Preeclampsia remains a major cause of maternal and perinatal morbidity, and low-dose aspirin is the most established pharmacological preventive strategy for pregnancies at increased risk. However, preventive benefit depends on more than drug prescription. This scoping review mapped the evidence from risk identification through aspirin optimization and real-world implementation. Scopus was searched using a predefined TITLE-ABS-KEY strategy combining low-dose aspirin, preeclampsia, pregnancy, and prevention terms. Of 494 records identified, 35 studies were included in the core evidence map after temporal, document-type, language, and topical screening. Evidence was charted across four domains: risk identification and screening; aspirin dose, timing, adherence, and biological responsiveness; maternal, fetal, neonatal, and safety outcomes; and implementation barriers and facilitators. Clinical risk-factor approaches were accessible but variably sensitive, whereas multimodal strategies incorporating mean arterial pressure, uterine artery Doppler, placental growth factor, pregnancy-associated plasma protein-A, and individualized competing-risks models generally improved risk stratification. Aspirin regimens ranged from approximately 60–81 mg to 150–162 mg, with emerging evidence that earlier initiation, adherence, obesity, baseline vascular risk, and pharmacodynamic response may modify benefit. Reported outcomes extended beyond preeclampsia to preterm birth, fetal growth, postpartum hypertension, and bleeding, with substantial heterogeneity across populations and study designs. Real-world studies repeatedly documented missed eligibility, under- prescription, delayed initiation, nonadherence, and health-system constraints, although structured screening, counseling, checklists, and integrated screen-and-prevent pathways improved uptake in several settings. The evidence therefore supports conceptualizing aspirin prophylaxis as a multistage prevention pathway rather than an isolated medication intervention. Future work should integrate phenotype-specific risk stratification, comparative dosing, standardized adherence measurement, biological response, cost, equity, and pragmatic implementation to translate established efficacy into reliable population-level prevention.