Following myocardial infarction, the heart undergoes a precisely choreographed repair sequence involving multiple cell types. Inflammatory cells first infiltrate damaged tissue to clear dead cardiomyocytes, followed by waves of leukocytes, fibroblasts, and endothelial cells guided by cytokine signals. These cells deposit collagen and other matrix proteins to form protective scar tissue that prevents cardiac rupture. This cellular orchestration represents one of medicine's most studied yet challenging repair processes. The inflammatory cascade mirrors wound healing elsewhere in the body, but cardiac muscle's limited regenerative capacity makes scarring the primary survival mechanism. However, this trade-off creates a clinical dilemma: while scarring prevents immediate death from cardiac rupture, excessive fibrosis reduces heart function long-term. Understanding these cellular dynamics has become crucial for developing therapies that optimize healing while minimizing functional impairment. Current research focuses on timing interventions to enhance beneficial inflammation while preventing excessive scarring. The complexity of these interactions explains why post-infarction outcomes vary dramatically between patients, and why therapeutic approaches must balance competing biological imperatives of structural stability versus functional preservation.