Besides cell death and loss of function in the brain, ischemic stroke is often associated with poor cardiac outcomes, increasing the risk for atrial fibrillation and myocardial infarction. This condition, known as stroke-induced heart injury (SIHI), has been well characterized for the four chambers of the heart and myocardial tissue, but the timeline and extent of injury in the coronary arteries remain unclear. To study the timeline of ischemic SIHI in the left coronary artery (LCA), we documented how the thickness, cross-sectional area, and immune cell recruitment in the LCA changed following an insular ischemic stroke in a rat model. Rats were divided into a stroke (endothelin-1 injection) and control (phosphate-buffered saline injection) group and sacrificed at various time-points post-treatment (6h, 24h, 7d, 14d, & 28d). Following a standard H&E staining protocol, we observed a general thickening and constriction in the vessel until 7 days post-stroke, corresponding to eutrophic remodelling. After immunohistochemistry staining for pan-leukocytes (CD45), neutrophils (myeloperoxidase), and B lymphocytes (CD45R), we observed a maximal recruitment of innate and adaptive immune cells occur concurrently at 24 hours post-stroke, indicating possible immunological memory in inflammation from stroke. These results extend our understanding of stroke-induced heart injury to vascular changes in the heart and lay the groundwork in addressing the relevant clinical problem of cardiac complications after stroke.