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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- DCM = LV dilatation + impaired systolic function (LVEF <45%) not due to CAD, hypertension, or valvular disease
- Causes: idiopathic (30–50%, many genetic), familial/genetic (20–35% — titin, lamin), post-viral myocarditis, alcohol, peripartum, drugs (doxorubicin), tachycardia-mediated
- Presents with heart failure symptoms; echo shows dilated, globally hypokinetic LV
- Manage as HFrEF: ACEi + beta-blocker + MRA + SGLT2i. CRT if LBBB + QRS ≥150 ms. ICD if LVEF ≤35% despite optimal therapy
- Screen first-degree relatives with echo + ECG (familial in up to 35%)
Overview
Dilated cardiomyopathy (DCM) is characterised by left ventricular (or biventricular) dilatation and systolic dysfunction that is not explained by coronary artery disease, hypertension, or valvular disease. It is the most common cardiomyopathy and the leading indication for cardiac transplantation. Pathologically, there is diffuse myocardial fibrosis and myocyte death. Genetic causes are increasingly recognised, with mutations in titin (TTN, ~25% of familial DCM), lamin A/C (associated with conduction disease and high arrhythmia risk), and other sarcomeric/cytoskeletal genes. Acquired causes include post-viral myocarditis, alcohol excess, peripartum cardiomyopathy, and cardiotoxic drugs.
Epidemiology
DCM prevalence is approximately 1 in 250–500. It can present at any age but is most commonly diagnosed in the 20s–50s. Male predominance (3:1). Familial DCM accounts for 20–35% of cases — autosomal dominant inheritance is most common. Alcohol-related DCM is an important reversible cause if diagnosed early. Peripartum cardiomyopathy develops in the last month of pregnancy or within 5 months postpartum. Prognosis has improved with modern heart failure therapies — 5-year survival is approximately 50–80%.
Clinical Features
Symptoms
Dyspnoea on exertion, progressing to orthopnoea and PND
Fatigue and exercise intolerance
Palpitations (AF or ventricular arrhythmias)
Peripheral oedema
Syncope (arrhythmia or low cardiac output)
Chest pain (less common, may occur with RV dilatation)
Signs
Displaced, diffuse apex beat (dilated LV)
S3 gallop (rapid ventricular filling)
Functional mitral regurgitation murmur (annular dilatation)
Raised JVP, bibasal crackles, peripheral oedema, hepatomegaly (biventricular failure)
AF (irregularly irregular pulse)
Investigations
First-line
EchocardiographyDilated LV (LVEDD >55 mm), globally reduced systolic function (LVEF <45%), often functional MR. Excludes valvular and pericardial disease
NT-proBNPElevated in symptomatic heart failure
ECGNon-specific: LBBB, poor R-wave progression, AF, LVH, non-specific ST/T changes
BloodsFBC, U&Es, LFTs, TFTs, ferritin/TSAT (iron deficiency), HbA1c, alcohol biomarkers
Second-line
Cardiac MRIMid-wall late gadolinium enhancement (fibrosis pattern distinguishes DCM from ischaemic cardiomyopathy — ischaemic = subendocardial; DCM = mid-wall)
Coronary angiography or CTCAExclude ischaemic cause (essential before labelling as DCM)
Specialist
Genetic testingRecommended for all DCM patients — especially if familial or if lamin A/C suspected (conduction disease + DCM)
Family screeningEcho + ECG for all first-degree relatives (repeat every 2–5 years)
Endomyocardial biopsyRarely needed; consider in fulminant presentation or suspected infiltrative/inflammatory disease
1
Heart failure therapy (four pillars)
- ACEi (ramipril) or ARNI (sacubitril-valsartan if LVEF ≤35% despite optimal therapy)
- Beta-blocker (bisoprolol, carvedilol) — start low, go slow
- MRA (spironolactone or eplerenone)
- SGLT2 inhibitor (dapagliflozin or empagliflozin)
- Loop diuretics for congestion (symptom relief, not disease-modifying)
2
Device therapy
- ICD: if LVEF ≤35% despite ≥3 months optimal medical therapy (primary prevention SCD)
- CRT: if LBBB with QRS ≥150 ms and LVEF ≤35% — significant mortality benefit
- Lamin A/C DCM: ICD threshold may be lower due to higher arrhythmia risk
3
Specific causes
- Alcohol: complete abstinence — LV function may recover significantly
- Tachycardia-mediated: control heart rate — LV function often normalises
- Peripartum: standard HF therapy; bromocriptine may be beneficial; risk of recurrence in future pregnancies
4
Advanced heart failure
- Cardiac transplantation for end-stage disease refractory to optimal therapy
- LVAD as bridge to transplant or destination therapy
Complications
- Heart failure: Progressive LV dysfunction and refractory symptoms
- Arrhythmias: AF (very common), VT/VF (risk of sudden death)
- Thromboembolism: Mural thrombus formation in dilated, hypokinetic LV; stroke with AF
- Functional MR/TR: Annular dilatation from ventricular enlargement
- Sudden cardiac death: Leading cause of death in younger DCM patients
UKMLA Exam Tips
- 1DCM = dilated LV + globally reduced function + normal coronaries. Distinguish from ischaemic cardiomyopathy (regional wall motion abnormalities)
- 2Cardiac MRI: mid-wall LGE = DCM. Subendocardial LGE = ischaemic
- 3Lamin A/C mutation + DCM = high arrhythmia risk → earlier ICD implantation
- 4Screen first-degree relatives of all DCM patients — familial in up to 35%
- 5Alcoholic cardiomyopathy can reverse with abstinence — important to identify
- 6Peripartum cardiomyopathy: last month of pregnancy to 5 months postpartum
practicetest your knowledge on dilated cardiomyopathyApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — cardiovascular and beyond.
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