In this issue of the Journal, Jackson et al.(1) describe infarct extension after anteroapical myocardial infarction (MI) in sheep that surprisingly occurs in the face of normal border zone (BZ) blood flow. Briefly, sheep were instrumented with an array of sonomicrometry crystals on a long-term basis. Crystals were placed within the area at risk, at the edge of the area at risk, and in the remote non-infarcted myocardium, and data were collected before and eight weeks after anteroapical MI (2). The BZ was defined as those chords that both remodeled (increase in chord length at end-systole) and had decreased function (decreased percent fractional shortening). Using these criteria, the BZ increased in size from 6 to 11 chords (of 20 total non-infarct chords) in the anterolateral left ventricular (LV) wall. Histology showed progressive fibrosis. This is demonstrated in Figure 6A of the Jackson et al.(1) article, in which tongues of fibrosis are seen infiltrating into the noninfarcted myocardium. At the edge of the advancing fibrosis were myocytes with pale cytoplasm and enlarged nuclei (myocytolysis)(Fig. 6C of Jackson et al.[1]) that the authors suggest are undergoing apoptosis.