Dhruv Mahtta1,2, Deepthi Sudhakar2, Srikanth Koneru3, Guilherme Vianna Silva3, Mahboob Alam3, Salim S Virani1,2,4, Hani Jneid5,6. 1. Health Policy, Quality & Informatics Program,, Michael E. DeBakey VA Medical Center Health Services Research & Development Center for Innovations in Quality, Effectiveness, and Safety, Houston, TX, USA. 2. Division of Cardiovascular Medicine, Baylor College of Medicine, Houston, TX, USA. 3. Division of Cardiovascular Medicine,, Texas Heart Institute and Baylor College of Medicine, Houston, TX, USA. 4. Section of Cardiology, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, 77030, USA. 5. Division of Cardiovascular Medicine, Baylor College of Medicine, Houston, TX, USA. Jneid@bcm.edu. 6. Section of Cardiology, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, 77030, USA. Jneid@bcm.edu.
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.
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.