We have reported previously that local, patent microvascular networks support long-term survival of adult cardiac myocytes in subendocardial and subepicardial regions of large transmural post-myocardial infarction (MI) scars induced by left coronary artery ligation in middle-aged rats. According to our findings, such microvascular beds become perfused retrogradely from the left ventricular chamber via Thebesian vessels linked to residual veins. However, considering that surviving cardiac myocytes may serve as an endogenous source of contractile cells in healing scars, it is vital to determine whether the original arterial bed can be salvaged as a conduit for blood reperfusion. Therefore, in the current study, we aimed to investigate structural integrity of residual coronary arteries in healing post-MI scars. In order to achieve this goal, a large transmural MI was induced in 12-month-old male Sprague-Dawley rats by permanent ligation of the left coronary artery. Post-MI rats were euthanized 4 and 12 weeks after surgery and their hearts were processed into paraffin for histological evaluations. Eight micron transverse sections of each heart were stained with picrosirius red, Masson’s trichrome and Verhoeff’s elastic tissue stains. In addition, sections were labeled with TUNEL technique and an anti-smooth muscle (SM) alpha-actin antibody. Images of stained arteries were captured using an Olympus BX53 microscope equipped with DP72 digital camera. Furthermore, in each heart, the entire scar, stained for fibrillar collagen and SM alpha-actin, was digitized and then analyzed with Image-Pro Analyzer v.7.0 software to determine the fractional volumes of intravascular collagen and vascular SM cells. We found that the profiles of residual coronary arteries could be identified clearly in 4- and 12-week-old scars. Although some vessels appeared normal, most nonperfused arteries revealed gross structural alterations including accumulation of perivascular collagen and a prominent centripetal neointimal growth narrowing the vessel lumen. In the latter case, vascular SM cell hyperplasia was accompanied by a perecellular accumulation of collagen and elastic fibrils. Consistent with the progressive nature of these changes, in 12-week-old scars we often observed a complete obliteration of arterial lumens that occurred concurrently with disappearance of vascular SM cells and their replacement by collagenous tissue. The positive TUNEL stain in the walls of residual arteries indicates that the reduction in vascular SM cells might be related to their death via apoptosis. Importantly, our quantitative assessment of 4- and 12-week-old scars did confirm that the overall dynamic of structural changes observed in residual coronary arteries was associated with progressive accumulation of intravascular collagen (0.52±0.17% vs. 0.80±0.12%, respectively) and reduction in the content of vascular SM cells (2.27±0.51% vs. 1.53±1.19%, respectively). Therefore, our current findings provide additional support for the necessity of earlier reperfusion of the residual coronary arterial bed in healing scars in order to preserve its capacity to serve as a potential conduit for restored blood supply.