dilated cardiomyopathy

5 min read Updated 2026-03-25
Contents
dilated cardiomyopathy

LV (or biventricular) dilatation with systolic dysfunction not explained by abnormal loading conditions (HTN, valve disease) or coronary artery disease. Aetiologies range from genetic (30–50% of “idiopathic” DCM) to toxic, inflammatory, and metabolic. Management follows standard HFrEF GDMT. Key distinguishing features: the role of cardiac MRI in aetiology, genetic testing and family screening, the ICD debate (DANISH), and the possibility of myocardial recovery.


aetiology

CategoryExamples
geneticTTN (titin — most common, ~25%), LMNA (lamin A/C — high arrhythmia risk), MYH7, DSP, FLNC, RBM20, PLN
toxicalcohol (>80 g/day for >5 years), cocaine, methamphetamine, chemotherapy (anthracyclines, trastuzumab)
inflammatorypost-viral myocarditis (enterovirus, parvovirus B19, SARS-CoV-2), autoimmune (SLE, sarcoidosis), giant cell myocarditis
metabolic / endocrinethyroid disease, phaeochromocytoma, acromegaly, nutritional (thiamine, selenium, carnitine deficiency)
peripartumonset in last month of pregnancy to 5 months postpartum; may recover; recurrence risk with subsequent pregnancies
tachycardia-mediatedsustained tachycardia (AF, incessant SVT/VT) → reversible LV dysfunction; often underdiagnosed
infiltrativeamyloidosis, haemochromatosis (iron overload — ferritin, TSAT; consider in young males)
idiopathicdiagnosis of exclusion — but ~30–50% have identifiable genetic variants on panel testing
reversible causes — always exclude

Tachycardia-mediated CM, alcohol, thyroid disease, and peripartum CM can fully recover with cause removal + GDMT. These are the “don’t miss” diagnoses.


investigation

cardiac MRI — central role in non-ischaemic CM

FeatureInterpretation
mid-wall LGE (septal stripe)typical of idiopathic/genetic DCM; predicts arrhythmia risk and mortality independently of LVEF
subendocardial LGE (coronary territory)suggests ischaemic aetiology — pursue coronary assessment
epicardial / patchy LGEmyocarditis pattern
diffuse subendocardial LGEamyloidosis
elevated native T1 / T2active inflammation (myocarditis, sarcoidosis)
no LGEbetter prognosis; higher likelihood of myocardial recovery
mid-wall fibrosis and ICD decisions

Mid-wall LGE on CMR predicts SCD risk independently of LVEF. In NICM patients with borderline LVEF (e.g. 36–40%), mid-wall fibrosis may tip the balance toward ICD implantation. This is relevant to the DANISH debate.

genetic testing

  • recommended for all patients with DCM — ESC Cardiomyopathy Guidelines 2023
  • clinical gene panel (typically 50–100 genes); whole exome/genome for research or unresolved cases
  • high-risk genotypes requiring closer surveillance and lower ICD threshold:
    • LMNA — high risk of malignant arrhythmias even with mild LV dysfunction; ICD indicated with ≥2 risk factors (male sex, NSVT, LVEF <45%, non-missense variant)
    • FLNC (filamin C) — arrhythmogenic, associated with LGE and SCD
    • DSP (desmoplakin) — overlap with ARVC; episodic myocardial injury (troponin flares)
    • PLN (phospholamban) — Dutch founder variant; progressive, arrhythmogenic
    • RBM20 — arrhythmogenic, aggressive course

family screening

  • first-degree relatives: clinical screening (ECG + echo) at diagnosis and every 2–3 years
  • cascade genetic testing if pathogenic variant identified
  • early detection allows GDMT initiation before advanced remodelling

standard workup

  • coronary assessment (CT angiography or invasive) to exclude ischaemic aetiology
  • iron studies (ferritin + TSAT) — haemochromatosis
  • TSH — thyroid disease
  • autoimmune screen if clinical suspicion (ANA, complement, CRP)
  • viral serology rarely changes management — not routinely recommended
  • endomyocardial biopsy: reserved for suspected giant cell myocarditis, eosinophilic myocarditis, sarcoidosis, or unexplained rapidly deteriorating CM

management

GDMT — same as HFrEF

Quadruple therapy backbone: ARNI + BB + MRA + SGLT2i — see HFrEF management for details.

cause-specific modifications
  • alcohol-related: complete abstinence is mandatory — LVEF recovery occurs in ~50% with abstinence + GDMT
  • tachycardia-mediated: rate/rhythm control of the underlying arrhythmia; LVEF often normalises within weeks to months
  • chemotherapy-related: cardio-oncology co-management; dexrazoxane for anthracycline cardioprotection; trastuzumab-related CM is often reversible (stop agent + GDMT)
  • peripartum: standard GDMT (avoid ACEi/ARB if breastfeeding — use hydralazine/ISDN); bromocriptine (experimental, some evidence); contraception counselling critical; high recurrence risk
  • LMNA mutation carriers: low threshold for ICD — arrhythmia risk exceeds what LVEF alone predicts
  • sarcoidosis: immunosuppression (corticosteroids ± steroid-sparing agents); ICD threshold is lower due to granulomatous arrhythmia substrate

anticoagulation

  • no routine anticoagulation for DCM in sinus rhythm — trials have not shown net benefit
  • anticoagulate if: AF (standard indications), LV thrombus, prior embolic event
  • consider if LVEF severely reduced (<20%) with large akinetic segments (individualised)

ICD in non-ischaemic DCM — the DANISH debate

TrialYearKey finding
DEFINITE (2004)2004ICD reduced arrhythmic death but not overall mortality (trend only)
SCD-HeFT (2005)2005ICD reduced all-cause mortality in NYHA II–III HF (mixed ischaemic/non-ischaemic)
DANISH (2016)2016ICD did not reduce all-cause mortality in NICM; reduced SCD but offset by non-SCD deaths. Subgroup: benefit in age <68
interpreting DANISH

DANISH was conducted in the era of modern GDMT (including CRT in 58% of patients). SCD rate was low (~4% over 5 years) — GDMT and CRT may reduce the arrhythmia substrate enough that prophylactic ICD adds less incremental benefit than in older trials.

Current practice:

  • guidelines still recommend ICD for NICM with LVEF ≤35% and NYHA II–III (class I in CCS/AHA) — DANISH has not changed this
  • shared decision-making is emphasised, particularly in older patients
  • CMR with mid-wall LGE may identify higher-risk subgroups who benefit more
  • age <59 had clear benefit in DANISH subgroup analysis
  • LMNA and other high-risk genotypes warrant ICD at higher LVEF thresholds

myocardial recovery

DCM has a real chance of LV recovery — unlike ischaemic CM where scar is permanent.

  • ~40% of “new” DCM patients improve LVEF to ≥50% with GDMT
  • absence of LGE on CMR predicts recovery
  • shorter symptom duration predicts recovery
  • tachycardia-mediated, alcohol, peripartum CM have highest recovery rates
do not stop GDMT after recovery

TRED-HF (2019) — withdrew GDMT in recovered DCM (LVEF normalised): 40% relapsed within 6 months. GDMT must be continued lifelong even after LVEF normalisation. The substrate remains — the drugs are compensating, not curing.

Key references

All sources (5)