LATITUDE-TIMI: is there still hope for anti-inflammatory therapy in acute myocardial infaction?

Matthias Dewenter, Michael Wagner, Ali El-Armouche


Inflammation is a crucial feature of atherosclerotic plaque formation as well as post myocardial infarction (MI) remodeling and thus thought to play an essential role in the pathogenesis of ischemic heart disease and its complications (1,2). The regenerative processes after MI involve inflammatory, proliferative and maturation phases that are crucial for wound healing and reparation (3). However, an overactive inflammatory and fibrotic response is associated with maladaptive structural and electrophysiological remodeling, leading to systolic as well as diastolic dysfunction and contributing to the development of an arrhythmogenic substrate (2,4). Moreover, elevated cytokine levels also correlate with increased risk for recurrent coronary events in patients with MI (5).

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