Introduction: Genetic reference panels and imputation approaches have improved greatly in the last 10 years. The development of the TOPMed reference plane has led to enhanced imputation quality and quantity of single nucleotide polymorphisms (SNPs) due to greater sample diversity among various population ancestries. We revisited our prior GWAS of recurrent stroke by utilizing the TOPMed imputation server. Methods: This GWAS used a Cox proportional hazards model of time to recurrent stroke with the Vitamin Intervention for Stroke Prevention clinical trial cohort. There were 2,100 genotyped patients (64% male) in total with an average age of 67.2 (±10.8) years and ancestry distribution of 1,725 (82%) European, 258 (12%) African, and 117 (6%) Other or Mixed ancestry. Genotyped samples underwent a strict quality control process. We utilized TOPMed for imputation which totaled 10,467,887 biallelic SNPs which was 14 times greater in number compared the original analysis. Results: Recurrent stroke was observed in 182 (8.7%) patients. We identified seven novel SNPS on chromosome 1 in addition to our previous finding, rs6664786. Interestingly all chromosome 1 SNPs were located within the LINCO1362 gene. This gene has an acute change in expression in the presence of smoking even after adjustment of relevant clinical factors. Two novel SNPs were found on chromosome 16 located in gene desert nearest the pseudo-gene RNU6-21P in an intergenic region downstream of the Cadherin-8 (CDH8) gene. Both SNPs and RNU6-21P have no previously reported clinical relevance, except for their relative position to CDH8. CDH8 is highly expressed in brain tissue. Conclusions: We identified several novel SNPs associated with recurrent stroke. Capitalizing on genetic imputation advancements allows potential new insights and discoveries with past trial cohorts. Understanding these insights may provide further mechanistic knowledge of recurrent stroke to develop potential therapeutic targets.