QT prolongation causes torsades de pointes sudden death from heritable, pharmacologic, metabolic, nutritional triggers. Its dimensions have been studied separately. This integrative review synthesizes research on molecular pathogenesis, acquired/metabolic/nutritional risks, clinical stratification, therapy, and AI prediction. Dual-function channel mutations and post-translational defects underlie congenital LQTS beyond classic three genes. Drug-gene-metabolic interactions amplify acquired risk; insulin resistance, NAFLD, and adiposity are independent risk factors. Nutritional exposures (grapefruit juice, licorice, energy drinks) compound arrhythmic risk. QTc threshold alone is insufficient; T-wave morphology, genotype, electromechanical window dynamics, and M-FACT score add prognostic value. Nonpenetrant LQTS carries near-population-level event risk. Genotype-targeted mexiletine and left cardiac sympathetic denervation are validated alternatives. Machine learning outperforms clinical scores; deep learning distinguishes congenital from acquired QT prolongation on ECG. Precision QT management requires integrated strategies including nutritional and metabolic determinants, QTc measurement, and AI-enhanced prediction. Prospective data remain essential before algorithmic tools guide decisions.