This federated electronic health record analysis of 97,882 matched adults found no association between elevated lipoprotein(a) levels and incident ischemic stroke or TIA, contradicting expected cardiovascular risk patterns. Patients with Lp(a) ≥50 mg/dL showed identical stroke rates (2.45% vs 2.69%) compared to those with lower levels, with similar null findings at alternative thresholds and across dose-response analyses. The disconnect between this real-world evidence and established causal links between Lp(a) and atherosclerotic disease likely reflects clinical practice patterns rather than biological reality. When physicians identify high Lp(a) patients, they typically initiate aggressive preventive interventions—statins, blood pressure management, lifestyle counseling—that may neutralize the genetic risk factor's impact. Additionally, testing-indication bias means Lp(a) measurements often occur in patients already receiving cardiovascular care, creating populations that don't reflect true population-level risk. This preprint awaits peer review, and results may change following expert evaluation. While confirmatory of treatment benefits rather than paradigm-shifting for Lp(a) biology, the findings underscore how real-world clinical management can modify genetic cardiovascular risk factors through proactive intervention strategies.