# Transthyretin Amyloid Cardiomyopathy (ATTR-CM) [RHC Comprehensive Guide](https://urinenephrology.org/mastery/rhc/index.html) [Restrictive vs Constrictive](https://urinenephrology.org/mastery/rhc/restrictive-vs-constrictive.html) [ATTR Cardiac Amyloidosis](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html) ## Quick Navigation [Executive Summary](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#executive-summary) [1. Introduction](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#introduction) [2. Epidemiology](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#epidemiology) [3. Pathophysiology](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#pathophysiology) [4. Clinical Presentation](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#clinical-presentation) [5. Diagnosis](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#diagnosis) [6. Differential Diagnosis](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#differential) [7. Treatment](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#treatment) [8. Prognosis](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#prognosis) [9. Nephrology Considerations](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#nephrology) [10. Summary](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#summary) [References](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html#references) ## Executive Summary **Key Points** - ATTR-CM is an underdiagnosed infiltrative cardiomyopathy resulting from extracellular deposition of misfolded transthyretin protein, producing restrictive physiology with preserved ejection fraction (1,2) - Wild-type ATTR-CM (ATTRwt) may affect 10–15% of older adults with HFpEF, with strong male predominance and typical onset after age 65 (2,3) - Ejection fraction is unreliable in restrictive cardiomyopathy; critically low cardiac output can coexist with preserved EF (1,4) - Congestive hepatopathy from ATTR-CM can produce imaging findings indistinguishable from cirrhosis; ascitic fluid analysis provides insight into sinusoidal integrity (5,6) - Noninvasive diagnosis: grade 2–3 uptake on Tc-99m PYP scintigraphy in the absence of monoclonal protein, with sensitivity \> 99% and specificity approaching 100% (7) - Disease-modifying therapies — tafamidis and acoramidis — significantly reduce mortality and cardiovascular hospitalization (8,9) ## 1. Introduction and Clinical Relevance Cardiac amyloidosis has undergone a paradigm shift from a rare, untreatable diagnosis to an increasingly recognized and therapeutically addressable cause of heart failure. The convergence of noninvasive diagnostic imaging, epidemiologic data revealing higher prevalence, and disease-modifying pharmacotherapy has driven this transformation (1). ATTR-CM is of particular relevance to clinicians in nephrology, hepatology, and primary care because its clinical manifestations frequently masquerade as more common conditions — refractory ascites attributed to cirrhosis, progressive renal dysfunction from cardiorenal syndrome, or HFpEF managed with standard therapy that proves ineffective (1,4). This review was developed from an illustrative clinical case in which a 75-year-old male (Patient A) with diuretic-refractory ascites and CT findings reported as cirrhosis was ultimately found to have severely elevated biventricular filling pressures with cardiogenic shock-range cardiac output (CI 1.15 L/min/m²) despite a preserved ejection fraction of 55%. The patient died before therapy could be initiated. ## 2. Epidemiology ATTRwt-CM was historically considered rare and was previously termed "senile cardiac amyloidosis." Contemporary data indicate substantially higher prevalence. Autopsy studies have identified transthyretin amyloid deposits in approximately 25% of individuals older than 80 years (2,3). Systematic screening has identified ATTR-CM in: approximately **13% of patients hospitalized with HFpEF**, **16% of patients undergoing TAVR** for severe aortic stenosis, and **5–9% of patients with bilateral carpal tunnel syndrome** (2,3). ATTRwt-CM predominantly affects elderly males (\> 90% male; median age at diagnosis \> 75 years). Hereditary ATTR-CM (ATTRv) results from pathogenic TTR gene variants, of which \> 120 have been identified. The Val122Ile variant is present in approximately 3–4% of African Americans (1,2). **Clinical Pearl:** Any male patient over 65 with unexplained HFpEF, particularly with increased wall thickness, bilateral carpal tunnel syndrome, lumbar spinal stenosis, or biceps tendon rupture, should be evaluated for ATTR-CM. These extracardiac manifestations may precede cardiac diagnosis by years (1,4). ## 3. Pathophysiology ### 3.1 Transthyretin Biology and Amyloidogenesis Transthyretin (TTR) is a 55-kDa homotetrameric protein synthesized predominantly in the liver. In ATTR amyloidosis, tetramer destabilization leads to dissociation into monomers, which misfold and aggregate into insoluble amyloid fibrils (2,8). In ATTRwt, the sequence is normal but age-related factors promote instability. In ATTRv, pathogenic variants directly destabilize the tetramer (2,9). ### 3.2 Cardiac Infiltration and Restrictive Physiology Amyloid fibrils deposit in the myocardial interstitium, expanding the extracellular space and progressively increasing wall thickness and stiffness. This produces severely impaired diastolic filling with reduced stroke volume despite preserved systolic contraction (1,2). The critical consequence is **EF–cardiac output dissociation**: a ventricle filling 50 mL and ejecting 28 mL produces an EF of 55% while delivering a stroke volume less than half of normal (1,4). ### 3.3 Congestive Hepatopathy Elevated right atrial pressure transmits retrograde through hepatic veins into sinusoids. Chronic sinusoidal hypertension produces centrilobular necrosis, fibrosis, and nodular regeneration — indistinguishable from cirrhosis on cross-sectional imaging. This "cardiac cirrhosis" is distinct from primary liver disease: inflammation plays no significant role, and the histologic pattern differs (5,6). ### 3.4 Sinusoidal Physiology and Ascites Formation | Ascitic Fluid Parameter | Cirrhotic Ascites | Cardiac Ascites | |-----------------------------|-----------------------|-----------------| | SAAG | ≥ 1.1 g/dL | ≥ 1.1 g/dL | | Ascitic fluid total protein | \< 2.5 g/dL | ≥ 2.5 g/dL | | Sinusoidal fenestrations | Closed (capillarized) | Open (intact) | | Hepatic synthetic function | Impaired | Preserved | **In cirrhosis:** Sinusoidal capillarization restricts protein passage → low-protein ascites. **In cardiac congestion:** Intact fenestrations allow free protein passage → high-protein ascites. **Warning:** The ascitic fluid protein cutoff of 2.5 g/dL has sensitivity and specificity in the 70–80% range. Early cirrhosis may produce higher-protein ascites, and longstanding cardiac congestion may cause true secondary cirrhosis with low-protein ascites. The protein value is a Bayesian probability modifier, not a definitive test (10). ## 4. Clinical Presentation ### 4.1 The Preserved EF Trap The cardinal presentation is progressive heart failure with preserved ejection fraction in an older male patient. The 2020 AHA Scientific Statement explicitly identifies preserved EF as the primary barrier to diagnosis (1). The quantitative evidence is compelling: - **Median diagnostic delay of 13 months** from HF to ATTRwt diagnosis (Ladefoged et al., 2020) (14) - Cardiac amyloidosis can be underrecognized. The 2023 ACC consensus supports a structured evaluation using monoclonal-protein testing, cardiac imaging, and tissue diagnosis when indicated. Diagnostic delay is clinically important, but no universal misdiagnosis percentage or mortality multiplier is established here. [ACC consensus](https://pubmed.ncbi.nlm.nih.gov/36697326/) - Cardiac amyloidosis can be underrecognized. The 2023 ACC consensus supports a structured evaluation using monoclonal-protein testing, cardiac imaging, and tissue diagnosis when indicated. Diagnostic delay is clinically important, but no universal misdiagnosis percentage or mortality multiplier is established here. [ACC consensus](https://pubmed.ncbi.nlm.nih.gov/36697326/) **Warning:** Preserved EF is the primary cognitive trap driving diagnostic failure in cardiac amyloidosis. In any elderly patient with HFpEF — particularly males over 65 with unexplained LV hypertrophy, disproportionate symptoms, or diuretic resistance — the EF must not be used to exclude significant cardiac disease. The preserved EF is not reassuring; it is the disease's camouflage (1,14,15,16). Echocardiographic clues: increased biventricular wall thickness (IVS \> 12 mm), biatrial enlargement, thickened interatrial septum and valves, small LV cavity, restrictive diastolic filling. **Global longitudinal strain (GLS) with apical sparing** is a more sensitive indicator than EF (1,4). ECG: low voltage in limb leads (25–40%), pseudo-infarction pattern, conduction abnormalities. The discordance between echo wall thickness and ECG voltage is an important clue. ### 4.2 Extracardiac Manifestations Bilateral carpal tunnel syndrome (often preceding cardiac diagnosis by 5–10 years), lumbar spinal stenosis, spontaneous biceps tendon rupture, peripheral and autonomic neuropathy, GI dysmotility (1,4). ### 4.3 Hepatic and Ascitic Manifestations CT/ultrasound may show nodular liver morphology interpreted as cirrhosis. **Preserved serum albumin (≥ 3.5 g/dL) with massive ascites argues strongly against cirrhosis** as the primary etiology (10). **Clinical Pearl:** In anticoagulated patients with ascites, never use the INR to assess hepatic synthetic function or calculate MELD scores. A supratherapeutic INR on warfarin creates the misleading appearance of hepatic failure when the liver is functionally intact. Albumin and factor V are the interpretable markers. ### 4.4 Diuretic-Refractory Ascites In the illustrative case, bumetanide 4 mg PO BID (~furosemide 320 mg daily), dapagliflozin 10 mg, and spironolactone 50 mg failed to prevent rapid reaccumulation of 5.7 liters of ascites. This degree of diuretic resistance — failure targeting three nephron segments — is a hallmark of severely compromised cardiac output driving cardiorenal physiology (11). Mechanisms are multiplicative: critically reduced CO limits renal blood flow; elevated RA pressure (23 mmHg) reduces the transrenal perfusion gradient; gut edema impairs oral diuretic bioavailability; neurohormonal activation overwhelms the diuretic effect. ### 4.5 The Absence of Lower Extremity Edema Patients with cardiac amyloidosis may present with massive ascites but minimal peripheral edema. This reflects preferential targeting of the splanchnic circulation — the hepatic venous bed experiences enormous hydrostatic pressure across uniquely permeable sinusoidal endothelium. **"Massive ascites with dry legs"** should prompt cardiac investigation rather than excluding it (5,6). ## 5. Diagnosis ### 5.1 The Diagnostic Algorithm **Step 1: Clinical Suspicion.** HFpEF with increased wall thickness in an older patient, especially with extracardiac features. Discordance between echo wall thickness and ECG voltage (1,2). **Step 2: Monoclonal Protein Screening.** Serum free light chains, serum protein immunofixation, and urine protein immunofixation must all be performed to exclude AL amyloidosis and enable interpretation of the scintigraphy result (4,7). **Step 3: Tc-99m Bone Scintigraphy.** Tc-99m PYP/DPD/HMDP with planar and SPECT imaging at 1 and 3 hours. | Perugini Grade | Visual Description | H/CL Ratio (1 hour) | |----------------|---------------------------------|---------------------| | 0 | No myocardial uptake | \< 1.0 | | 1 | Mild uptake, less than rib | 1.0–1.5 | | 2 | Moderate uptake, equal to rib | ≥ 1.5 | | 3 | Strong uptake, greater than rib | \>\> 1.5 | **Noninvasive Diagnostic Criteria for ATTR-CM (Gillmore et al., 2016):** Grade 2 or 3 myocardial uptake on Tc-99m PYP/DPD/HMDP scintigraphy PLUS absence of monoclonal protein = diagnostic of ATTR-CM without endomyocardial biopsy (7). **Step 4: Genetic Testing.** TTR gene sequencing distinguishes ATTRwt from ATTRv. A positive TTR gene test does NOT obviate the need for PYP scintigraphy — the gene test answers "what type?" while scintigraphy answers "is it there?" (4,7). **Clinical Pearl:** Think of TTR gene testing as answering "what type?" while PYP scintigraphy answers "is it there?" A positive gene test without scintigraphic confirmation could lead to misattribution. The noninvasive pathway requires appropriate scintigraphy and exclusion of AL; typed biopsy provides a separate diagnostic route. ### 5.2 The Role of Right Heart Catheterization Invasive hemodynamic assessment is critically important when the clinical presentation is disproportionate to echocardiographic findings. In the illustrative case, echo suggested mild disease (EF 55%), while catheterization revealed cardiogenic shock-range hemodynamics (CI 1.15). RHC also excludes constrictive pericarditis, which requires different management. ### 5.3 Cardiac Magnetic Resonance Imaging CMR with late gadolinium enhancement (LGE) and parametric mapping (native T1, ECV) provides supportive diagnostic information. Characteristic: diffuse subendocardial or transmural LGE, elevated native T1, increased ECV. Cannot reliably distinguish ATTR from AL (1,2). **Clinical Pearl:** Very high NT-proBNP levels (disproportionate to clinical HF severity) combined with chronically elevated troponin in a patient with echocardiographic hypertrophic phenotype is strongly suggestive of cardiac amyloidosis (4). ## 6. Differential Diagnosis | Condition | Distinguishing Features | |----|----| | AL (light chain) amyloidosis | Monoclonal protein detected; rapid progression; multiorgan involvement including nephrotic syndrome; requires urgent chemotherapy | | Hypertensive cardiomyopathy | History of hypertension; concentric hypertrophy without disproportionate diastolic dysfunction | | Hypertrophic cardiomyopathy | Asymmetric septal hypertrophy; dynamic outflow obstruction; younger presentation; sarcomere mutations | | Fabry disease | X-linked; alpha-galactosidase A deficiency; angiokeratomas; corneal opacities; younger onset | | Constrictive pericarditis | Pericardial thickening/calcification; dip-and-plateau; ventricular interdependence; surgically treatable | | Cardiac sarcoidosis | Younger patients; conduction disease; patchy LGE; PET avidity; responsive to immunosuppression | | Iron overload cardiomyopathy | Low T2\* on CMR; history of transfusions or hemochromatosis | ## 7. Treatment ### 7.1 Disease-Modifying Therapy: TTR Stabilizers **Tafamidis (Vyndaqel/Vyndamax):** Binds to TTR tetramer, preventing dissociation. The ATTR-ACT trial (Maurer et al., *NEJM* 2018): 441 patients, 30 months. All-cause mortality 29.5% vs. 42.9% placebo (p = 0.0006). Reduced CV hospitalization (0.48 vs. 0.70/year). Tafamidis free acid 61 mg is the current formulation (8). ATTRibute-CM randomized 632 patients to acoramidis or placebo. Its four-component hierarchical primary analysis favored acoramidis (win ratio 1.8, 95% CI 1.4–2.2). The outcome incorporated death, cardiovascular hospitalization, NT-proBNP change, and six-minute walk distance; the win ratio is not a mortality hazard ratio. [ATTRibute-CM](https://pubmed.ncbi.nlm.nih.gov/38197816/) ### 7.2 Gene Silencing Therapies RNA interference and antisense oligonucleotide therapies reduce hepatic TTR production 80–90%. Vutrisiran (RNAi, subcutaneous q3 months) demonstrated 28% reduction in composite of death and recurrent CV events in HELIOS-B (12). CRISPR-Cas9 gene editing (NTLA-2001) has shown \> 90% sustained TTR knockdown after a single IV dose; phase 2/3 trials ongoing (2). ### 7.3 Anti-Amyloid Antibodies: Toward Disease Reversal The phase 1 NI006 trial enrolled 40 patients. At higher doses, imaging-based surrogate markers of amyloid load appeared to decrease during follow-up. These early findings do not establish improved survival or a proven clinical amyloid-removal treatment. [Phase 1 trial](https://pubmed.ncbi.nlm.nih.gov/37212440/) Biological plausibility was reinforced by a 2023 *NEJM* correspondence reporting three patients with spontaneous near-complete regression of cardiac amyloidosis via endogenous anti-TTR amyloid antibodies (12). ### 7.4 Can ATTR-CM Be Cured? A Realistic Assessment | Therapeutic Class | Mechanism | Status | "Cure" Potential | |----|----|----|----| | TTR stabilizers (tafamidis, acoramidis) | Prevent tetramer dissociation | FDA-approved | No — slows progression, does not remove deposits | | Gene silencers (vutrisiran, patisiran) | Reduce hepatic TTR production 80–90% | Approved (neuropathy); HELIOS-B positive | Partial — stops production; native clearance may slowly reduce burden | | CRISPR gene editing (NTLA-2001) | Permanent TTR gene knockdown (\> 90%) | Phase 2/3 | Partial — single dose, permanent production halt | | Anti-amyloid antibodies (NI006) | Phagocytic removal of deposited fibrils | Phase 3 | Highest — direct amyloid removal demonstrated on imaging | | Combination (silencer + depleter) | Halt production + remove deposits | Theoretical | Greatest — addresses both supply and accumulated burden | ### 7.5 Heart Failure Management **Diuretics** remain the cornerstone of volume management but frequently prove inadequate in advanced ATTR-CM. Strategies: conversion to IV loop diuretics, addition of metolazone or chlorothiazide for sequential nephron blockade, and serial large-volume paracentesis. **Warning:** Beta-blockers and non-dihydropyridine calcium channel blockers should be avoided or used with extreme caution in cardiac amyloidosis. The stiff, infiltrated ventricle is rate-dependent for cardiac output — stroke volume is fixed, so CO is directly proportional to heart rate. Rate-slowing agents may precipitate hemodynamic collapse (1,4). Digoxin binds preferentially to amyloid fibrils, potentially causing toxicity at standard levels. ## 8. Prognosis Untreated ATTRwt-CM: median survival approximately 2.5–3.5 years from diagnosis. Staging systems incorporating NT-proBNP, troponin T, and eGFR provide prognostic stratification (2,3). With disease-modifying therapy: tafamidis reduced 30-month mortality from 42.9% to 29.5%. Acoramidis achieved 80.7% 30-month survival, approaching the 85% estimated for age-matched general population (8,9). Earlier treatment initiation confers greater benefit. ## 9. Special Considerations for Nephrology ### 9.1 Cardiorenal Syndrome ATTR-CM with reduced CO and elevated right-sided pressures produces cardiorenal syndrome through: reduced renal arterial perfusion (forward failure), elevated renal venous pressure (congestive nephropathy), neurohormonal activation, and impaired diuretic delivery. This directly explains the diuretic resistance (11). ### 9.2 Renal Amyloid Deposition While cardiac involvement dominates, TTR amyloid deposits can occur in the kidney, particularly in ATTRv. Manifests as proteinuria or progressive renal insufficiency. Monitor renal function and urinary protein in all ATTR-CM patients (4). ### 9.3 Diuretic Optimization in Low-Output States Key principles: recognize impaired oral bioavailability from gut edema; use IV diuretics when oral response is inadequate; sequential nephron blockade; monitor electrolytes; avoid excessive preload reduction in the rate-dependent amyloid ventricle. ### 9.4 Drug Dosing Considerations Both tafamidis and acoramidis are hepatically metabolized — no renal dose adjustment needed. However, ATTRibute-CM excluded eGFR \< 30, and limited data exist in advanced CKD or dialysis (9). ### 9.5 Transplant Considerations Combined heart-liver transplantation has been performed for ATTRv. With gene silencing therapies available, isolated heart transplant combined with pharmacologic TTR suppression is an emerging alternative (2,4). ## 10. Summary and Key Teaching Points **Key Points** - ATTR-CM is an underdiagnosed, treatable cause of HFpEF — consider in any elderly male over 65 with unexplained HF, increased wall thickness, or clinical severity disproportionate to echo findings - Preserved EF is the single most dangerous cognitive trap: median 13-month delay, 44% misdiagnosis rate, 3- to 5-fold mortality increase - Congestive hepatopathy can mimic cirrhosis on imaging; diagnose with caution when hepatic synthetic function is preserved - In anticoagulated patients, INR cannot assess hepatic synthetic function or MELD scores - "Massive ascites with dry legs" should prompt cardiac investigation, not exclude it - High SAAG with high fluid protein (≥ 2.5 g/dL) suggests cardiac congestion through intact sinusoidal fenestrations - An appropriate scintigraphy pathway or typed tissue can establish ATTR-CM; TTR gene testing alone does not confirm cardiac involvement - TTR stabilizer therapy (tafamidis or acoramidis) reduces mortality; beta-blockers and calcium channel blockers should be avoided - The therapeutic trajectory is evolving from stabilization toward reversal; anti-amyloid antibodies have demonstrated amyloid removal on imaging - The nephrologist plays an essential role in managing cardiorenal syndrome, interpreting diuretic resistance as a hemodynamic signal, and monitoring renal involvement ## References 1. Kittleson MM, Maurer MS, Ambardekar AV, et al. Cardiac amyloidosis: evolving diagnosis and management. *Circulation*. 2020;142(1):e7-e22. [PubMed](https://pubmed.ncbi.nlm.nih.gov/32476490/) 2. Ruberg FL, Grogan M, Hanna M, et al. Transthyretin amyloid cardiomyopathy: JACC state-of-the-art review. *J Am Coll Cardiol*. 2019;73(22):2872-2891. [PubMed](https://pubmed.ncbi.nlm.nih.gov/31171094/) 3. Lane T, Fontana M, Martinez-Naharro A, et al. Natural history, quality of life, and outcome in cardiac transthyretin amyloidosis. *Circulation*. 2019;140(1):16-26. [PubMed](https://pubmed.ncbi.nlm.nih.gov/31109193/) 4. Kittleson MM, Ruberg FL, Ambardekar AV, et al. 2023 ACC expert consensus decision pathway on cardiac amyloidosis. *J Am Coll Cardiol*. 2023;81(11):1076-1126. [PubMed](https://pubmed.ncbi.nlm.nih.gov/36697326/) 5. Fortea JI, et al. Congestive hepatopathy. *Int J Mol Sci*. 2020;21(24):9420. [PubMed](https://pubmed.ncbi.nlm.nih.gov/33321947/) 6. Wells ML, et al. Imaging findings of congestive hepatopathy. *Radiographics*. 2016;36(4):1024-1037. [PubMed](https://pubmed.ncbi.nlm.nih.gov/27284758/) 7. Gillmore JD, Maurer MS, Falk RH, et al. Nonbiopsy diagnosis of cardiac transthyretin amyloidosis. *Circulation*. 2016;133(24):2404-2412. [PubMed](https://pubmed.ncbi.nlm.nih.gov/27143678/) 8. Maurer MS, et al. Tafamidis treatment for patients with transthyretin amyloid cardiomyopathy. *N Engl J Med*. 2018;379(11):1007-1016. [PubMed](https://pubmed.ncbi.nlm.nih.gov/30145929/) 9. Gillmore JD, Judge DP, Cappelli F, et al. Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy. *N Engl J Med*. 2024;390(2):132-142. [PubMed](https://pubmed.ncbi.nlm.nih.gov/38197816/) 10. Runyon BA; AASLD. Management of adult patients with ascites due to cirrhosis 2012. *Hepatology*. 2013;57(4):1651-1653. [PubMed](https://pubmed.ncbi.nlm.nih.gov/23463403/) 11. Rangaswami J, Bhalla V, Blair JEA, et al. Cardiorenal Syndrome: AHA Scientific Statement. *Circulation*. 2019;139(16):e840-e878. [PubMed](https://pubmed.ncbi.nlm.nih.gov/30852913/) 12. Fontana M, et al. Vutrisiran in patients with transthyretin amyloidosis with cardiomyopathy. *N Engl J Med*. 2024;391(17):1582-1593. [PubMed](https://pubmed.ncbi.nlm.nih.gov/39213194/) 13. Garcia-Pavia P, et al. Phase 1 trial of antibody NI006 for depletion of cardiac transthyretin amyloid. *N Engl J Med*. 2023;389(3):239-250. [PubMed](https://pubmed.ncbi.nlm.nih.gov/37212440/) 14. Ladefoged B, Dybro A, Povlsen JA, et al. Diagnostic delay in wild type transthyretin cardiac amyloidosis. *Int J Cardiol*. 2020;304:138-143. [PubMed](https://pubmed.ncbi.nlm.nih.gov/32033783/) 15. Wechalekar AD, Fontana M, Quarta CC, et al. AL Amyloidosis for Cardiologists: Awareness, Diagnosis, and Future Prospects. *JACC CardioOncol*. 2022;4(4):427-441. [PubMed](https://pubmed.ncbi.nlm.nih.gov/36444232/) 16. Shchendrygina A, Mewton N, Niederseer D, et al. Cardiac Amyloidosis Screening and Management in HFpEF: An International Survey. *Am J Cardiol*. 2024;236:42-48. [PubMed](https://pubmed.ncbi.nlm.nih.gov/39481586/) [RHC Comprehensive Guide](https://urinenephrology.org/mastery/rhc/index.html) [Restrictive vs Constrictive](https://urinenephrology.org/mastery/rhc/restrictive-vs-constrictive.html) [ATTR Cardiac Amyloidosis](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html) [← Back to Mastery](https://urinenephrology.org/mastery/index.html) This educational review was prepared by the Medical Associates Department of Nephrology in collaboration with the University of Illinois College of Medicine at Peoria, the University of Dubuque Physician Assistant Program, and the UDPA Butler School of Medicine. © 2026 Medical Associates Department of Nephrology — Cardiorenal Education Series --- [Website version](https://urinenephrology.org/mastery/rhc/cardiac-amyloidosis.html) · Markdown synchronized October 3, 2026.