Targeting inflammation after myocardial infarction
Document Type
Article
Department
Office of the Provost; Cardiology
Abstract
Purpose of review: Inflammation plays a key role in clearing cellular debris and recovery after acute myocardial infarction (AMI). Dysregulation of or prolonged inflammation may result in adverse cardiac remodeling and major adverse clinical events (MACE). Several pre-clinical studies and moderate sized clinical trials have investigated the role of immunomodulation in improving clinical outcomes in patients with AMI.
Recent findings: Clinical data from the Canakinumab Atherothrombosis Outcome (CANTOS) and Colchicine Cardiovascular Outcomes Trial (COLCOT) have provided encouraging results among patients with AMI. Several other clinical and pre-clinical trials have brought about the prospect of modulating inflammation at various junctures of the inflammatory cascade including inhibition of complement cascade, interleukins, and matrix metalloproteinases. In patients with AMI, modulation of residual inflammation via various inflammatory pathways and mediators may hold promise for further reducing MACE. Learning from current data and understanding the nuances of immunomodulation in AMI are key for future trials and before widespread dissemination of such therapies.
Publication (Name of Journal)
Current Cardiology Reports
DOI
10.1007/s11886-020-01358-2
Recommended Citation
Mahtta, D.,
Sudhakar, D.,
Koneru, S.,
Silva, G. V.,
Alam, M.,
Virani, S. S.,
Jneid, H.
(2020). Targeting inflammation after myocardial infarction. Current Cardiology Reports, 22(10), 110.
Available at:
https://ecommons.aku.edu/provost_office/573
Comments
Pagination is not provided by the author/publisher. This work was published before the author joined Aga Khan University.