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Cardiovascular Research 1999 43(2):291-299; doi:10.1016/S0008-6363(99)00132-7
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Inflammation in ischemic heart disease: Response to tissue injury or a pathogenetic villain?

J.L Mehtaa,b,* and D.Y Lia

aDepartment of Medicine, University of Florida, College of Medicine, 1600 Archer Rd., P.O. Box 100277, JHMHC, Gainesville, FL, USA
bVA Medical Center, Gainesville, FL, USA

* Corresponding author. Tel.: +1-352-379-4160; fax: +1-352-379-4161 mehta@medmac.ufl.edu

Received 9 December 1998; accepted 8 March 1999

The first 150 words of the full text of this article appear below.


    1 Introduction
 
The presence of inflammatory cells in the ischemic myocardial tissues has traditionally been believed to represent pathophysiologic response to injury [1]. It is only recently that inflammation has been related to the pathogenesis of acute coronary syndromes [2,3], reperfusion injury to ischemic myocardium [4], restenosis after angioplasty [5–7], failure of cardiac transplant [8], and chronic heart failure [9]. Accordingly, the relationship between inflammation with atherosclerosis and myocardial ischemia is now an area of active investigation.

Accumulation of polymorphonuclear leukocytes (PMN) and their activation are key features of inflammatory reaction associated with acute myocardial ischemia-reperfusion [3]. Experimental studies have shown that influx of PMNs into tissues results in tissue injury beyond that caused by ischemia alone [10,11]. It has also become apparent that the recruitment of PMNs during ischemia-reperfusion involves numerous mediators [3,4]. The causative role of PMNs in reperfusion injury in . . . [Full Text of this Article]


    2 Role of inflammation in atherogenesis
 

    3 Inflammation in precipitation of acute myocardial ischemia
 

    4 Inflammation in patients with ischemic heart disease
 
4.1 Stable/unstable ischemic heart disease
4.2 Coronary artery interventions

    5 Clinical studies directed at modulation of inflammation in IHD
 

    6 Integration of studies on inflammation in IHD
 

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