Anti-Inflammatory Strategies for Ventricular Remodeling Following ST-Segment Elevation Acute Myocardial Infarction

被引:342
作者
Seropian, Ignacio M. [1 ]
Toldo, Stefano [2 ,3 ]
Van Tassell, Benjamin W. [2 ,3 ,4 ]
Abbate, Antonio [2 ,3 ]
机构
[1] FLENI Fdn, Dept Cardiol, Buenos Aires, DF, Argentina
[2] Virginia Commonwealth Univ, VCU Pauley Heart Ctr, Richmond, VA USA
[3] Virginia Commonwealth Univ, Victoria Johnson Res Lab, Richmond, VA USA
[4] Virginia Commonwealth Univ, Sch Pharm, Richmond, VA USA
基金
美国国家卫生研究院;
关键词
TUMOR-NECROSIS-FACTOR; PERCUTANEOUS CORONARY INTERVENTION; IMPROVES CARDIAC-FUNCTION; ISCHEMIA-REPERFUSION INJURY; ANTI-C5 COMPLEMENT ANTIBODY; C1 ESTERASE INHIBITOR; HEART-FAILURE; P-SELECTIN; INTRAVENOUS IMMUNOGLOBULIN; PHARMACOLOGICAL INHIBITION;
D O I
10.1016/j.jacc.2014.01.014
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
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. (C) 2014 by the American College of Cardiology Foundation
引用
收藏
页码:1593 / 1603
页数:11
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