Granulation Tissue and Collagen Scar Formation | AI Learning Guide

The reparative macrophages do more than clean up. They release growth factors that recruit fibroblasts and trigger new capillary growth, and the result is granulation tissue — a loose, vascular tissue full of myofibroblasts sitting in a matrix of type three collagen. That tissue starts replacing dead myocytes around day three and dominates the infarct between about day seven and week two. The myofibroblasts are the workhorses here: they make collagen and they can contract, pulling the wound edges together. Over the next few weeks the matrix matures — type three collagen is swapped for stronger type one collagen, cross-linking increases, and the blood supply drops. By six to eight weeks you have a dense scar with almost no cells. It is tough, so it resists rupture, but it has no sarcomeres, so it cannot contract. That is the trade-off: you get mechanical stability at the cost of permanent loss of pump tissue. And notice the timing problem — during the granulation phase, the dead tissue is gone but the new collagen is still weak, so days three to fourteen are when the wall is most likely to rupture.

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From granulation tissue to mature scar

Reparative macrophages release growth factors that recruit fibroblasts and stimulate angiogenesis. The resulting granulation tissue — capillaries, fibroblasts, myofibroblasts, and loose type III collagen — replaces necrotic myocytes from about day 3 and dominates the infarct between day 7 and week 2. Over the following weeks, type III collagen is replaced by stronger type I collagen, cross-links increase, vascularity falls, and the tissue becomes a dense acellular scar by roughly 6–8 weeks.

The weak window

During the granulation phase the dead tissue has been digested but the new collagen scaffold is still immature. This makes roughly days 3 to 14 the period of greatest risk for ventricular free wall rupture, papillary muscle rupture, and septal rupture. Once the scar matures, rupture risk falls sharply — but the loss of contractile tissue is permanent.