Aetiology

Monogenic (Mendelian): ~30–40% of idiopathic DCM, up to ~50–60% with a family history (TTN, LMNA, FLNC)^[1]^[8]

Acquired: common, exclude first: myocarditis, alcohol, tachycardia-mediated, peripartum, chemotherapy, thyroid, nutritional^[1]

Complex (likely polygenic): part of "idiopathic" DCM after exclusion reflects polygenic susceptibility with environmental triggers^[1]

Genetics

Inheritance: Predominantly autosomal dominant (penetrance 30-50% by age 40-50); some X-linked and recessive forms

Genetic yield: ~30-40% in unselected DCM, up to 50-60% with family history

Major genes with arrhythmic risk stratification:

Gene	Protein	% Familial DCM	Penetrance	Arrhythmic Risk
TTN (A-band truncating)	Titin	20–25%	30–40%	Standard
LMNA	Lamin A/C	5–8%	>90%	High, early ICD
FLNC (truncating)	Filamin C	2–4%	60–70%	High, early ICD
MYH7	β-myosin heavy chain	~5%	70–80%	Standard
TNNT2	Cardiac troponin T	~3%	High	Standard
BAG3	BAG cochaperone	2–3%	>80%	Moderate, HF progression + skeletal myopathy
RBM20	RNA-binding motif 20	2–3%	>90%	Moderate-High; early onset; high atrial fibrillation burden
SCN5A	Nav1.5 (Na⁺ channel)	2–3%	30–60%	Moderate, conduction disease
Dystrophin (DMD)	Dystrophin	X-linked	~100% males	Standard, see DMD/BMD section

Pathophysiology: Gene-specific mechanisms → cytoskeletal disruption (TTN, FLNC), nuclear envelope dysfunction (LMNA), sarcomeric dysfunction (MYH7, TNNT2), RNA splicing defects (RBM20) → progressive cardiomyocyte loss, fibrosis, chamber dilatation, and contractile dysfunction

TTN variants: Interpretation challenging; truncating variants in A-band region pathogenic (~1% general population has TTN variant)

Gene frequencies and penetrance figures derive largely from referral cohorts and vary with variant class and ascertainment; treat them as indicative rather than fixed.

LMNA Cardiomyopathy: Natural History (Hasselberg et al, Eur Heart J 2018^[11])

Single-centre longitudinal study of 79 LMNA genotype-positive patients (mean age 42±16 yrs, EF 45±13%):

LMNA mutations found in 6.2% of familial DCM in Norway
Asymptomatic LMNA carriers: 9% annual incidence of newly documented cardiac phenotype; 61% developed phenotype by 4.4 years follow-up^[11]
Of early-phenotype carriers: 95% had conduction/arrhythmic disease before DCM, AV block (32%), AF (23%), non-sustained VT (39%)
72% overall developed AV block; 37% became pacemaker-dependent
Sustained ventricular arrhythmia predicted by: AV block (log-rank P=0.03) and LVEF <45%, AV block negative predictive value for VA = 100%
Heart transplantation in 19% of this cohort over 7.8±6.3 years, higher than typically seen in other DCM aetiologies^[11]

Clinical implications: Early and regular follow-up of asymptomatic LMNA carriers from point of genetic diagnosis; ECG/Holter at every review; ICD consideration before LVEF falls to standard HFrEF threshold

Arrhythmic Risk by Genotype in DCM^[1]

Gene	Risk	% Familial DCM	Key Features	ICD Threshold
LMNA	High	6–8%	Conduction disease before DCM; VT with preserved LVEF; mid-wall septal LGE	LVEF <50% OR NSVT OR conduction disease (≥2 risk factors)
FLNC (truncating)	High	3–4%	Ring-like/circumferential LGE; VT with mild LV dysfunction	ANY LV dysfunction + NSVT
DSP	High	2–3%	LV-dominant or biventricular; ring-like LGE; ARVC overlap	VT + any LV dysfunction
PLN p.Arg14del	Mod-High	<1%*	Founder mutation (Netherlands); low voltage ECG; variable progression	Low threshold; individualised
RBM20	Mod-High	2–3%	Early onset; >80% AF rate; rapid progression	Standard + low threshold
BAG3	Mod-High	2–3%	HF progression; skeletal myopathy	Standard
TTN (A-band truncating)	Standard	15–25%	Most common; lower arrhythmic risk; reverse remodeling possible	Standard (LVEF ≤35%)

*PLN p.Arg14del high prevalence in Dutch population. ICD thresholds per ESC 2023 cardiomyopathy guidelines.^[1]

Prevalence

1 in 250–400 individuals in the general population^[1]

~30–40% of cases are familial/genetic; a pathogenic or likely pathogenic variant is identifiable in ~20–35% of DCM probands^[8]

Most common indication for cardiac transplantation

Wide age range at presentation (childhood to elderly)

Population-level epidemiology (UK Biobank, Shah et al 2022^[8]): Among 18,665 individuals who underwent whole-exome sequencing, ECG and CMR, 7.8% carried ≥1 putative pathogenic variant in 44 DCM genes; over 90% of these carriers had no known history of DCM. Combined clinical/subclinical penetrance was ≤30% across all three variant-filtering strategies. The most common early DCM manifestation was arrhythmia or conduction disease (15.2%), occurring before ventricular dilation or dysfunction, highlighting the importance of ECG surveillance in variant carriers.

Diagnosis

Diagnostic Criteria:

Left ventricular ejection fraction (LVEF) <45%
LV end-diastolic diameter >117% predicted (adjusted for age and BSA)
Exclusion of alternative causes (ischemic heart disease, hypertension, valvular disease)

Clinical Presentation:

Heart failure symptoms: dyspnea, fatigue, edema
Arrhythmias: AF, VT, heart block
Thromboembolic events
Sudden cardiac death (particularly in LMNA and FLNC)
May be asymptomatic with incidental finding

Investigations

First-line:

12-lead ECG (may show AF, BBB, Q waves, low voltage)
Transthoracic echocardiography (LVEF, chamber dimensions, valves)
NT-proBNP
24-hour Holter monitoring (arrhythmia burden, heart block)

Advanced imaging:

Cardiac MRI - precise LVEF, LGE pattern (mid-wall suggests genetic/inflammatory)
Consider coronary angiography to exclude ischemic cause

Specialist investigations:

Genetic testing (especially if young onset, family history, or specific features)
Myocardial biopsy (selected cases: suspected myocarditis, infiltrative disease)
Screening for metabolic/storage diseases if indicated

Treatments

Guideline-directed medical therapy (GDMT), four pillars (ESC HF 2021^[2]):

1. ACE inhibitor / ARB / ARNI

Ramipril: start 1.25–2.5 mg once daily; uptitrate every 2 weeks → target 10 mg once daily (or 5 mg bd)
Lisinopril: start 2.5–5 mg once daily → target 20–35 mg once daily
Sacubitril/valsartan (Entresto®)^[2]^[12] (PARADIGM-HF), PREFERRED if LVEF ≤40%, tolerating ACEi/ARB:
- Start 24/26 mg twice daily; leave 36-hour washout after last ACEi dose
- Double dose every 2–4 weeks as tolerated → target 97/103 mg twice daily
- Monitor BP and eGFR; hold if systolic BP <90 mmHg or eGFR <30 ml/min/1.73m²
Candesartan (if ACEi-intolerant), start 4–8 mg once daily → target 32 mg once daily

2. Beta-blockers (mortality benefit established by MERIT-HF^[17], CIBIS-II^[18] and COPERNICUS^[19])

Bisoprolol: start 1.25 mg once daily; uptitrate every 2 weeks → target 10 mg once daily
Carvedilol: start 3.125 mg twice daily; uptitrate every 2 weeks → target 25 mg twice daily (50 mg bd if >85 kg)
Metoprolol succinate (CR/XL): start 12.5–25 mg once daily → target 200 mg once daily
Only initiate when euvolaemic; do not start in acutely decompensated HF

3. Mineralocorticoid receptor antagonist (MRA) (RALES^[15], EMPHASIS-HF^[16])

Eplerenone: start 25 mg once daily → target 50 mg once daily; preferred post-MI or in males (avoids gynaecomastia)
Spironolactone: start 25 mg once daily → target 25–50 mg once daily
Monitor K⁺ and eGFR at 1–2 weeks after initiation; hold if K⁺ >5.5 mmol/L or eGFR <30

4. SGLT2 inhibitor

Dapagliflozin 10 mg once daily (DAPA-HF^[13]; NICE TA679^[5])
Empagliflozin 10 mg once daily (EMPEROR-Reduced^[14]; NICE TA773^[6])
Fixed doses, no uptitration required; hold if eGFR <20 ml/min/1.73m² (empagliflozin) or <25 (dapagliflozin)
Interrupt 3–5 days before planned surgery; advise sick-day rules

Device therapy:

ICD for primary prevention if LVEF ≤35% after ≥3 months GDMT, NYHA II–III, life expectancy >1 year (SCD-HeFT^[20], MADIT-II^[21]; note DANISH^[25] showed no overall mortality benefit of primary-prevention ICD in non-ischaemic cardiomyopathy, so device decisions are individualised, weighing arrhythmic risk markers such as LGE and genotype)
CRT-D if LVEF ≤35%, LBBB morphology, QRS ≥130 ms (greatest benefit QRS ≥150 ms) (COMPANION^[22], CARE-HF^[23], RAFT^[24])

Advanced heart failure:

Heart transplantation assessment, refer if NYHA III–IV, peak VO₂ <12–14 ml/kg/min despite GDMT
LVAD as bridge to transplant or destination therapy

Gene-specific considerations:

LMNA: ICD if ≥2 of, NSVT, LVEF <45%, male sex, non-missense variant (Wahbi 2019, ESC 2023^[1])
FLNC: Consider ICD if truncating variant with any additional risk factor

Related Resources

Complications

Progressive heart failure: the dominant clinical course, advancing to refractory heart failure, LVAD or transplant^[1]
Ventricular arrhythmia and sudden cardiac death: can precede severe systolic dysfunction in arrhythmogenic genotypes (LMNA, FLNC, PLN, DSP)^[1]
Conduction disease and high-grade AV block: especially with LMNA variants, which can demand pacing or ICD before the ejection fraction falls
Atrial fibrillation.
Intracardiac (LV) thrombus and systemic embolism: in low-flow, severely impaired ventricles
Functional mitral regurgitation: from annular dilatation, worsening the heart failure spiral

Risk Stratification

ICD for primary prevention:

LVEF ≤35% despite ≥3 months optimal medical therapy
NYHA Class II-III symptoms
Life expectancy >1 year with good functional status

High arrhythmic risk genes (consider ICD even if LVEF >35%):

LMNA: ICD if ≥2 risk factors: NSVT, LVEF <45%, male sex, non-missense variant (Wahbi 2019, ESC 2023). Additionally, LMNA variants localising to the IgD domain (C-terminal immunoglobulin-like domain, e.g. p.Arg471His, p.Arg541His) present a distinct apical pseudo-infarct LGE pattern (transmural fibrosis) and independently predict major ventricular arrhythmias (HR 2.39, 95% CI 1.05–5.46; Castrichini et al 2025^[10]); these variants also carry higher thromboembolic risk, consider prophylactic anticoagulation when apical fibrosis/aneurysm detected on CMR
FLNC: Consider ICD if truncating variant with any additional risk factor
DSP: Associated with ARVC phenotype; arrhythmic risk

CMR Late Gadolinium Enhancement (LGE) and Prognosis in DCM (Halliday et al, JACC Imaging 2018^[9])

In 874 DCM patients followed for a median of 4.9 years, 34.3% had nonischemic LGE. Even small LGE amounts predicted substantially higher SCD risk:

LGE 0–2.55%: SCD adjusted HR 2.79 (95% CI 1.42–5.49)
LGE 2.55–5.10%: SCD adjusted HR 3.86 (95% CI 2.09–7.13)
LGE >5.10%: SCD adjusted HR 4.87 (95% CI 2.78–8.53)
Septal + free-wall LGE combined = highest SCD risk (the combination outperforms extent or pattern alone)
Predictive models using LGE presence and location were superior to models based on LVEF alone

CMR with LGE should be performed in all DCM patients, LGE presence, location (septal vs free-wall), and extent all independently inform ICD decision-making beyond LVEF.

Heart transplant referral considerations:

NYHA Class III-IV despite optimal therapy
Peak VO2 <12-14 ml/kg/min
Recurrent hospitalizations for heart failure
Refractory arrhythmias
Seattle Heart Failure Model or HFSS can aid prognostication

Pregnancy Management

ESC 2018 Pregnancy Guidelines - DCM (mWHO Class III-IV)

PRECONCEPTION COUNSELLING:

Risk stratification:
- LVEF ≥45%, NYHA I: mWHO II-III (moderate risk but generally manageable)
- LVEF 30-45%, NYHA II: mWHO III (high risk)
- LVEF <30% or NYHA III-IV: mWHO IV (PREGNANCY CONTRAINDICATED)
- Peripartum cardiomyopathy history with recovered LVEF: mWHO III (high recurrence risk 25-50%)
Mandatory assessment:
- Full echo (LVEF, chamber dimensions, MR severity, PA pressure)
- NT-proBNP baseline
- ECG and Holter monitoring (arrhythmia, conduction disease)
- Functional capacity (6-minute walk test or CPET if available)
Genetic considerations:
- 50% transmission risk if autosomal dominant gene identified
- LMNA, FLNC: Inform of high arrhythmic risk in offspring
- X-linked (DMD): 50% risk sons affected, 50% risk daughters carriers
Medication optimization:
- STOP before conception: ACE-I/ARB (switch to hydralazine + nitrates), spironolactone (teratogenic), sacubitril-valsartan
- CONTINUE: Beta-blockers (metoprolol, bisoprolol, carvedilol safe)
- SWITCH: Warfarin to LMWH if on anticoagulation
- Digoxin, ivabradine: Limited data but used if needed
Device considerations:
- ICD safe during pregnancy - maintain if already implanted
- CRT: Pregnancy not contraindication but limited data
- LVAD: Case reports only; extremely high risk

PREGNANCY MANAGEMENT:

Monitoring frequency:
- Monthly cardiology review minimum (LVEF >40%)
- Fortnightly if LVEF 30-40% or symptomatic
- Echo each trimester PLUS any clinical deterioration
- NT-proBNP each trimester (rising trend indicates decompensation)
Physiological challenges:
- Plasma volume ↑40-50% (peak 28-32 weeks) → preload stress on failing ventricle
- Cardiac output ↑30-50% → afterload reduction compensates but limited reserve
- 10-15% risk clinical deterioration (new/worsening HF symptoms)
Medical therapy adjustments:
- Heart failure: Hydralazine 75-300mg/day + isosorbide dinitrate 60-120mg/day (replace ACE-I/ARB)
- Beta-blocker: Uptitrate if tachycardia or worsening HF (metoprolol target 100-200mg)
- Diuretics: Furosemide safe if needed (bumetanide less data)
- Digoxin: Safe (0.0625-0.25mg/day); monitor levels (pregnancy alters clearance)
- Ivabradine: Limited data; case reports suggest safe if essential
Arrhythmia management:
- AF: LMWH anticoagulation (enoxaparin 1mg/kg BD); rhythm control if possible
- NSVT common (physiological) - only treat if symptomatic or haemodynamic compromise
- VT: Urgent cardiology review; beta-blockers first-line; amiodarone if refractory (thyroid monitoring)
Admission thresholds:
- New/worsening NYHA class
- LVEF drop >10% absolute
- NT-proBNP >2x baseline
- Sustained arrhythmia, syncope, chest pain

LABOUR & DELIVERY:

Timing and location:
- Deliver at tertiary centre with cardiac expertise, ICU, cardiac surgery backup
- MDT planning at 32 weeks (cardiology, obstetrics, anaesthetics, neonatology)
- Aim delivery 37-39 weeks (balance prematurity vs maternal decompensation risk)
Mode of delivery:
- Vaginal delivery: Preferred if LVEF >30%, NYHA I-II, haemodynamically stable
- Elective caesarean section: If LVEF <30%, NYHA III, decompensated, on anticoagulation
- Assisted second stage (forceps/ventouse) to minimize maternal effort
Anaesthesia:
- Epidural: Preferred for vaginal delivery - slowly titrated to avoid hypotension
- Spinal: Avoid if poor LV function (rapid vasodilation poorly tolerated)
- GA for CS: High-risk (fluid shifts, positive pressure ventilation); senior anaesthetist essential
Intrapartum monitoring:
- Continuous ECG, pulse oximetry
- Invasive BP monitoring (arterial line) if LVEF <35% or haemodynamic instability
- Consider PA catheter if severe LV dysfunction (LVEF <25%) - guide fluid management
- Careful fluid balance - avoid overload but maintain perfusion
Third stage management:
- Syntocinon safe but give SLOWLY (5U over 5 minutes, not bolus - risk hypotension)
- Avoid ergometrine (hypertension, vasoconstriction)
- If PPH: Crystalloid cautiously, tranexamic acid, uterotonics as guided by obstetrics

POSTPARTUM:

Critical first 72 hours: Autotransfusion from uterine contraction + third-space fluid mobilization = highest HF risk
- CCU/HDU monitoring 48-72 hours (all LVEF <40%)
- Daily weights, strict fluid balance
- Monitor for pulmonary oedema, arrhythmia
Peripartum cardiomyopathy (PPCM) risk:
- Pre-existing DCM can WORSEN postpartum (mimic PPCM)
- Echo within 48 hours if any deterioration
- Bromocriptine 2.5mg BD for 2 weeks if acute severe PPCM features (inhibits prolactin, may aid recovery)
Restart medications:
- Reintroduce ACE-I (enalapril, captopril compatible with breastfeeding)
- Spironolactone if needed (excreted in breast milk - consider formula feeding or use eplerenone)
- Resume GDMT as per standard HF protocols
Follow-up:
- Echo 6 weeks postpartum
- Recovery expected by 6 months (if pregnancy-related deterioration)
- Persistent LVEF <40% at 6 months suggests underlying progressive disease
Contraception:
- COCP contraindicated (thrombosis risk)
- Progesterone-only methods safe (POP, implant, Mirena)
- LARC strongly recommended
Breastfeeding: Encouraged if stable; most medications compatible (ACE-I, beta-blockers, digoxin safe)

ABSOLUTE CONTRAINDICATIONS TO PREGNANCY:

LVEF <30%
NYHA Class III-IV at baseline
Previous peripartum cardiomyopathy with persistently reduced LVEF (<40%)
Recent acute decompensation (<6 months)
Severe pulmonary hypertension (>60 mmHg)

GENE-SPECIFIC CONSIDERATIONS:

LMNA: High arrhythmic risk - ensure ICD in place, very close monitoring
DMD carriers: 10-30% develop DCM; pregnancy may unmask carrier state - baseline echo essential
PPCM history with full recovery: 25-50% recurrence risk - counsel strongly against further pregnancy

Follow-up

Based on ESC 2023 Cardiomyopathy & ESC Heart Failure guidelines^[1]^[2].

Advanced / complicated = LVEF <35%, NYHA III–IV symptoms, recurrent arrhythmia, high-risk genotype (LMNA, FLNC, RBM20, PLN, DSP), or a device in situ.

Genotype-positive / phenotype-negative (G+/P−) = a confirmed pathogenic-variant carrier with no overt disease expression yet.

	Genotype+ / Phenotype−	Uncomplicated / Stable	Advanced / Complicated
Frequency	Every 2–3 yrs (annual if LMNA/FLNC)	Every 1–2 years	Every 3–6 months
Clinical review	Symptoms, BP	Symptoms, NYHA, BP, weight	As above + fluid status, device check
ECG	Each screening visit	Annual 12-lead	Each visit
Echocardiography	Each screening visit (early dysfunction)	Every 1–2 years (LVEF, dimensions)	6-monthly
Holter / ambulatory	If high-risk genotype (LMNA/FLNC)	Every 1–2 years (more often if LMNA/FLNC)	6-monthly
Bloods	NT-proBNP if indicated	Annual (renal function, NT-proBNP)	Each visit
CMR	Consider (early fibrosis)	Baseline; repeat if phenotype changes	As clinically indicated
Family screening	–	Cascade ECG + echo (genotype-guided)	–

Disclaimer: This table is general guidance based on published guidelines and does not replace clinical judgement. The responsible clinician is accountable for determining the appropriate, individualised follow-up plan for each patient.

Key Points

Ensure optimal medical therapy before considering devices (wait 3-6 months on GDMT)^[1]
Screen first-degree relatives (clinical + genetic if variant identified)
LMNA carriers - do NOT wait for LVEF ≤35% to consider ICD^[1]
Anticoagulation if AF, LV thrombus, or severely impaired LV function^[1]
Excess alcohol should be avoided; complete abstinence is recommended where alcohol-related cardiomyopathy is suspected
Preconception counselling essential - pregnancy contraindicated if LVEF <30% or NYHA III-IV
Address reversible causes: thyroid, nutritional deficiency, toxins
TTN variants common in population - clinical correlation essential

References & Review Date

Last reviewed: June 2026

Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J. 2023;44(37):3503–3626. doi:10.1093/eurheartj/ehad194
McDonagh TA, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599–3726. doi:10.1093/eurheartj/ehab368
Zeppenfeld K, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997–4126. doi:10.1093/eurheartj/ehac262
Regitz-Zagrosek V, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J. 2018;39(34):3165–3241. doi:10.1093/eurheartj/ehy340
NICE Technology Appraisal TA679 (2021). Dapagliflozin for treating chronic heart failure with reduced ejection fraction. nice.org.uk/guidance/ta679
NICE Technology Appraisal TA773 (2022). Empagliflozin for treating chronic heart failure with reduced ejection fraction. nice.org.uk/guidance/ta773
Joint Formulary Committee. British National Formulary (BNF). bnf.nice.org.uk
Shah RA, Asatryan B, et al. Frequency, penetrance, and variable expressivity of dilated cardiomyopathy–associated putative pathogenic gene variants in UK Biobank participants. Circulation. 2022;146(2):110–124. doi:10.1161/CIRCULATIONAHA.121.058143
Halliday BP, Baksi AJ, Gulati A, et al. Outcome in dilated cardiomyopathy related to the extent, location, and pattern of late gadolinium enhancement. JACC Cardiovasc Imaging. 2019;12(8 Pt 2):1645–1655. doi:10.1016/j.jcmg.2018.07.015
Castrichini M, Garmany R, Siontis KC, et al. Variant-specific late gadolinium enhancement patterns influence clinical outcomes in LMNA-related cardiomyopathy. J Am Heart Assoc. 2025;14:e041230. doi:10.1161/JAHA.124.041230
Hasselberg NE, Haland TF, Saberniak J, et al. Lamin A/C cardiomyopathy: young onset, high penetrance, and frequent need for heart transplantation. Eur Heart J. 2018;39(10):853–860. doi:10.1093/eurheartj/ehx596
McMurray JJV, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure (PARADIGM-HF). N Engl J Med. 2014;371(11):993–1004. doi:10.1056/NEJMoa1409077
McMurray JJV, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction (DAPA-HF). N Engl J Med. 2019;381(21):1995–2008. doi:10.1056/NEJMoa1911303
Packer M, et al. Cardiovascular and renal outcomes with empagliflozin in heart failure (EMPEROR-Reduced). N Engl J Med. 2020;383(15):1413–1424. doi:10.1056/NEJMoa2022190
Pitt B, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure (RALES). N Engl J Med. 1999;341(10):709–717. doi:10.1056/NEJM199909023411001
Zannad F, et al. Eplerenone in patients with systolic heart failure and mild symptoms (EMPHASIS-HF). N Engl J Med. 2011;364(1):11–21. doi:10.1056/NEJMoa1009492
MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure (MERIT-HF). Lancet. 1999;353(9169):2001–2007. doi:10.1016/S0140-6736(99)04440-2
CIBIS-II Investigators and Committees. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial. Lancet. 1999;353(9146):9–13. doi:10.1016/S0140-6736(98)11181-9
Packer M, et al. Effect of carvedilol on survival in severe chronic heart failure (COPERNICUS). N Engl J Med. 2001;344(22):1651–1658. doi:10.1056/NEJM200105313442201
Bardy GH, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure (SCD-HeFT). N Engl J Med. 2005;352(3):225–237. doi:10.1056/NEJMoa043399
Moss AJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction (MADIT-II). N Engl J Med. 2002;346(12):877–883. doi:10.1056/NEJMoa013474
Bristow MR, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure (COMPANION). N Engl J Med. 2004;350(21):2140–2150. doi:10.1056/NEJMoa032423
Cleland JGF, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure (CARE-HF). N Engl J Med. 2005;352(15):1539–1549. doi:10.1056/NEJMoa050496
Tang ASL, et al. Cardiac-resynchronization therapy for mild-to-moderate heart failure (RAFT). N Engl J Med. 2010;363(25):2385–2395. doi:10.1056/NEJMoa1009540
Køber L, et al. Defibrillator implantation in patients with nonischemic systolic heart failure (DANISH). N Engl J Med. 2016;375(13):1221–1230. doi:10.1056/NEJMoa1608029

Dilated Cardiomyopathy (DCM)