Background: Lipoprotein(a) [Lp(a)] is increasingly recognized as an independent and genetically determined cardiovascular risk factor. However, its clinical role in patients with established coronary artery disease (CAD), particularly in relation to premature disease onset, remains incompletely defined. This study aimed to evaluate the association between Lp(a) levels and early-onset CAD, as well as the relative contribution of Lp(a) compared with traditional cardiovascular risk factors. Methods: We conducted a retrospective observational study including 225 patients with established CAD admitted to a tertiary care center in 2023. Lp(a) levels were measured at admission. Patients were stratified according to revascularization strategy and age at first cardiovascular event (<50 vs. ≥50 years). Logistic regression and receiver operating characteristic (ROC) curve analyses were performed to assess associations and determine predictive performance. Results: Thirty-eight patients (17%) experienced early-onset CAD. Patients with early events showed significantly higher Lp(a) levels compared with those with later events (median 42 [19–75] vs. 21 [10–66] mg/dL; p = 0.020), despite lower LDL and non-HDL cholesterol levels. In multivariate analysis, both Lp(a) (OR 2.835, 95% CI 1.226–6.556, p = 0.015) and smoking (OR 2.516, 95% CI 1.116–5.673, p = 0.026) were independently associated with early-onset CAD. Lp(a) showed modest discriminative ability (AUC 0.619), with a cut-off value of 23 mg/dL providing 74% sensitivity and 52% specificity, and a high negative predictive value (91%). Lp(a) levels did not differ across revascularization subgroups. Conclusions: Elevated Lp(a) levels are independently associated with premature CAD, even in patients with lower traditional lipid risk factors and intensive lipid-lowering therapy. Routine Lp(a) assessment may improve cardiovascular risk stratification, particularly in younger patients.