State-of-the-Art Paper
Anti-Inflammatory Strategies for Ventricular Remodeling Following ST-Segment Elevation Acute Myocardial Infarction

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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.

Key Words

acute myocardial infarction
inflammation
ventricular remodeling

Abbreviations and Acronyms

AAT
alpha1-trypsin
AMI
acute myocardial infarction
COX
cyclooxygenase
CRP
C-reactive protein
CVF
cobra venom factor
HF
heart failure
IL
interleukin
IL-1R1
interleukin 1 receptor 1
IVIG
intravenous immunoglobulin
MACE
major adverse cardiac event(s)
MMP
metalloproteinase
PCI
percutaneous coronary intervention
PI3K
phosphoinositide 3-kinase
RCT
randomized clinical trial
STEMI
ST-segment elevation myocardial infarction
TNF
tumor necrosis factor
TNFR
tumor necrosis factor receptor

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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.