Genome-wide association studies have identified over 300 genetic loci linked to coronary artery disease risk, with polygenic risk scores now explaining approximately 15-20% of disease heritability. Key pathways include lipid metabolism disruption, endothelial dysfunction, and inflammatory cascade activation, with variants in genes like PCSK9, LDLR, and CRP showing the strongest effect sizes. This genetic framework represents a fundamental shift toward precision cardiovascular medicine. Traditional risk factors like cholesterol and blood pressure capture only part of an individual's true cardiac risk profile. Polygenic scoring can identify high-risk patients decades before symptoms appear, potentially enabling aggressive early intervention in those with genetic predisposition despite normal conventional markers. The clinical implications extend beyond risk prediction to drug development, as genetic variants often point directly to druggable pathways. However, current polygenic scores perform poorly in non-European populations due to research bias, limiting their universal application. While promising for personalized prevention strategies, the complexity of gene-environment interactions means genetic risk remains probabilistic rather than deterministic. This genomic approach could revolutionize preventive cardiology, but equitable implementation across diverse populations remains a critical challenge requiring expanded genetic research inclusivity.