01Approach to the Critical Patient/attcp56

Immediate priorities

›Airway and breathing threats

›Acute pulmonary edema

›Severe dyspnea at rest

›SpO2 < 90% on room air

›Bilateral crackles with frothy sputum

›Ventilatory failure

›Rising PaCO2

›Respiratory fatigue with accessory muscle use

›If acute pulmonary edema with respiratory failure, initiate non-invasive ventilation

›BiPAP preferred over CPAP for hypercapnic patients

›Class I recommendation

›Cardiogenic shock recognition

›Hemodynamic criteria

›SBP < 90 mmHg for > 30 minutes

›MAP < 65 mmHg despite adequate preload

›End-organ hypoperfusion

›Cool clammy extremities

›Urine output < 30 mL/hour

›Altered mental status

›Lactate >= 2 mmol/l

›If cardiogenic shock, initiate vasopressor or inotrope support immediately

›Avoid aggressive fluid resuscitation in pulmonary edema

›Class I recommendation for early revascularization if ischemic etiology

Monitoring and targets

›Hemodynamic monitoring bundle

›Continuous cardiac monitoring

›Arrhythmia detection priority

02History/hx80

Presentation pattern

›Classic heart failure symptoms

›Dyspnea on exertion

›Onset and progression timeline

›NYHA functional class estimation

›Orthopnea

›Number of pillows required

›Onset timing after lying flat

›Paroxysmal nocturnal dyspnea

›Awakening from sleep with dyspnea

›Time to symptom relief upon sitting up

›Fatigue and exercise intolerance

›Functional decline from baseline

›Limitation of activities of daily living

›Congestion symptoms

›Peripheral edema

›Bilateral leg swelling

›Abdominal distension and early satiety

›Weight gain

›Rate of weight gain over days to weeks

›Tight fitting shoes or clothing

Risk factors and triggers

›Toxic and medication exposures

›Alcohol use

›Quantity >= 80 g/day for > 5 years suggests alcoholic cardiomyopathy

›Dose-dependent cardiotoxicity

›Chemotherapy history

›Anthracyclines (doxorubicin) — cumulative dose dependent

03Physical Exam/exam73

Vital signs and general appearance

›Hemodynamic snapshot

›Heart rate

›Tachycardia common in decompensation

›Narrow pulse pressure suggesting low output

›Blood pressure

›Hypotension (SBP < 90 mmHg) suggests shock

›Elevated BP may indicate hypertensive decompensation

›Respiratory rate

›>= 25 per minute as severity marker

›Respiratory distress pattern

›Oxygen saturation

›Room air value compared to baseline

›Exertional desaturation if ambulatory

›General appearance

›Increased work of breathing

›Accessory muscle use

›Inability to speak full sentences

›Diaphoresis

›Sympathetic activation in low output state

›Cachexia

›Chronic severe HF with cardiac cachexia

Cardiovascular exam

›Jugular venous assessment

›Elevated JVP

›Estimate cm above sternal angle

›Hepatojugular reflux sign

›Waveform abnormalities

04Differential Diagnosis/ddx46

Life threats and close mimics

›Ischemic etiologies

›Ischemic cardiomyopathy

›ICD-10 I25.5

›Most important to exclude — coronary angiography or stress testing required

›Acute coronary syndrome with LV dysfunction

›Troponin elevation

›Regional wall motion abnormalities on echo

›Other cardiomyopathies

›Hypertrophic cardiomyopathy burned out

›End-stage HCM with LV dilation

›Prior HCM diagnosis or family history

›Arrhythmogenic cardiomyopathy

›Left-dominant ARVC can phenotypically overlap with DCM

›ICD-10 I42.8

›Left ventricular noncompaction

›Prominent trabeculations on imaging

›ICD-10 I42.8

›Stress (Takotsubo) cardiomyopathy

›Acute onset, apical ballooning pattern

›Emotional or physical stressor trigger

›Systemic and toxic causes

›Alcoholic cardiomyopathy

›ICD-10 I42.6

›Reversible with cessation in early stages

›Tachycardia-induced cardiomyopathy

›Persistent tachyarrhythmia > 100 bpm

›Expect recovery within 4 weeks of rate/rhythm control

05Laboratory Tests/lt64

Core cardiac biomarkers

›Natriuretic peptides

›BNP or NT-proBNP

›Elevated in volume overload and LV dysfunction

›BNP > 100 ng/L or NT-proBNP > 300 ng/L supports HF diagnosis

›Guides severity stratification and treatment response

›Lower levels may occur in obese patients (false negatives)

›Trend monitoring

›Decline with effective decongestion

›Persistently elevated despite treatment is poor prognostic marker

›Troponin

›High-sensitivity troponin I or T

›Myocardial injury marker

›Elevated in myocarditis, ischemic etiology, or severe decompensation

›Serial measurement to differentiate pattern

›Pattern interpretation

›Acute rise and fall suggests ACS

›Chronically mildly elevated in advanced DCM

Metabolic and organ function

›Renal function

›Creatinine and eGFR

›Cardiorenal syndrome common in decompensated HF

›Baseline essential before initiating diuretics and RAAS agents

›Electrolytes

›Sodium — hyponatremia common in advanced HF

›Potassium — critical before initiating MRA and RAAS therapy

›Magnesium — arrhythmia risk with hypomagnesemia

›Hepatic function

06Diagnostic Tests/dt103

Scoring Systems

›Heart failure severity and prognosis tools

›NYHA Functional Classification

›Class I: no limitation of physical activity

›Class II: slight limitation — comfortable at rest

›Class III: marked limitation — comfortable at rest only

›Class IV: symptoms at rest or with any activity

›Guides GDMT targets and device therapy eligibility

›MAGGIC Risk Score

›Mortality prediction tool in chronic HF

›Incorporates EF, NYHA class, age, comorbidities

›Device therapy eligibility criteria

›ICD eligibility

›LVEF <= 35% after >= 3 months of optimal GDMT

›NYHA Class II or III on optimal therapy

›DANISH trial: attenuated benefit in non-ischemic DCM, especially older patients

›CRT eligibility

›LVEF <= 35%

›LBBB with QRS >= 150 ms

›NYHA Class II to IV in sinus rhythm

›Class I recommendation for LBBB + QRS >= 150 ms

›Advanced HF referral triggers

›I-NEED-HELP mnemonic criteria

›IV inotropes required

›NYHA Class III to IV despite optimal GDMT

›End-organ dysfunction

›EF <= 35%

›Defibrillator shocks

›Hospitalizations >= 2 in past year

›Edema refractory to diuretics

›Low BP limiting GDMT titration

›Prognostic medication intolerance

MRI

›Cardiac MRI (CMR) role in DCM

›Indications

›Etiology characterization when echo is non-diagnostic

›Late gadolinium enhancement (LGE) for risk stratification

›Preferred imaging for myocarditis, sarcoidosis, and amyloidosis evaluation

›Viability assessment before revascularization in ischemic-DCM overlap

›LGE patterns and significance

›Midwall linear LGE — characteristic of non-ischemic DCM

›Subendocardial or transmural LGE — suggests ischemic etiology

›LGE presence associated with higher SCD risk and adverse outcomes (JAMA 2024 meta-analysis)

›LGE extent correlates with arrhythmia burden

›Tissue characterization sequences

›T1 mapping for diffuse fibrosis quantification

›T2 mapping for active myocardial inflammation

›Extracellular volume (ECV) fraction

›Performance characteristics

›Superior to echocardiography for characterizing myocardial tissue

›No ionizing radiation

›CMR contraindications

›Hemodynamically unstable patient

›Defer until stabilized

›Non-MRI-compatible devices

›Legacy pacemakers or ICDs

›Certain cochlear implants and metallic implants

›Claustrophobia and inability to cooperate

›Sedation consideration in selected cases

CT

›CT coronary angiography

›Indications

›New DCM — exclude ischemic etiology as first-line non-invasive option

›Low to intermediate pretest probability of CAD

›Calcium scoring to guide further testing

›Performance characteristics

›High negative predictive value for CAD exclusion

›Sensitivity > 95% for obstructive coronary disease

›Limitations with heavy calcification or high heart rate

›CT chest indications in DCM

›Pulmonary cause evaluation

›Severe pulmonary hypertension workup

›Sarcoidosis pulmonary involvement assessment

›Pre-LVAD or pre-transplant workup

›Aortic anatomy and vascular access planning

›Radiation considerations

›Reserve for specific indications

›ECG gating for cardiac CT

Ultrasound

›Echocardiography — primary diagnostic modality

›Transthoracic echocardiogram (TTE) findings in DCM

›LV dilation — LV end-diastolic dimension > 5.5 cm (men) or > 5.0 cm (women)

›Global systolic dysfunction — EF < 50% by biplane Simpson method

›Global wall motion abnormality distinguishes from regional ischemic pattern

›Functional mitral regurgitation from annular dilation

›LA enlargement secondary to elevated filling pressures

›Diastolic function grading

›Elevated E/e' ratio indicates elevated LV filling pressures

›Restrictive filling pattern (E/A > 2) indicates advanced disease

›Right ventricular assessment

›RV dilation and dysfunction as adverse prognostic marker

›Tricuspid annular plane systolic excursion (TAPSE) < 17 mm

›TR jet velocity for estimated RVSP

›Point-of-care ultrasound (POCUS)

›Lung ultrasound

›B lines in multiple zones — pulmonary congestion pattern

›Bilateral B lines in >= 2 bilateral zones suggest pulmonary edema

›IVC assessment

›Dilated non-collapsing IVC suggests elevated right atrial pressure

›IVC diameter > 2.1 cm with < 50% collapse with inspiration

›Pericardial effusion screen

›Exclude pericardial tamponade in hemodynamically unstable patient

›Transesophageal echocardiogram (TEE)

›Indications

›Intracardiac thrombus assessment before cardioversion

›LA appendage thrombus exclusion

›Superior valvular assessment when TTE inadequate

07Disposition/dispo53

Admission indications

›Criteria for hospitalization

›Hemodynamic instability

›Cardiogenic shock or impending shock

›Symptomatic hypotension

›Severe decompensation

›New-onset HF with significant symptoms

›Acute decompensated HF requiring IV diuretics or vasoactive agents

›High-risk arrhythmias

›Sustained ventricular tachycardia

›High-grade AV block

›New rapid atrial fibrillation

›Syncope in setting of known or suspected DCM

›Until arrhythmic cause excluded

›End-organ dysfunction

›Acute renal failure (cardiorenal syndrome)

›Hepatic congestion with coagulopathy

›Need for urgent advanced workup

›Endomyocardial biopsy consideration

›Urgent cardiac catheterization

Level of care selection

›ICU indications

›Cardiogenic shock with vasopressor or inotrope requirement

›Hemodynamic monitoring

›Mechanical circulatory support consideration

›Acute pulmonary edema requiring BiPAP or intubation

›Ventilatory monitoring

›Refractory ventricular arrhythmias

08Treatment/t173

Acute decompensation management

›Decongestion therapy

›IV furosemide

›Initial dose 40 mg IV if diuretic naive

›2.5 times the home oral dose IV if on chronic diuretics

›Titrate to urine output 3 to 5 mL/kg/hour

›Convert to oral when euvolemic

›IV bumetanide alternative

›1 to 3 mg IV per dose

›Equivalent to furosemide at 40:1 ratio

›Diuretic resistance management

›Add thiazide diuretic (metolazone) for sequential nephron blockade

›Metolazone 2.5 to 10 mg PO 30 minutes before loop diuretic

›Monitor electrolytes closely with combination diuresis

›Vasodilation for congestion with adequate BP

›Nitroglycerin sublingual or IV

›Sublingual 0.4 mg every 5 minutes for acute pulmonary edema

›IV 10 to 20 mcg/min starting dose

›Titrate to relief or SBP > 90 mmHg

›Avoid if SBP < 90 mmHg or recent phosphodiesterase-5 inhibitor use

›Sodium nitroprusside IV

›For severe hypertensive decompensated HF

›0.3 mcg/kg/min starting dose

›Titrate to hemodynamic targets with arterial line monitoring

Cardiogenic shock

›Vasopressor therapy

›Norepinephrine

›0.01 to 3 mcg/kg/min IV infusion

›First-line vasopressor in cardiogenic shock

›Titrate to MAP >= 65 mmHg

›Vasopressin adjunct

›0.03 to 0.04 units/min IV

›Norepinephrine sparing agent

›Inotropic therapy

›Dobutamine

›2 to 20 mcg/kg/min IV infusion

›Positive inotrope for low output state

›Risk of tachyarrhythmia and increased oxygen demand

›Milrinone

›0.375 to 0.75 mcg/kg/min IV infusion

›PDE3 inhibitor — inodilator

›Preferred in patients on beta-blockers (bypasses beta receptor)

›Renal dose adjustment required

›Levosimendan

›0.1 mcg/kg/min over 24 hours

›Calcium sensitizer — inodilator

›Not available in all centers

›Mechanical circulatory support

›Intra-aortic balloon pump (IABP)

›Counterpulsation to reduce afterload and augment diastolic pressure

›Impella or other percutaneous LVAD

›Higher hemodynamic support for refractory cardiogenic shock

›VA-ECMO

›Biventricular failure or cardiac arrest with refractory shock

Guideline-directed medical therapy (GDMT)

›ACE inhibitor or ARB therapy

›Lisinopril

›Starting dose 2.5 to 5 mg PO daily

›Target dose 20 to 40 mg PO daily

›Monitor renal function and potassium

›Ramipril

›Starting dose 1.25 to 2.5 mg PO twice daily

›Target dose 5 mg PO twice daily

›Class I recommendation — reduces mortality and hospitalizations

›Sacubitril-valsartan (ARNI)

›Sacubitril-valsartan

›Starting dose 24/26 mg PO twice daily

›Target dose 97/103 mg PO twice daily

›Superior to ACEi for CV death and HF hospitalization reduction (PARADIGM-HF)

›36-hour washout required after ACEi to prevent angioedema

›Class I recommendation for symptomatic HFrEF despite ACEi/ARB

›Beta-blocker therapy

›Carvedilol

›Starting dose 3.125 mg PO twice daily

›Target dose 25 mg PO twice daily (50 mg if > 85 kg)

›Non-selective beta-blocker with alpha-1 blockade

›Bisoprolol

›Starting dose 1.25 mg PO daily

›Target dose 10 mg PO daily

›Cardioselective

›Metoprolol succinate (CR/XL)

›Starting dose 12.5 to 25 mg PO daily

›Target dose 200 mg PO daily

›Class I recommendation — titrate to highest tolerated dose

›Do NOT initiate during acute decompensation with fluid overload

›Mineralocorticoid receptor antagonist (MRA)

›Spironolactone

›Starting dose 12.5 to 25 mg PO daily

›Target dose 25 to 50 mg PO daily

›Monitor potassium and renal function

›Avoid if eGFR < 30 mL/min/1.73m2 or potassium > 5.0 mmol/l

›Eplerenone alternative

›Starting dose 25 mg PO daily

›Target dose 50 mg PO daily

›Fewer anti-androgenic side effects than spironolactone

›Class I recommendation — reduces mortality and hospitalizations

›SGLT2 inhibitor

›Dapagliflozin

›10 mg PO daily

›Class I recommendation (DAPA-HF trial)

›Empagliflozin

›10 mg PO daily

›Class I recommendation (EMPEROR-Reduced trial)

›Benefits independent of diabetes status

›Avoid if eGFR < 20 mL/min/1.73m2 (dapagliflozin) or < 25 (empagliflozin)

Additional pharmacotherapy

›Diuretics for congestion

›Loop diuretics for symptom control

›No mortality benefit but essential for quality of life

›Furosemide 20 to 80 mg PO daily or twice daily

›Titrate to minimize congestion while preserving renal function

›Ivabradine

›Starting dose 5 mg PO twice daily

›Target dose 7.5 mg PO twice daily

›For heart rate > 70 bpm in sinus rhythm despite maximally tolerated beta-blocker

›Contraindicated in AF, sinus bradycardia, or significant AV block

›Hydralazine-isosorbide dinitrate

›Hydralazine and isosorbide dinitrate combination

›Hydralazine 25 to 50 mg PO three times daily (target 75 mg three times daily)

›Isosorbide dinitrate 20 to 40 mg PO three times daily

›Class I recommendation for self-identified Black patients with NYHA III-IV

›ACEi/ARB intolerant patients as alternative

›Anticoagulation

›Indications

›Atrial fibrillation — rate or rhythm control with anticoagulation

›Intracardiac thrombus on imaging

›LMNA-related DCM — higher risk for thromboembolic events

›Agents

›DOACs preferred over warfarin for AF in non-valvular context

›Warfarin for intracardiac thrombus or mechanical valves

›Medications to avoid in DCM

›Non-dihydropyridine calcium channel blockers

›Verapamil and diltiazem contraindicated if EF <= 50%

›Negative inotropic effect worsens LV function

›NSAIDs

›Sodium and water retention

›Reduced efficacy of diuretics

›Renal function deterioration

›Thiazolidinediones

›Fluid retention and HF hospitalization risk

Device therapy

›Implantable cardioverter-defibrillator (ICD)

›Primary prevention criteria

›LVEF <= 35% on optimal GDMT for >= 3 months

›NYHA Class II or III

›Genetic subtypes (LMNA, RBM20, FLNC, DSP) may warrant ICD at higher EF

›Class IIa recommendation in non-ischemic DCM based on DANISH trial data

›Secondary prevention

›Survived VF arrest or hemodynamically unstable VT

›Class I recommendation

›Cardiac resynchronization therapy (CRT)

›CRT-D or CRT-P criteria

›LVEF <= 35%

›LBBB with QRS >= 150 ms

›NYHA Class II to IV on optimal GDMT

›Class I recommendation for LBBB + QRS >= 150 ms

›Expected benefits

›Improvement in LVEF and symptoms

›Reduction in HF hospitalization and mortality

Etiology-specific treatment

›Reversible cause treatment

›Alcohol cessation

›Mandatory for alcoholic cardiomyopathy

›Partial EF recovery possible within weeks to months

›Tachycardia-induced cardiomyopathy

›Rate or rhythm control of causative arrhythmia

›Expect EF recovery within 4 weeks

›Peripartum cardiomyopathy

›Bromocriptine 2.5 mg PO twice daily for 2 weeks then once daily for 6 weeks

›Reduces prolactin — emerging evidence for benefit

›Standard GDMT (modify for breastfeeding)

›Inflammatory cardiomyopathy

›Giant cell myocarditis

›Immunosuppression with corticosteroids and additional agents

›High mortality without prompt treatment

›Cardiac sarcoidosis

›Prednisone 40 to 60 mg PO daily tapering over months

›18F-FDG PET guided monitoring

09Special Populations/sp78

Pregnancy

›Peripartum cardiomyopathy considerations

›Diagnosis timing

›Last month of pregnancy to 5 months postpartum

›EF < 45% is diagnostic threshold

›Exclude pre-existing DCM and other causes

›Incidence and prognosis

›Approximately 1 in 1,000 to 4,000 pregnancies

›EF recovery occurs in 50% within 6 months

›Mortality risk highest in low EF at diagnosis

›Medication safety in pregnancy

›Safe in pregnancy

›Hydralazine for afterload reduction

›Beta-blockers (labetalol, metoprolol) — monitor for neonatal bradycardia

›Loop diuretics with caution — placental perfusion risk

›Heparin or low-molecular-weight heparin for anticoagulation

›Contraindicated in pregnancy

›ACE inhibitors — teratogenic (renal and skeletal abnormalities)

›ARBs — contraindicated throughout pregnancy

›SGLT2 inhibitors — insufficient safety data

›Spironolactone — anti-androgenic effects

›Obstetric management

›Multidisciplinary team including maternal-fetal medicine

›Delivery planning with cardiac anesthesia involvement

›Epidural analgesia preferred for hemodynamic stability

›Future pregnancy counseling

›High recurrence risk if EF not fully recovered

›Contraception discussion essential

Geriatric

›Physiologic and presentation differences

›Atypical presentations more common

›Fatigue and confusion rather than classic dyspnea

›Reduced exercise capacity attributed to deconditioning

›Comorbidity burden

›CKD complicating diuresis and RAAS therapy

›Polypharmacy and drug interactions

›Baseline cognitive impairment affecting self-care adherence

›Medication modifications

›GDMT initiation

›Start at lowest doses and titrate slowly

›Beta-blockers — increased fall risk with orthostatic hypotension

›ACEi and ARBs — monitor renal function and potassium more frequently

›Diuretic caution

›Dehydration and electrolyte disturbance risk higher

›Frailty increases fall risk with excessive diuresis

›Device therapy in elderly

›ICD benefit attenuated in patients > 70 years per DANISH subgroup analysis

›Individualized risk-benefit discussion

›Competing non-cardiac mortality risk

›CRT benefit preserved across age groups

›Symptom improvement and quality of life justification

›Goals of care

›Palliative care integration in advanced HF

›Symptom management priority

›Device deactivation discussion

Pediatrics

›Epidemiology in children

›Most common cardiomyopathy in children

›Incidence approximately 0.57 per 100,000 per year

›Familial in approximately 50% of pediatric cases

›Age of presentation

›Bimodal distribution — infancy and adolescence

›Infants present with acute decompensation

›Etiology differences

›Genetic causes predominate

›TTN, MYH7, MYBPC3 mutations

›Neuromuscular disease association (Duchenne, Barth syndrome)

›Myocarditis as common preceding event

›Viral etiology frequent

›Risk of progression to DCM

›Treatment approach

›GDMT principles similar but weight-based dosing

›Carvedilol 0.05 mg/kg/dose PO twice daily — titrate to 0.35 mg/kg/dose

›Enalapril 0.05 to 0.1 mg/kg/dose PO twice daily — titrate to effect

›Furosemide 1 to 2 mg/kg/dose IV or PO

›Device therapy in children

›ICD for secondary prevention of SCA — Class I recommendation (AHA 2023)

›ICD for primary prevention if LVEF severely reduced and high-risk features

›Advanced therapy

›LVAD as bridge to transplant in refractory pediatric DCM

›Heart transplantation — most common indication in children

10Background/b93

Epidemiology

›Prevalence and incidence

›Prevalence approximately 1 in 2,500 people in general population

›True prevalence likely higher due to underdiagnosis

›More common in men across most genetic subtypes

›Annual incidence approximately 7 per 100,000 person-years

›Increasing with better diagnostic recognition and population aging

›Typical age of presentation

›4th to 6th decade of life for adult-onset

›Earlier presentation in genetic and familial subtypes

›Burden of disease

›Most common indication for heart transplantation globally

›Accounts for approximately 45% of transplant indications

›Approximately 25% of patients with recent-onset DCM may have spontaneous recovery

›Higher recovery rates with short symptom duration < 3 months

›Mortality

›Median survival without transplantation historically 5 to 10 years from diagnosis

›Improving with contemporary GDMT including SGLT2 inhibitors

›Sex differences

›Men more frequently affected with most genetic subtypes

›DSP mutations may be more penetrant in women

›Women with DCM have better EF recovery rates

›Peripartum DCM has higher recovery potential

›Underdiagnosis in women is a recognized gap (JACC 2026)

Pathophysiology

›Structural and functional changes

›Primary myocyte dysfunction

›Sarcomere protein dysfunction (MYH7, TNNT2 mutations)

›Nuclear envelope disruption (LMNA mutations)

›Cytoskeletal dysfunction (dystrophin, desmin)

›Maladaptive remodeling cascade

›LV dilation from volume overload compensation

›Eccentric hypertrophy with sarcomere replication in series

›Progressive fibrosis replacing functional myocardium

›Neurohormonal activation

›RAAS activation — sodium retention, vasoconstriction, fibrosis

›Sympathetic nervous system overactivation

›Natriuretic peptide release as compensatory counterregulation

›Etiology-specific mechanisms

›Toxic cardiomyopathy

›Anthracyclines — topoisomerase II inhibition and free radical injury

›Alcohol — direct mitochondrial toxicity and acetaldehyde effects

›Immune-mediated

›Myocardial inflammation with T-cell infiltration

›Autoantibodies against adrenoreceptors and sarcomeric proteins

›Tachycardia-induced

›Energy depletion and calcium overload from sustained rapid rate

›Reversal with rate control demonstrates causal relationship

›Complication pathways

›Atrial fibrillation

›Left atrial dilation and elevated pressures trigger AF

›AF worsens LV dysfunction — bidirectional relationship

›Ventricular arrhythmias

›Fibrosis creates re-entry substrate for VT and VF

›LMNA mutations carry highest arrhythmic risk per kg fibrosis burden

›Intracardiac thrombus

›Stasis in dilated LV cavity

›Global hypokinesis without regional predilection

Therapeutic Considerations

›GDMT initiation and titration principles

›All four pillars initiated simultaneously when possible

›ACEi or ARB or ARNI + beta-blocker + MRA + SGLT2i within 4 to 6 weeks

›Rapid up-titration to target doses improves outcomes

›GDMT not withdrawn even if EF normalizes

›TRED-HF trial: 44% relapse rate within 6 months of GDMT withdrawal despite normalized EF

›Sequencing pragmatics

›Beta-blocker avoided in acutely decompensated wet patient

›RAAS agents avoided in acute shock or severe renal failure

›Introduce low doses as hemodynamics allow with goal to reach target

›Reversibility and recovery

›Alcoholic cardiomyopathy

›Up to 80% may show EF improvement with abstinence

›Delay device decisions 3 to 6 months after abstinence

›Tachycardia-induced cardiomyopathy

›Expect substantial or complete recovery within 4 weeks of rhythm control

›Requires persistent arrhythmia > 100 bpm as causative

›Chemotherapy-induced

›Monitoring and early intervention with GDMT may improve recovery

›Cardio-oncology collaboration for continued cancer treatment

›Genetic testing and cascade screening

›Genetic testing recommended in all familial or unexplained DCM

›Gene panels include TTN, LMNA, MYH7, SCN5A, RBM20, DSP, FLNC

›Pathogenic variant identified in 30 to 40% of tested patients

›Cascade screening of first-degree relatives

›Echocardiography every 3 to 5 years if initially normal

›More frequent if borderline abnormalities detected

›LMNA and high-risk gene carriers — ECG and Holter monitoring for conduction disease

›Arrhythmia and conduction disease management

›LMNA-specific management

›High risk of sudden death even at EF > 35%

›ICD often warranted at higher EF thresholds in LMNA carriers

›Early pacemaker for AV block (may require ICD given SCD risk)

›AF management

›Rate control with beta-blocker or digoxin

›Rhythm control with amiodarone or catheter ablation in symptomatic patients

›Anticoagulation for thromboembolic prevention

11Patient Discharge Instructions/pdi54

copy discharge instructions

›What is dilated cardiomyopathy

›Condition where the heart muscle weakens and the heart becomes enlarged

›The heart pumps less effectively than normal

›This causes fluid to back up into the lungs and body

›Your medications are critical

›Take all heart medications exactly as prescribed every day

›Do not stop any heart medication without calling your doctor first

›Missing doses can cause serious worsening of heart function

›Your medications likely include some combination of

›ACE inhibitor or ARB or sacubitril-valsartan to protect and strengthen the heart

›Beta-blocker to slow heart rate and reduce strain

›Water pill (diuretic) to remove excess fluid

›Spironolactone or eplerenone to reduce scarring

›SGLT2 inhibitor to reduce hospitalizations and protect the heart

›Daily weight monitoring is mandatory

›Weigh yourself every morning after using the bathroom and before eating

›Use the same scale at the same time each day

›Record your weight in a diary or app

›If you gain more than 1 to 1.5 kg in 24 hours or 2 to 2.5 kg in a week

›Call your cardiologist or return to the emergency department

›Diet and lifestyle

›Salt restriction

›Limit sodium to less than 2 g (2,000 mg) per day

›Avoid processed foods, canned soups, deli meats, fast food

›Read nutrition labels — look for sodium content

›Fluid restriction if advised by your cardiologist

›Typically 1.5 to 2 litres per day

12References/r37

Guidelines and key sources

›Society guidelines

›2022 AHA/ACC/HFSA Heart Failure Guideline

›Quadruple therapy (ACEi/ARB/ARNI + BB + MRA + SGLT2i) Class I recommendations

›ICD and CRT candidacy criteria

›2023 ESC Guidelines for Heart Failure

›GDMT titration targets and monitoring recommendations

›AHA Scientific Statement on Specific Dilated Cardiomyopathies (Bozkurt et al 2016)

›Etiology-specific diagnostic and treatment guidance

›Landmark trials

›PARADIGM-HF — sacubitril-valsartan versus enalapril in HFrEF

›20% reduction in CV death and HF hospitalization

›DAPA-HF — dapagliflozin in HFrEF with and without diabetes

›26% reduction in worsening HF or CV death

›EMPEROR-Reduced — empagliflozin in HFrEF

›25% reduction in CV death or worsening HF hospitalization

›DANISH trial — ICD in non-ischemic HF

›Attenuated all-cause mortality benefit vs ischemic cardiomyopathy

›Benefit seen in younger patients

›TRED-HF — GDMT withdrawal in recovered DCM

›44% relapse within 6 months — support for indefinite GDMT

›Key evidence sources

›Hershberger RE, Jordan E. Dilated Cardiomyopathy Overview. GeneReviews 2024

›Familial DCM genetics, cascade screening recommendations

›Eichhorn C et al. Risk Stratification in Nonischemic DCM Using CMR. JAMA 2024

›LGE as predictor of adverse outcomes

›Heymans S et al. Dilated Cardiomyopathy: Causes, Mechanisms, and Treatment. Lancet 2023

›Comprehensive pathophysiology and treatment review

Evidence & Review