🧬 Genetic testing in Dilated Cardiomyopathy: are we using it right? A new ESC consensus highlights a key shift: genetics in DCM is no longer just about family screening—it’s now central to clinical decision-making. 🔍 Key messages 🧠 Not just monogenic anymore DCM is increasingly seen as a continuum: Rare variants (high impact) common variants (polygenic background) environmental triggers ➡️ Disease = interaction, not a single mutation 🧬 Who should be tested? → almost everyone Genetic testing is recommended when results can impact: ✔️ diagnosis ✔️ prognosis ✔️ treatment (e.g. ICD decisions) ✔️ family screening ➡️ Even “acquired” DCM does NOT exclude genetics 📊 Yield is variable but meaningful ~8–36% overall up to 55% in familial DCM ➡️ Still clinically impactful despite imperfect yield ⚠️ Gene panels: bigger ≠ better Large panels increase VUS Limited gain in actionable variants ➡️ Focus on validated disease genes is key 🔥 Genotype matters clinically Some genes carry higher arrhythmic risk: LMNA, FLNC, DSP, RBM20, PLN ➡️ Can influence ICD decision-making beyond EF 🧩 The real paradigm shift: interpretation Genetic results must be read in context: phenotype environment (e.g. myocarditis, chemo, pregnancy) penetrance ➡️ A variant alone is NOT the diagnosis 👨‍👩‍👧 Family impact is huge Enables cascade screening Can discharge gene-negative relatives Opens reproductive options 💡 Take-home message Genetic testing in DCM is no longer optional or “nice to have”— it’s becoming a core part of precision cardiology. 👉 But its value depends entirely on how well we interpret it. #Cardiology #DCM #Genetics #Cardiomyopathy #PrecisionMedicine #HeartFailure #ESC #MedEd 🧬🫀 doi.org/10.1093/eurheartj/eh…