Coagulative necrosis and the wavefront across the wall

Once myocytes cross into irreversible injury, the tissue dies by coagulative necrosis. The defining feature is that the architectural outline of the tissue is preserved for days: the myocytes remain in place, their cytoplasm becomes intensely eosinophilic (pink on H&E staining), and the nuclei disappear as DNA is degraded. The sarcolemma is breached, so cytosolic enzymes such as troponin and creatine kinase MB leak into the interstitium and eventually into the bloodstream. An inflammatory infiltrate appears at the border zone within hours and moves inward over the following days. The distribution of necrosis across the ventricular wall is not uniform, and the pattern is best described as a wavefront. Because the subendocardium is the most vulnerable region, necrosis begins there and spreads outward toward the epicardium as occlusion time lengthens. In the classic experiments of Reimer and Jennings, occlusion of a coronary artery for 20 minutes produced necrosis confined to a small subendocardial zone; 40 minutes extended it to roughly the inner third of the wall; 3 hours reached the mid-myocardium; and 6 hours or more produced transmural necrosis involving the full thickness. The practical implication is that the fraction of the wall that infarcts is determined mainly by how long the artery remained occluded, which is why restoring flow quickly limits infarct size. A thin rim of subepicardial myocardium often survives even in large infarcts because it receives some flow from epicardial collateral vessels.