Myocardial Infarction (MI) in young adults aged 18–30 years is an emerging clinical concern with a steadily increasing global incidence. Although traditionally attributed to premature atherosclerosis, growing evidence suggests that early-onset MI results from a complex interplay of endothelial dysfunction, coronary vasospasm, thrombophilia, genetic susceptibility, metabolic syndrome, and substance exposure. These mechanisms may precipitate acute coronary events even in the absence of advanced atherosclerotic plaque burden. Unlike previous reviews that primarily emphasize premature coronary artery disease, this short communication provides an integrated multisystem pathophysiological perspective on early-onset MI. Understanding these interacting mechanisms is essential for early cardiovascular risk stratification, targeted preventive strategies, and timely intervention beginning in adolescence and early adulthood.