Cardiomyopathies & Myocarditis

Overview & definition

The cardiomyopathies are diseases of the heart muscle, classified into four morphological types — dilated (the commonest), hypertrophic, restrictive, and arrhythmogenic right ventricular — to which Takotsubo (stress) cardiomyopathy is often added as a fifth, reversible, mimic. Myocarditis is an inflammation of the myocardium (most commonly viral) that can mimic an ACS and may progress to a dilated cardiomyopathy.[1][1]

The 2023 ESC cardiomyopathy guideline reframes these around a phenotype-first, genotype-driven approach: define the phenotype (dilated, hypertrophic, restrictive, non-compaction, ARVC) from imaging, then hunt systematically for the cause (genetic, acquired), and cascade-screen first-degree relatives.[1]

The phenotype-first approach (2023 ESC)[1]

Dilated cardiomyopathy (DCM)

The commonest cardiomyopathy. An enlarged, thin-walled LV with a reduced ejection fraction (a systolic failure) — LVEDD usually >6 cm with an EF <40%.[1][6]

Causes (the mnemonic "ABCD GET SMASHED" is overkill — learn the high-yield six):[1][6]

• Genetic — a family history in 30-40 per cent of "idiopathic" cases; autosomal dominant truncating variants in titin (TTNtv) are the single commonest genetic cause (found in ~15-20 per cent of familial and ~10 per cent of sporadic DCM). Truncate screening of first-degree relatives is now standard.[1]
• Post-viral myocarditis — the progression to DCM (the "burnt-out" myocarditis); a viral prodrome weeks to months earlier is the clue.
• Toxic — alcohol (a direct myocardial toxin; >7-8 drinks/day over ≥5 years), anthracycline chemotherapy (doxorubicin — dose-dependent, cumulative, via iron-mediated free-radical injury; dexrazoxane is cardioprotective; the newer anti-HER2 trastuzumab causes a usually-reversible dysfunction), cocaine/methamphetamines, and clozapine (myocarditis/cardiomyopathy within the first 8 weeks).
• Peripartum — the last month of pregnancy to 5 months postpartum; the diagnosis requires the timing plus an EF <45%; higher rates in pre-eclampsia, older maternal age, and multiparity. It recovers more often than other DCMs (≈50-70 per cent recover LV function by 12 months with GDMT). A subsequent pregnancy carries a recurrence risk of ~30-50 per cent if the EF has not normalised.
• Tachycardia-induced — chronic AF/SVT with a rate >110-130 for weeks-months; the EF recovers with rate control — the only DCM that is essentially curable.
• Endocrine/nutritional — thyrotoxicosis, hypothyroidism, selenium deficiency (Keshan disease in parts of China), carnitine deficiency, thiamine (beriberi — high-output).
• Idiopathic — a diagnosis of exclusion after the above are excluded; ~30 per cent.

Pathophysiology: the cardinal defects are loss of myocytes (necrosis, apoptosis), interstitial fibrosis, and adverse remodelling — leading to wall thinning, chamber dilation, reduced contractility, and functional mitral/tricuspid regurgitation from annular dilation. Neurohormonal activation (RAAS, sympathetic) drives progressive remodelling — which is exactly what GDMT blocks. [1]

Investigations:

• Echocardiography — the first test: LV dilation, global or regional hypokinesia, reduced EF, functional MR. Strain imaging (reduced global longitudinal strain) is more sensitive than EF.
• ECG — non-specific; may show AF, LBBB (a CRT consideration), low voltage, or Q waves (mimicking old infarction).
• Cardiac MRI — the most informative single test: confirms LV/RV size and function, shows mid-wall LGE (the non-ischaemic pattern, typically in the septum — distinguishes from the subendocardial LGE of infarction), and identifies myocarditis or sarcoid patterns. Should be done in every new "idiopathic" DCM.[1]
• Coronary angiography — to exclude ischaemia as the cause (ischaemic vs non-ischaemic DCM).
• Genetic testing — multigene panel; cascade screening of first-degree relatives with clinical assessment + echo ± genetics.[1]

Management — the four pillars of GDMT (+ ARNI, loop diuretic, devices):[1][6]

• ACE inhibitor / ARB / ARNI — ARNI (sacubitril/valsartan) preferred over ACEi in HFrEF (PARADIGM-HF); use ACEi first then switch once stable.
• Beta-blocker — one of the three mortality-reducing ones: bisoprolol, carvedilol, or nebivolol (metoprolol tartrate is NOT — use succinate, but evidence base is the three).
• Mineralocorticoid receptor antagonist — spironolactone or eplerenone (for symptomatic HFrEF or post-MI EF <30).
• SGLT2 inhibitor — dapagliflozin or empagliflozin (DAPA-HF, EMPEROR-Reduced) — now first-line, mortality- and hospitalisation-reducing, irrespective of diabetes.
• Loop diuretic — furosemide/bumetanide for congestion relief (symptomatic only; no mortality benefit).
• Device therapy (for selected patients): ICD for the primary prevention of sudden cardiac death (EF ≤35%, NYHA II-III, ≥3 months of optimal GDMT, ≥1-year survival expectation); CRT (biventricular pacemaker) for QRS ≥150 ms with LBBB morphology.
• Advanced — LVAD (destination or bridge-to-transplant) or cardiac transplantation for refractory end-stage disease.
• Anticoagulation — for an LV thrombus, prior embolus, or AF; NOT routinely for low EF alone (no net benefit in sinus rhythm).

Prognosis: 5-year mortality ~20 per cent on modern GDMT (historically ~50 per cent); reversible causes (peripartum, tachycardia-induced, alcoholic with abstinence) do better. The predictors of a poor outcome are a low EF, RV dysfunction, advanced NYHA class, high NT-proBNP, and renal dysfunction.[6]

Hypertrophic cardiomyopathy (HCM)

A genetic sarcomeric disease (most commonly a beta-myosin heavy chain MYH7 or myosin-binding protein C MYBPC3 mutation) producing an asymmetric septal hypertrophy (wall ≥15 mm, or ≥13 mm in a first-degree relative) — inherited autosomal dominant, prevalence ~1 in 500.[1][2][4]

The pathophysiology of the dynamic LVOT obstruction: the thickened septum narrows the LV outflow tract, and the systolic anterior motion (SAM) of the mitral valve (the anterior leaflet is pulled into the narrowed outflow tract by the Venturi effect) worsens the obstruction and produces a mitral regurgitation. The dynamic LVOT obstruction — it varies with the preload, the afterload, and the contractility — is the hallmark. The obstruction is present at rest in ~one-third, labile/latent in one-third (provokable by Valsalva, standing, amyl nitrite, or exercise echo), and absent in one-third.[2]

The "four D's" that worsen the LVOT gradient — and the four that relieve it (an exam favourite): [1]

Clinical features:

• The murmur — a crescendo-decrescendo systolic ejection murmur at the left sternal edge, radiating to the apex (not the neck), that intensifies with Valsalva/standing (less preload) and softens with squatting/handgrip (more preload/afterload). The opposite of aortic stenosis (which softens with Valsalva).
• Symptoms — exertional dyspnoea (the commonest, from diastolic dysfunction and/or MR), angina (despite clean coronaries — microvascular dysfunction, increased muscle mass), pre-syncope/syncope (the LVOT gradient, arrhythmia), and sudden cardiac death — HCM is the commonest cause of SCD in the young athlete.[4]

Risk stratification for sudden death — the HCM Risk-SCD score:[3] a validated model (O'Mahony 2014) estimating 5-year SCD risk from age, maximal wall thickness, LA diameter, LVOT gradient, family history of SCD, NSVT, and unexplained syncope. An estimated 5-year risk ≥6 per cent warrants an ICD for primary prevention; 4-6 per cent is a shared decision; <4 per cent generally not. The 2020 AHA/ACC guideline supplements this with major risk factors (massive LVH ≥30 mm, family history of ≥1 SCD <50, unexplained syncope, NSVT, abnormal BP response).[2]

Management:[1][2]

• Beta-blockers (the first-line — they reduce the contractility and the heart rate, lowering the LVOT gradient). Non-dihydropyridine calcium-channel blockers (verapamil/diltiazem) are second-line (caution: avoid in heart block, severe gradient where the negative inotropy can transiently worsen filling).
• Disopyramide — a class Ia antiarrhythmic with strong negative inotropy, added for refractory symptoms/gradient.
• Mavacamten — a first-in-class cardiac myosin inhibitor that reduces actin-myosin cross-bridging, lowering the gradient; EXPLORER-HCM showed it improved symptoms and reduced the LVOT gradient in symptomatic obstructive HCM.[5]
• Avoid vasodilators and inotropes — they reduce the afterload and the preload, worsening the dynamic obstruction (the LVOT narrows further). This is the opposite of the dilated cardiomyopathy management.
• Avoid dehydration — maintain the preload (the LVOT is less obstructed with a fuller LV).
• Septal reduction therapy for the refractory symptomatic patient with a gradient ≥50 mmHg: surgical septal myectomy (the gold standard, performed at high-volume centres) or alcohol septal ablation (a percutaneous alternative inducing a controlled septal infarct; reserved for those unsuitable for surgery, higher pacemaker dependency).
• An ICD for the primary prevention of sudden cardiac death (HCM is the commonest cause of sudden cardiac death in the young athlete; risk stratify with the HCM Risk-SCD score).[3]

Restrictive cardiomyopathy

Stiff, non-compliant ventricles that cannot relax and fill in diastole (a diastolic failure) — small ventricles with massively enlarged atria, a near-normal EF, and high filling pressures.[1]

Causes:[1]

• Amyloidosis — the commonest and most important: AL (light-chain, from a plasma-cell dyscrasia; multisystem — macroglossia, periorbital purpura, nephrotic-range proteinuria) and ATTR (transthyretin; wild-type/senile in elderly men, or hereditary from a TTR mutation). The red-flag clue on echo is a thick LV with low voltages on the ECG (the "discordance" between echo and ECG) and a global longitudinal strain with apical sparing ("cherry-on-the-top" pattern) on strain imaging.[7]
• Sarcoidosis — granulomatous infiltration; may cause heart block, ventricular arrhythmia, and a sarcoid cardiomyopathy. Cardiac MRI shows focal LGE in a basal inferolateral/subepicardial distribution; PET-CT shows active inflammation.
• Eosinophilic (Loeffler endocarditis) — eosinophilic myocarditis with mural thrombus and endocardial fibrosis; in the tropics (endomyocardial fibrosis) or with hypereosinophilic syndrome, Churg-Strauss, or parasitic infestation.
• Storage diseases — haemochromatosis (iron; also a DCM phenotype), Fabry disease (alpha-galactosidase A deficiency; an X-linked mimicker of HCM with concentric LVH), glycogen storage diseases (Danon, Pompe).
• Radiation — a late consequence of mediastinal radiotherapy (years to decades); may cause concomitant constriction, valvular disease, and coronary ostial disease.
• Idiopathic.

The cardiac amyloidosis workup (the workflow examiners love):

1. Index of suspicion — elderly man with "hypertension" that has become refractory, heart failure with preserved EF, carpal tunnel syndrome (often bilateral, often preceding the cardiac disease by years), biceps tendon rupture (the "Popeye sign"), spinal stenosis, and orthostatic hypotension.
2. ECG + echo discordance — thick LV on echo but low voltages on ECG (especially in AL).
3. Strain imaging — apical sparing pattern.
4. Scintigraphy (the non-biopsy route for ATTR) — ^99mTc-DPD, PYP or HMDP uptake grade 2-3, with no monoclonal protein on serum/urine immunofixation, makes ATTR without biopsy (Perugini criteria — avoid the endomyocardial biopsy for ATTR).
5. Serum/urine immunofixation + serum free light chains — for AL amyloid.
6. Endomyocardial biopsy — the gold standard for AL when scintigraphy is not diagnostic (Congo red apple-green birefringence). [1]

Treatment of cardiac amyloidosis (ATTR-ACT changed the landscape):[7]

• Tafamidis — a transthyretin stabiliser that slows ATTR progression (ATTR-ACT, Maurer 2018, reduced all-cause mortality and cardiovascular hospitalisations in ATTR-CM).[7]
• AL amyloid — treat the underlying plasma-cell dyscrasia with chemotherapy/bortezomib ± autologous stem-cell transplant (haematology-led).
• Heart failure — cautious diuretics (the stiff ventricles are preload-dependent — over-diuresis causes a catastrophic fall in cardiac output); AVOID ACE inhibitors/ARBs/ARNI (often intolerant — hypotension), calcium-channel blockers (negatively inotropic, bind amyloid fibrils), and digoxin (binds amyloid fibrils → toxicity).
• Anticoagulation for atrial fibrillation (high thromboembolic risk).

Sarcoid cardiomyopathy — corticosteroids (prednisolone 0.5-1 mg/kg) ± steroid-sparing agents (methotrexate) for active inflammation; an ICD (even primary prevention) for the arrhythmic risk, which is disproportionate to the EF.[1]

The key distinction — restriction vs constriction: restrictive cardiomyopathy is distinguished from constrictive pericarditis (both present with right heart failure and equalised diastolic pressures — see the pericardial-disease topic). Restriction has a normal pericardium and a thick, infiltrated LV (amyloid on the MRI or the biopsy); constriction has a thickened pericardium and a normal LV.[1]

Management: treat the underlying cause (amyloid — treat the underlying plasma cell dyscrasia or the ATTR; sarcoid — corticosteroids). The heart failure is diastolic — cautious diuretics, avoid over-diuresis (the stiff ventricles are preload-dependent).[1]

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

A genetic desmosomal cardiomyopathy (most commonly PKP2 encoding plakophilin-2; also DSG2, DSC2, JUP) in which the right-ventricular myocardium is progressively replaced by fibrofatty tissue — leading to RV dilation, regional akinesia/dyskinesia, ventricular arrhythmia, and a risk of sudden death. Autosomal dominant, prevalence ~1 in 2000-5000.[1][1]

The 2010 revised Task Force Criteria diagnose ARVC from a combination of:[1]

• Imaging — RV regional akinesia/dyskinesia/aneurysm + RV dilation/dysfunction (echo, MRI, or angiography).
• Cardiac MRI — RV regional wall-motion abnormalities + fibrosis (late gadolinium enhancement); fatty infiltration is suggestive but hard to confirm reliably.
• Biopsy — residual myocytes <60 per cent by area with fibrous replacement ± fat (endomyocardial biopsy).
• ECG repolarisation — T-wave inversion in V1-V3 (without RBBB).
• ECG depolarisation — the epsilon wave (a small deflection at the end of the QRS in V1-V3 — a near-pathognomonic but late sign), late potentials on signal-averaged ECG, a prolonged terminal activation duration.
• Arrhythmia — NSVT or sustained VT of left-bundle-branch-block morphology (RV origin) with a superior axis.
• Family history / genetics — a confirmed disease-causing desmosomal mutation.

Management:[1]

• Sports restriction — competitive and endurance sport is prohibited (it accelerates the disease and precipitates arrhythmia).
• Beta-blocker first-line for symptomatic arrhythmia.
• ICD for the secondary prevention of VF/VT and for primary prevention in high-risk phenotypes (sustained VT, syncope, extensive RV involvement).
• Catheter ablation for recurrent VT (often recurrent at a new focus — the disease is diffuse).
• Heart failure therapy for the biventricular failure of advanced disease; transplantation for end-stage.

Takotsubo (stress) cardiomyopathy

A transient, reversible regional systolic dysfunction, typically apical ballooning, triggered by intense emotional or physical stress ("broken-heart syndrome"), in the absence of a culprit coronary occlusion.[12][13]

Pathophysiology: catecholamine surge (the apex is rich in beta-receptors and more vulnerable to calcium overload and microvascular spasm); the basal hyperkinesis squeezes against a stunned apex, producing the characteristic akinesia of the apex with hyperkinesis of the base (the octopus-pot shape, tako-tsubo).[12]

The Mayo/InterTAK diagnostic criteria (all four required):[13]

1. Transient regional wall-motion abnormality (apical, mid-ventricular, basal, or focal) that usually extends beyond a single epicardial vascular territory.
2. No obstructive epicardial coronary disease (or acute plaque rupture) on angiography.
3. A new ECG abnormality (ST elevation, T-wave inversion, or QTc prolongation) or a modest troponin rise (disproportionately small compared with the wall-motion abnormality).
4. The syndrome is not explained by myocarditis or pheochromocytoma.

Presentation: post-menopausal women (>90 per cent) hours-days after a trigger (grief, sepsis, surgery, subarachnoid haemorrhage, an asthma attack, or even a surprise party); chest pain, dyspnoea, syncope, or an arrhythmia. The InterTAK registry (Templin 2015) showed an in-hospital mortality of ~4 per cent and serious complications in ~20 per cent — it is NOT always benign.[12]

The variants — not all are apical:

• Apical ballooning (~80 per cent) — the classic.
• Mid-ventricular — a "mitral systolic motion" variant; can co-apical-ballooning with HCM-like SAM and an LVOT gradient.
• Basal (reverse Takotsubo) — basal akinesia, hyperkinetic apex.
• Focal. [1]

Complications that demand ICU vigilance:

• LV apical thrombus (stasis in the akinetic apex) — anticoagulate during the acute phase (echo to detect; anticoagulate for ~3 months until the LV recovers).
• LVOT obstruction (from the basal hyperkinesis + SAM) — avoid inotropes; treat with a beta-blocker and fluids, as in HCM.
• Acute heart failure and cardiogenic shock.
• Arrhythmia — Torsades de pointes (the QTc is markedly prolonged), VT/VF, high-grade AV block.
• Free-wall rupture (rare but lethal; typically day 3-7). [1]

Management:[13]

• Supportive — treat as acute heart failure; diuretics and nitrates for pulmonary oedema (provided there is no LVOT obstruction — echo first).
• ACE inhibitor/ARB, beta-blocker — conventional, though beta-blocker benefit is debated; most continue it for 3-6 months then stop once the EF normalises.
• Anticoagulation for an LV thrombus or severe apical akinesia.
• Avoid inotropes if there is an LVOT gradient; if shock with NO LVOT obstruction, cautious low-dose inotrope or MCS.
• Recovery within weeks to months in the majority (~95 per cent recover the EF); recurrence ~5-10 per cent over years.

Myocarditis

An inflammation of the myocardium, most commonly viral (coxsackie B, parvovirus B19, SARS-CoV-2, influenza, adenovirus, HHV-6, Epstein-Barr, HIV), but also autoimmune, drug (anthracyclines, clozapine, immune-checkpoint inhibitors), toxic, and hypersensitivity (DRESS, eosinophilic).[1][9]

Aetiology — the exam-friendly breakdown:[9]

Clinical:[1][9]

• Chest pain (mimics an ACS), a flu-like prodrome in the preceding 1-2 weeks.
• Arrhythmia (atrial and ventricular — from the inflamed myocardium; the most common cause of death in the acute phase).
• Heart failure (from the LV dysfunction — may be fulminant).
• Sudden death in young athletes — myocarditis is the third commonest cause of SCD in the under-35s (after HCM and arrhythmogenic syndromes).
• A rising troponin with normal coronary arteries on the angiogram.
• A rub or pericardial features if there is a concomitant pericarditis (myopericarditis).

Diagnosis:[1][9][10]

• Echocardiography — an LV dysfunction (may be regional or global; may be normal early). Look specifically for RV involvement (a poor prognostic sign) and a pericardial effusion.
• Cardiac MRI — the gold-standard non-invasive test. The Lake Louise criteria (updated 2018) require both a tissue-characterisation abnormality (T1 mapping, ECV, late gadolinium enhancement) and an inflammatory signal (T2 mapping/STIR oedema). The classic pattern is mid-wall or subepicardial late gadolinium enhancement in the lateral/inferolateral wall (the non-ischaemic pattern — distinguishes from the subendocardial LGE of an infarct).[10]
• Endomyocardial biopsy — the historical gold standard; the Dallas criteria (a lymphocytic infiltration with myocyte necrosis = active myocarditis; borderline if infiltrate without necrosis). Rarely done in clinical practice (the MRI has largely replaced it for diagnosis), but remains indicated for the fulminant case in a middle-aged adult to exclude giant-cell myocarditis — because giant-cell changes the management to immunosuppression/transplant.[9][11]
• Viral PCR on blood and (if biopsied) myocardial tissue.
• Coronary angiography — to exclude an ACS as the cause of the troponin rise.

The fulminant vs acute distinction (McCarthy, NEJM 2000):[8] fulminant myocarditis presents with sudden severe haemodynamic compromise needing inotropes/MCS within hours-days, often with a distinct viral prodrome and fever; non-fulminant acute myocarditis is more insidious. Paradoxically, fulminant myocarditis has a BETTER long-term survival (93 per cent at 11 years vs 45 per cent for acute) — because the fulminant inflammation is a single, robust, self-limited immune response, whereas the indolent form smolders into a dilated cardiomyopathy.[8]

Treatment:[1][9][11]

• Supportive — heart-failure therapy (ACEi, beta-blocker, diuretic), treat the arrhythmia, anticoagulate if an LV thrombus.
• Rest — avoid exercise for 6 months (exercise during the acute phase increases the viral replication and the mortality; the classic example is athletes who collapse on returning to sport).
• NSAIDs for the pericarditis component (myopericarditis) — colchicine may be added.
• Treat the cause — antiviral for the specific virus if available; immunosuppression for the giant-cell or the autoimmune myocarditis (confirmed on the biopsy) — Kandolin 2015 showed combined immunosuppression (cyclosporine + azathioprine + steroids) improved survival in giant-cell myocarditis; a trial of corticosteroids for virus-negative, biopsy-proven lymphocytic myocarditis may be considered.[11]
• Most recover fully; some progress to a dilated cardiomyopathy; the fulminant case (a severe acute presentation with cardiogenic shock) may need mechanical support (VA-ECMO, an Impella) as a bridge to recovery, or a transplant.[1][8]

COVID-19 and vaccine myocarditis

SARS-CoV-2 can cause myocarditis directly (viral tropism via the ACE2 receptor) or indirectly (the cytokine storm, the multisystem inflammatory syndrome in children [MIS-C], and critical illness). The mRNA vaccines (BNT162b2, mRNA-1273) carry a small but real risk of myopericarditis, predominantly in young males within 1 week of the second dose, that is generally mild and self-limiting — distinct from classical viral myocarditis, with a prompt recovery of the EF and a low complication rate.[14] The overall risk-benefit strongly favours vaccination.

Mechanical circulatory support for fulminant myocarditis

The principle: support the failing ventricle while the inflammation resolves (most fulminant cases recover within days to weeks), with a defined exit strategy — bridge to recovery, to decision, to a durable LVAD, or to transplant.[1][8]

Trials that changed practice

[1]

[1] [1] [1]

Red flags

References

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2. [2]Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Circulation, 2020.PMID 33215938
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