Restrictive Cardiomyopathy

Meet the patient

A 72-year-old man is back on the cardiology ward for the third time in a year with "HFpEF" that will not settle. He has bilateral carpal tunnel releases behind him, a ruptured biceps tendon he blames on the gym, and now a JVP that does not fall, an abdomen full of ascites, and an ECG whose voltages you can barely see.[1][9]

He is the patient every cardiology firm admits as "diuretic-resistant right heart failure" — and he is the patient you must not send for pericardiectomy. Two questions are now live, and the whole topic exists to answer them: is this restriction or constriction? and what is stiffening his ventricle?[1][6]

A stiff ventricle with a preserved pump — the first mark in the viva

This is a stiff-ventricle problem, not a pump problem. Systolic ejection is normal early; the ventricle simply cannot accept the blood returning to it. Filling pressures climb, the atria hypertrophy and balloon, and the patient drowns in venous congestion on a normal ejection fraction.[5]

RCM is the least common of the three WHO cardiomyopathies — hypertrophic and dilated sit ahead of it. The label is the easy part; the skill is recognising that a stiff ventricle underlies the "HFpEF", naming the infiltrate, and separating it from constriction.[5]

Why is systole spared at first? The contractile machinery is intact — amyloid, iron and granulomas sit in the interstitium, so myocyte shortening survives. Only late, once the load is heavy and replacement fibrosis sets in, does the pump fail — the "burnt-out" phase that predicts a poor outcome.[1]

The AMISH list — what is stiffening this ventricle?

When the ventricle is stiff, name the cause before you name the drug. The aetiology decides everything that follows, and the AMISH mnemonic keeps the five families in one breath.[1]

The two anatomical axes that earn a sub-mark. Split each cause by where the disease sits: myocardial RCM (amyloid, sarcoid, radiation, scleroderma, idiopathic) infiltrates the muscle itself; endomyocardial RCM (Löffler, tropical EMF, carcinoid) scars the lining under a coat of thrombus. The split predicts the imaging — apical obliteration is the endomyocardial fingerprint.[1][7]

Is this restriction or constriction? (The question that decides surgery)

This is the single most important decision in restrictive cardiomyopathy, because pericardiectomy cures constriction and is futile — even harmful — in RCM. The bedside signs overlap almost perfectly: raised JVP, Kussmaul, hepatomegaly, ascites. The discrimination happens on imaging and catheter, not at the bedside.[6]

[6]

The one-line discriminator to carry into the viva: BNP high plus no calcification points to restriction; BNP normal plus calcification points to constriction. Add a preserved septal e-prime (annulus paradoxus) and the case is closed.[6]

The dip-and-plateau sign will not save you — it is shared

The square-root (dip-and-plateau) sign is the trap, because it appears in BOTH restriction and constriction and so does not discriminate. Early diastolic filling is rapid and then abruptly arrested in each — the ventricle fills fast, hits its limit, and the pressure plateaus. Seeing it confirms only that filling is restricted; it tells you nothing about the pericardium.[6]

The three tests that actually separate the two are BNP, pericardial calcification and annulus paradoxus — not the square-root sign. Reach for those before you reach for the catheter tracings.[6]

Kussmaul's sign is the other shared finding — use it for a different fork. A JVP that rises on inspiration is present in BOTH restriction and constriction, because the stiff right ventricle cannot accept the augmented venous return — but it is absent in tamponade. That makes it a three-way discriminator: restriction and constriction yes, tamponade no.[6]

Voltage-mass discordance — amyloid until you exclude it

The classic trap: low voltages on the ECG with thick LV walls on the echo is amyloidosis until you have proven otherwise. Normally a thick wall means more muscle means bigger voltages; in amyloid the fibrils displace myocardium, so the wall is thick but the QRS is small. That discordance is the bedside signature of infiltration.[1]

Add the apical sparing pattern on longitudinal strain — the "cherry on top", where basal and mid-wall strain fall away but the apex is preserved — and the picture is virtually diagnostic. On cardiac MRI the matched finding is diffuse subendocardial late gadolinium enhancement that will not null: the blood pool and myocardium null together because so much amyloid holds the gadolinium.[1]

Etymology for viva gold: amyloid comes from the Greek amylon, "starch". Virchow named it because the deposits stained like starch with iodine. It is not starch — it is misfolded protein in beta-pleated sheets that takes up Congo red and glows apple-green under polarised light. The name is wrong; it stuck.[3][4]

AL versus ATTR — read the amyloid type, because the treatment is opposite

Once amyloid is confirmed, the next question decides the drug: is it AL or ATTR? They share the stiff-ventricle phenotype but diverge completely in cause, pace and treatment. Light chains are directly toxic to myocytes, so AL is aggressive and chemo-responsive; transthyretin deposits more slowly, so ATTR runs for years and answers to a stabiliser.[1][3]

[1] [3]

The one-line discriminator: light chains, macroglossia, periorbital purpura and a fast decline point to AL; carpal tunnel, biceps rupture, spinal stenosis in an elderly man point to ATTR.[3][9]

Why the atria balloon and the patient drowns — the mechanism in three steps

Three structural problems converge on one haemodynamic phenotype. Whatever the infiltrate — amyloid fibrils, granulomas, iron, fibrous tissue — it displaces contractile myocardium and shifts the passive pressure-volume curve up and to the left, so a small gain in volume produces a large rise in pressure.[1][4]

That produces restrictive early filling: the E-wave inflow is rapid and then stops dead as the stiff ventricle hits its limit, and atrial contraction adds almost nothing — the dip-and-plateau signature on catheter and the E-dominant, short-deceleration pattern on echo.[1]

The atria pay the price. Pumping against a non-compliant ventricle they hypertrophy, dilate and finally fibrillate — the bi-atrial enlargement that is the radiological and echocardiographic hallmark, and the substrate for the atrial standstill and thrombus that complicate the disease.[1]

Who walks through the door — the red-flag patient

RCM is rare, but its causes cluster so tightly that the patient often hands you the diagnosis in the history. Ask about age, ancestry, occupation and region, past radiotherapy, chronic inflammation, and the orthopaedic and soft-tissue signs that precede ATTR by years.[1]

• AL amyloidosis — incidence 8 to 12 per million per year; cardiac involvement in about half at diagnosis; slight male predominance; usually a lambda clone.[3]
• ATTR wild-type — underdiagnosed; autopsy prevalence around 25 percent in those over 80; elderly men with HFpEF, bilateral carpal tunnel, spinal stenosis or biceps rupture years before the heart.[9]
• ATTRv V122I — carried by 3 to 4 percent of African Americans; penetrant cardiac amyloid in late life; the classic "hypertensive heart failure" mislabel.[3]
• Cardiac sarcoidosis — clinical involvement in 2 to 5 percent of systemic sarcoid, subclinical in 20 to 25 percent on PET or autopsy; over-represented in African Americans, Scandinavians and Japanese; young and middle-aged adults.[11]
• Endomyocardial fibrosis — the tropical equatorial belt (Uganda, Nigeria, Mozambique, the Kerala coast); a leading cause of heart failure in young people there, with eosinophilia and poverty as risk factors.[7]
• Hereditary haemochromatosis — HFE C282Y homozygosity in 1 in 200 Northern Europeans; cardiac deposition in about a third of untreated adults.[8]

Read the bedside like the consultant — the JVP and the systemic clues

The JVP is the most important bedside sign, and the waveform tells you more than the height. In RCM the y descent is rapid and deep (Friedreich's sign) — early diastolic filling is fast, then arrested — alongside a preserved x descent. Kussmaul's sign sits on top, marking the stiff right ventricle that cannot accept venous return.[6]

Heart sounds split RCM from constriction at the bedside. An S3 in RCM marks the rapid deceleration of early filling; the pericardial knock of constriction is its higher-pitched, earlier mirror — filling arrested by the pericardium itself. An S4 appears while the atrium still contracts in sinus rhythm.[1]

Then hunt for the cause in the skin, mouth and hands — the systemic clues that hand you the aetiology before any scan.[1]

• Tongue — macroglossia with teeth scalloping (AL); eyelids — periorbital purpura, the raccoon sign (AL).
• Skin — bronze pigmentation and angiokeratomas (haemochromatosis, Fabry); wrists and shoulders — carpal tunnel and biceps tendon rupture (ATTR).
• Joints — second and third metacarpophalangeal arthritis (haemochromatosis); lymph nodes, skin and eyes — erythema nodosum and uveitis (sarcoid).[1]

Phenotype, then constrict, then cause — the staged diagnostic strategy

Run the work-up in three deliberate steps, in order. Confirm the restrictive phenotype, separate it from constriction, then name the infiltrate. Skipping straight to a biopsy without the first two is how patients reach an operating table they should never have been on.[1][5]

Step one — phenotype, on ECG and echo. Low limb-lead voltages under 0.5 mV with a thick granular LV, a pseudoinfarct Q-wave pattern with no infarct, and first-degree or higher AV block build the amyloid case. Echo shows massive bi-atrial enlargement and an E-dominant restrictive inflow — E-over-A above 2, deceleration time under 150 ms — with an annular e-prime under 5 cm/s at both septal and lateral walls.[1]

Step two — separate from constriction. BNP is markedly raised in RCM and normal in constriction; pericardial calcification and septal bounce belong to constriction alone; annulus paradoxus (preserved septal e-prime) points to constriction. On simultaneous catheter tracings the dip-and-plateau appears in both, but in RCM LVEDP exceeds RVEDP by over 5 mmHg at end-expiration while in constriction they equalise within 5 mmHg.[6]

Step three — name the infiltrate, with the modality matched to the cause.[1]

• Cardiac MRI — diffuse subendocardial LGE that will not null, native T1 over 1040 ms and extracellular volume over 40 percent for amyloid; patchy basal subepicardial LGE with FDG uptake for sarcoid; native T2-star under 20 ms for iron.[8]
• Bone-tracer scintigraphy (PYP, DPD or HMDP) at Perugini grade 2 to 3 diagnoses ATTR non-invasively, once light chains are excluded.[12]
• Serum free light chains with ratio, serum and urine immunofixation, bone marrow biopsy find the AL clone.[3]
• Endomyocardial biopsy with Congo red and apple-green birefringence plus mass-spectrometry typing remains the gold standard when non-invasive work-up is inconclusive.[1]

[1] [6] [1] [2]

Treat the cause — and never reach for digoxin or a calcium-channel blocker

[1]

The single most important step in RCM is to treat the underlying cause; everything else is symptomatic. Modern therapy has transformed the prognosis of AL and ATTR amyloid, which is exactly why early, accurate typing now changes lives.[1][3]

ATTR amyloidosis — tafamidis 61 mg orally once daily. The ATTR-ACT trial showed a 30 percent reduction in all-cause mortality and a 32 percent reduction in cardiovascular hospitalisations over 30 months in ATTR-CM, wild-type and hereditary together. Diflunisal, patisiran and the antisense or RNA-interference agents target hereditary ATTR with polyneuropathy; acoramidis is the next-generation stabiliser with a positive phase-3 trial.[2]

AL amyloidosis — urgent plasma-cell-directed chemotherapy, never tafamidis. First-line is CyBorD — cyclophosphamide, bortezomib and dexamethasone — with bortezomib 1.3 mg per metre squared subcutaneously on days 1, 4, 8 and 11 of a 21-day cycle, dexamethasone 40 mg weekly and cyclophosphamide 300 mg per metre squared weekly. Daratumumab (anti-CD38, subcutaneous) is added for higher-risk disease; autologous stem cell transplant is reserved for fit patients with limited cardiac involvement.[3]

Cardiac sarcoidosis — corticosteroids first. Prednisolone 0.5 to 1 mg per kg per day (typically 30 to 40 mg daily), tapering over 6 to 12 months guided by symptoms, ECG and imaging; add methotrexate 7.5 to 15 mg weekly, mycophenolate 1 g twice daily or azathioprine 1 to 2 mg per kg per day for refractory disease or steroid toxicity. An ICD covers sustained VT; a pacemaker covers high-grade AV block.[11]

Hereditary haemochromatosis — get the iron out. Therapeutic phlebotomy of one unit (450 to 500 mL, about 200 to 250 mg of iron) weekly until the serum ferritin is under 50 microgram per litre, then maintenance phlebotomy every 1 to 3 months. For those who cannot tolerate phlebotomy, deferoxamine 20 to 40 mg per kg per day subcutaneously over 8 to 12 hours, or oral deferasirox 14 to 28 mg per kg per day.[8]

Endomyocardial disease. Löffler endocarditis (hypereosinophilic syndrome) takes prednisolone 1 mg per kg per day with or without hydroxyurea, or imatinib if FIP1L1-PDGFRA is positive, plus anticoagulation and surgical endocardiectomy in advanced disease. Carcinoid heart disease takes a somatostatin analogue — octreotide LAR 20 to 30 mg intramuscularly every 4 weeks or lanreotide autogel 120 mg deep subcutaneously every 4 weeks — and tricuspid or pulmonary valve replacement for symptomatic right-heart failure.[7]

The preventable-harm list — drugs you must not give in amyloidosis

Two drugs bind amyloid fibrils and predictably harm these patients; both belong on the avoid list. Reach for neither, and teach the team why.[1]

• Digoxin binds amyloid fibrils — it concentrates in the deposit, so toxicity and dangerous arrhythmias follow at "normal" doses. Digoxin is contraindicated in cardiac amyloidosis.[1]
• Non-dihydropyridine calcium-channel blockers — verapamil and diltiazem — bind amyloid fibrils and are negative inotropes, so they worsen heart failure. Avoid both.[1]
• Over-diuresis and vasodilators collapse a preload-dependent ventricle into cardiogenic shock — nitrates, ACE inhibitors, ARBs and hydralazine have no place in decompensated RCM.[10]

Diurese with your eyes open — the ventricle is preload-dependent

Acute decompensated RCM is a difficult combination — marked congestion, hypotension and renal dysfunction on a ventricle that cannot afford to lose preload. Cautious intravenous loop diuretic is the mainstay, titrated to urine output and renal function.[10]

• Furosemide 20 to 40 mg intravenously (or bumetanide 1 mg), with spironolactone 12.5 to 25 mg orally added for sodium retention; over-diuresis precipitates cardiogenic shock.[1]
• Avoid nitrates, ACE inhibitors, ARBs, hydralazine and high-dose beta-blockers in decompensated disease — the tachycardia is compensatory for a small fixed stroke volume, and slowing it drops cardiac output.[10]
• Atrial fibrillation with rapid ventricular response — rate control with small doses of metoprolol 25 to 50 mg orally twice daily (or 2.5 to 5 mg intravenously, cautiously); amiodarone 200 mg three times daily for one week then 200 mg once daily for rhythm control. Never digoxin, never a calcium-channel blocker.[1]
• Anticoagulate for atrial fibrillation, intracardiac thrombus or severe atrial standstill — apixaban 5 mg orally twice daily, or warfarin to an INR of 2 to 3, remembering that AL amyloid patients bleed easily.[1]

Pacemakers, ICDs and the combined heart-liver transplant

Devices follow the rhythm; transplantation follows the cause. A pacemaker covers symptomatic high-grade AV block, common in sarcoid and amyloid; an ICD covers sustained VT, with primary-prevention benefit weighed against competing risk in end-stage amyloid.[1]

Heart transplantation gives a 5-year survival of 70 to 80 percent in selected end-stage RCM with a treatable or absent extra-cardiac cause. For ATTRv the liver is the source of mutant transthyretin, so a combined heart-liver transplant prevents recurrence; for AL with renal failure a combined heart-kidney transplant is the equivalent move.[1]

The tropical and the temperate — EMF and Löffler

Endomyocardial disease is the great tropical cause of restrictive physiology, and Löffler is its temperate mirror. Both scar the endocardium and coat it with thrombus, producing the pathognomonic apical obliteration of one or both ventricles on echo — the cavity filled in from the apex upwards.[7]

Tropical endomyocardial fibrosis dominates the equatorial belt — Uganda, Nigeria, Mozambique, the Kerala coast — and is a leading cause of heart failure in young people there. The giveaway at the bedside is ascites out of proportion to the peripheral oedema, with AV-valve regurgitation from tethered leaflets. Endocardiectomy with valve repair offers symptomatic relief in selected patients.[7]

Löffler endocarditis is the temperate-zone hypereosinophilic syndrome — marked peripheral eosinophilia over 1500 per microlitre for over 6 months, endocardial thrombus, systemic thromboembolism and restrictive filling, often driven by FIP1L1-PDGFRA. Treat the eosinophilia with steroids, hydroxyurea or imatinib, anticoagulate, and reserve surgical endocardiectomy for advanced disease.[7]

Prognosis is cause-dependent — and it has been transformed

Prognosis tracks the cause, and modern therapy has rewritten it for AL and ATTR. Knowing the type tells you the timeline before you say a word about treatment.[1]

• AL amyloidosis — median survival under 6 months untreated from heart-failure onset; with CyBorD plus or minus daratumumab, median survival now exceeds 3 to 5 years. The Mayo 2013 stage (NT-proBNP, troponin T, free-light-chain difference) runs from stage I at over 90 percent five-year survival to stage IV under 25 percent.[3]
• ATTR wild-type — median 3 to 5 years untreated; tafamidis cut all-cause mortality by 30 percent over 30 months in ATTR-ACT.[2][9]
• ATTRv V122I — median 2 to 3 years untreated; tafamidis-responsive.[3]
• Cardiac sarcoidosis — variable, with a high sudden-death risk, but it responds to steroids if caught before scar establishes.[11]
• Tropical EMF — high early mortality around 25 percent in the first year; survivors stabilise with chronic heart failure.[7]
• Hereditary haemochromatosis — cardiac function often reverses with iron removal if caught before cirrhosis and diabetes.[8]
• Radiation-induced — progressive over decades; median survival under 2 years once cardiac symptoms appear.[1]

Special populations — who you screen, and how

Screening thresholds shift with ancestry, age and geography. Build the reflex into the history so the diagnosis finds you, not the other way around.[1]

• Elderly — ATTR wild-type dominates; suspect it in any man over 65 with "HFpEF" and bilateral carpal tunnel or biceps rupture, and send bone-tracer scintigraphy and serum free light chains at a low threshold.[9]
• African descent — screen TTR V122I in any patient presenting with "hypertensive heart failure" and LVH out of proportion; the carrier rate is 3 to 4 percent.[3]
• Tropical regions — EMF is the dominant cause and tuberculous constrictive pericarditis the dominant mimic; both are common.[7]
• Pregnancy — rare; avoid ACE inhibitors, ARBs and spironolactone, diurese cautiously with furosemide, and deliver in a cardiac centre.[10]
• Family screening — offer genetic testing to all first-degree relatives of ATTRv patients and to siblings of HFE C282Y haemochromatosis; cascade screening finds pre-symptomatic carriers.[1][8]

The guideline and trial backbone

Three documents and one trial carry the evidence weight in RCM. Name them in the viva and the marks follow.[1]

• 2021 ESC position statement on cardiac amyloidosis (Garcia-Pavia) — the red-flag screening algorithm, non-invasive bone-tracer scintigraphy for ATTR, serum free light chains for AL, and disease-specific therapy.[1]
• 2021 expert consensus on monitoring ATTR-CM (Garcia-Pavia) — surveillance echo, biomarkers and clinical review intervals for patients on tafamidis.[12]
• 2016 ESC heart-failure guideline (Ponikowski) — RCM sits within HFpEF and heart failure with mildly reduced EF, with early referral for cardiomyopathy assessment.[10]
• ATTR-ACT (Maurer 2018) — tafamidis 61 mg or 80 mg daily versus placebo over 30 months in ATTR-CM; all-cause mortality 29.5 percent versus 42.9 percent (hazard ratio 0.70), with fewer cardiovascular hospitalisations and a slower decline in six-minute walk.[2]
• HRS 2014 expert consensus on cardiac sarcoidosis (Birnie) — diagnostic criteria and arrhythmia management, and the role of steroids and immunosuppression.[11]
• Mayo 2004 and 2013 AL staging — biomarker staging (troponin, NT-proBNP, free-light-chain difference) driving transplant decisions and prognosis.[3]

Ward-round test — 3 stems

Work each stem out loud, then open the model answer. Each one rehearses a trap that costs marks.[1]

Stem 1 — the elderly man with refractory HFpEF and bilateral carpal tunnel

A 74-year-old man is admitted for the third time with "HFpEF" that will not settle. His ECG voltages are tiny, the echo shows a thick granular LV with an apical-sparing strain pattern, and he has bilateral carpal tunnel releases in his history. What two tests settle the diagnosis, and what drug do you reach for first? Model: Send serum free light chains with immunofixation (to exclude AL) and a 99mTc-PYP or DPD bone-tracer scan; grade 2 to 3 uptake with negative light chains non-invasively diagnoses ATTR wild-type amyloidosis. If ATTR-CM is confirmed, start tafamidis 61 mg once daily — it cut all-cause mortality by 30 percent in ATTR-ACT. Never give digoxin or a calcium-channel blocker in amyloidosis, and never send this patient for pericardiectomy.[1][2][9]

Stem 2 — raised JVP, Kussmaul and a preserved EF

A 60-year-old woman has a JVP that does not fall, a positive Kussmaul sign, hepatomegaly, ascites and a preserved ejection fraction. Is this restriction or constriction, and which three tests discriminate? Model: The bedside signs overlap completely — Kussmaul and the dip-and-plateau sign appear in BOTH, so they do not discriminate. The three tests that do are BNP (markedly raised in restriction, normal in constriction), pericardial calcification on CT (present in constriction, never in RCM) and annulus paradoxus on tissue Doppler (preserved septal e-prime in constriction, reduced in both walls in RCM). On catheter, LVEDP exceeding RVEDP by over 5 mmHg points to restriction; equalisation within 5 mmHg points to constriction. The decision matters because pericardiectomy cures constriction and is harmful in RCM.[6]

Stem 3 — the young African-descent patient with AV block

A 34-year-old man of African descent presents with complete heart block and an episode of sustained ventricular tachycardia, mild biventricular failure and bilateral hilar lymphadenopathy. What is the diagnosis, and what is the first treatment? Model: This is cardiac sarcoidosis until proven otherwise, not "hypertensive heart disease". Send cardiac MRI for patchy basal and subepicardial late gadolinium enhancement and an FDG-PET for active inflammation, and screen for extracardiac sarcoid. Start corticosteroids early — prednisolone 0.5 to 1 mg per kg per day — while the granulomas are still steroid-responsive, and consider an ICD for the sustained VT. Caught early, sarcoid responds to steroids; once scar establishes, the sudden-death risk climbs and steroids stop working.[11]

The mantra

Stiff ventricle, preserved EF, bi-atrial enlargement — find the cause, never digoxin or a calcium-channel blocker, never pericardiectomy.[1][6]

References

1. [1]Garcia-Pavia P, Rapezzi C, Adler Y, et al. Diagnosis and treatment of cardiac amyloidosis. A position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases Eur J Heart Fail, 2021.PMID 33826207
2. [2]Maurer MS, Schwartz JH, Gundapaneni B, et al. Tafamidis Treatment for Patients with Transthyretin Amyloid Cardiomyopathy N Engl J Med, 2018.PMID 30145929
3. [3]Muchtar E, Dispenzieri A, Magen H, et al. Systemic amyloidosis from A (AA) to T (ATTR): a review J Intern Med, 2021.PMID 32929754
4. [4]Falk RH. Diagnosis and management of the cardiac amyloidoses Circulation, 2005.PMID 16186440
5. [5]Rapezzi C, Arbustini E, Caforio AL, et al. Diagnostic work-up in cardiomyopathies: bridging the gap between clinical phenotypes and final diagnosis. A position statement from the ESC Working Group on Myocardial and Pericardial Diseases Eur Heart J, 2013.PMID 23211230
6. [6]Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography Circulation, 1989.PMID 2914352
7. [7]Mocumbi AO. Endomyocardial fibrosis: recent advances and future therapeutic targets Nat Rev Cardiol, 2025.PMID 40011660
8. [8]Murphy CJ, Oudit GY. Iron-overload cardiomyopathy: pathophysiology, diagnosis, and treatment J Card Fail, 2010.PMID 21055653
9. [9]Grogan M, Scott CG, Kyle RA, et al. Natural History of Wild-Type Transthyretin Cardiac Amyloidosis and Risk Stratification Using a Novel Staging System J Am Coll Cardiol, 2016.PMID 27585505
10. [10]Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure Rev Esp Cardiol (Engl Ed), 2016.PMID 27894487
11. [11]Birnie DH, Sauer WH, Bogun F, et al. HRS expert consensus statement on the diagnosis and management of arrhythmias associated with cardiac sarcoidosis Heart Rhythm, 2014.PMID 24819193
12. [12]Garcia-Pavia P, Bengel F, Brito D, et al. Expert consensus on the monitoring of transthyretin amyloid cardiomyopathy Eur J Heart Fail, 2021.PMID 33915002