholas van Bruggen, Juyong Brian Kim
1Genentech Research and Early Development, 1 DNA Way MS 453a, South San Francisco, CA 94080, USA.
Insights
Recurrent heart attacks after acute coronary syndrome (ACS) are linked to inflammation. New research suggests the sympathetic nervous system drives this inflammation, offering potential therapeutic targets to prevent future cardiac events.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Hematology
Background:
- High risk of recurrent myocardial infarction (MI) persists after acute coronary syndrome (ACS) despite advanced treatments.
- Acute inflammatory response following ACS correlates with recurrent event risk, suggesting a causal role.
- Pathophysiological mechanisms linking post-ACS inflammation to recurrent events remain incompletely understood.
Purpose of the Study:
- To review evidence implicating systemic inflammation post-ACS in atherosclerosis progression.
- To identify potential therapeutic targets for intervention in the post-ACS period.
- To highlight experimental therapies and clinical studies validating these targets.
Main Methods:
- Review of existing and emerging scientific literature on post-ACS inflammation and atherosclerosis.
- Synthesis of proposed mechanisms involving sympathetic nervous system activation and hematopoietic stem cell mobilization.
- Identification of therapeutic strategies based on current research and ongoing clinical trials.
Main Results:
- Evidence suggests sympathetic nervous system activation post-cardiac event mobilizes stem cells.
- Mobilized stem cells may differentiate into inflammatory monocytes that infiltrate plaques.
- This process can acutely lead to recurrent plaque rupture and myocardial infarction.
Conclusions:
- Post-ACS systemic inflammation, driven by sympathetic activation, plays a critical role in atherosclerosis progression and recurrent events.
- Targeting inflammatory pathways and stem cell mobilization presents a promising therapeutic strategy.
- Ongoing clinical studies are crucial for validating these novel therapeutic targets.
Abstract:
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.
Related Concept Videos
01:27Coronary Artery Disease V: Interprofessional Care
01:26Atherosclerosis III: Management
01:28Acute Coronary Syndrome IV: Interprofessional Care
01:26Angina IV: Management
01:27Peripheral Artery Disease III: Interprofessional Care
01:26Coronary Artery Disease IV: Preventive Measures