Infarct scar: a dynamic tissue

Infarct scar. a requisite to the rebuilding of necrotic myocardium followin g myocardial infarction (MI), has long been considered inert. Earlier morph ologic studies suggested healing at the infarct site was complete within 6- 8 weeks following MI and resultant scar tissue, albeit necessary, was acell ular and simply fibrillar collagen. Utilizing molecular and cellular biolog ic technologies. recent studies indicate otherwise. Infarct scar is compose d of phenotypically transformed fibroblast-like cells, termed myofibroblast s (myoFb) because they express alpha-smooth muscle actin (alpha-SMA) and th ese microfilaments confer contractile behavior in response to various pepti des and amines. These cells are nourished by a neovasculature and are persi stent at the MI site, where they are metabolically active expressing compon ents requisite to angiotensin (Ang) peptide generation, including convertin g enzyme, receptors for AngII and transforming growth factor (TCF)-beta 1. They continue to elaborate fibrillar type I collagen. Their generation of t hese peptides contribute to ongoing scar tissue collagen turnover and to fi brous tissue formation of noninfarcted myocardium. Infarct scar contraction accounts for its thinning and its tonus may contribute to abnormal ventric ular chamber stiffness with diastolic dysfunction. Infarct scar is a dynami c tissue: cellular, vascularized. metabolically active and contractile. Pha rmacologic interventions with angiotensin converting enzyme inhibitor or AT I receptor antagonist has proven effective in attenuating scar tissue metab olic activity and minimizing adverse accumulation of fibrous tissue in noni nfarcted myocardium. (C) 2000 Elsevier Science B.V. All rights reserved.