Author + information
- Received November 29, 2013
- Revision received December 28, 2013
- Accepted January 8, 2014
- Published online April 29, 2014.
- Ignacio M. Seropian, MD∗,
- Stefano Toldo, PhD†,‡,
- Benjamin W. Van Tassell, PharmD†,‡,§ and
- Antonio Abbate, MD, PhD†,‡∗ ()
- ∗Cardiology Department, FLENI Foundation, Buenos Aires, Argentina
- †VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia
- ‡Victoria Johnson Research Laboratory, Virginia Commonwealth University, Richmond, Virginia
- §School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia
- ↵∗Reprint requests and correspondence:
Dr. Antonio Abbate, Department of Medicine, VCU Pauley Heart Center, Virginia Commonwealth University, 1200 East Broad Street, Box 980281, Richmond, Virginia 23298.
Acute myocardial infarction (AMI) leads to molecular, structural, geometric, and functional changes in the heart in a process known as ventricular remodeling. An intense organized inflammatory response is triggered after myocardial ischemia and necrosis and involves all components of the innate immunity, affecting both cardiomyocytes and noncardiomyocyte cells. Inflammation is triggered by tissue injury; it mediates wound healing and scar formation and affects ventricular remodeling. Many therapeutic attempts aimed at reducing inflammation in AMI during the past 3 decades presented issues of impaired healing or increased risk of cardiac rupture or failed to show any additional benefit in addition to standard therapies. More recent strategies aimed at selectively blocking one of the key factors upstream rather than globally suppressing the response downstream have shown some promising results in pilot trials. We herein review the pathophysiological mechanisms of inflammation and ventricular remodeling after AMI and the results of clinical trials with anti-inflammatory strategies.
Drs. Abbate, Toldo, and Van Tassell are supported by research grants from the American Heart Association and the National Institutes of Health. Dr. Abbate has received research grants from Gilead, Novartis, and XOMA; has lectured for GlaxoSmithKline, Novartis, and XOMA; and has consulted for Gilead, Janssen, Omni Biopharma, Swedish Orphan Biovitrum, and XOMA. Dr. Van Tassell has received research grants from Gilead and Novartis; and has consulted for Novartis. Dr. Seropian has reported that he has no relationships relevant to the contents of this paper to disclose.
- Received November 29, 2013.
- Revision received December 28, 2013.
- Accepted January 8, 2014.
- American College of Cardiology Foundation