High-risk pathogenic variants in genes such as LMNA, DSP, FLNC, and others markedly increase ventricular arrhythmia and heart failure risk in DCM, independent of ejection fraction and clinical demographics.
Genetic diagnosis refines sudden cardiac death prevention strategies, identifying patients at risk even with preserved left ventricular ejection fraction (LVEF ≥ 50%).
Emerging evidence highlights novel pathogenic genes like NKX2-5 implicated in familial DCM with arrhythmias, expanding the genetic spectrum beyond sarcomeric proteins.
Polymorphisms in adrenergic receptor-related genes modulate cardiovascular event risk, underscoring the influence of genetic modifiers on arrhythmia susceptibility in DCM.
