Healing of myocardial infarcts depends on an inflammatory cascade that 
ultimately results in clearance of dead cells and matrix debris and formation of 
a scar. Myocardial necrosis activates complement, Nuclear Factor (NF)-kappaB and 
Toll-like Receptor (TLR)-dependent pathways, and generates free radicals, 
triggering an inflammatory response. Chemokines and cytokines are markedly 
induced in the infarct and mediate recruitment and activation of neutrophils and 
mononuclear cells. Extravasation of platelets and plasma proteins, such as 
fibrinogen and fibronectin, results in formation of a clot, consisting of 
platelets embedded in a mesh of crosslinked fibrin. This provisional matrix 
provides a scaffold for migration of cells into the infarct. Monocytes 
differentiate into macrophages and secrete fibrogenic and angiogenic growth 
factors inducing formation of granulation tissue, containing myofibroblasts and 
neovessels. Repression of proinflammatory cytokine and chemokine synthesis, 
mediated in part through Transforming Growth Factor (TGF)-beta and Interleukin 
(IL)-10, is critical for resolution of the inflammatory infiltrate and 
transition to fibrous tissue deposition. Infarct myofibroblasts deposit 
extracellular matrix proteins and a collagen-based scar is formed. As the wound 
matures, fibroblasts undergo apoptosis and neovessels regress, resulting in 
formation of a scar with a low cellular content containing dense, cross-linked 
collagen. The pathologic and structural changes associated with infarct healing 
directly influence ventricular remodeling and affect prognosis in patients with 
myocardial infarction. Understanding the mechanisms involved in the regulation 
of the post-infarction inflammatory response, and the spatial and temporal 
parameters of wound healing is necessary in order to identify specific molecular 
targets for therapeutic intervention.