ReviewHeart failure reviews2021
Practical recommendations for the diagnosis and management of transthyretin cardiac amyloidosis.
Review in Heart failure reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- A systematic review for the evidence of recommendations and guidelines in hybrid nuclear cardiovascular imaging.European journal of nuclear medicine and molecular imaging · 2024Pooled it
- Suspicion, screening, and diagnosis of wild-type transthyretin amyloid cardiomyopathy: a systematic literature review.ESC heart failure · 2022Pooled it
- An N-terminal ATTR Fibril Segment Promotes Transthyretin Amyloid Nucleation and Polymorphism.bioRxiv : the preprint server for biology · 2026Article
- QuantitativeEuropean journal of nuclear medicine and molecular imaging · 2026Article
- Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Functional Capacity Evaluation and Rehabilitation Strategies in Cardiac Amyloidosis: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Diagnostic Challenges in the Management of Aortic Valve Stenosis and the Role of Imaging: A Narrative Review.Journal of clinical medicine · 2025Review
- Prevalence of Transthyretin Amyloid Cardiomyopathy Among Acute Heart Failure Patients with Hypertrophy Across the Left Ventricular Ejection Fraction Spectrum.Journal of clinical medicine · 2024Article
- Examining the Difficulties in Identifying and Handling Cardiac Amyloidosis; Acquiring Important Knowledge and Robust Treatment Methods.Cardiovascular & hematological disorders drug targets · 2024Review
- A wolf in sheep's clothing-aortic stenosis and cardiac amyloidosis: "RAISE"ing awareness in clinical practice.Frontiers in cardiovascular medicine · 2024Article
- Article
- Quantitative SPECT/CT Parameters in the Assessment of Transthyretin Cardiac Amyloidosis-A New Dimension of Molecular Imaging.Journal of cardiovascular development and disease · 2023Review
- Drug and Gene Therapy for Treating Variant Transthyretin Amyloidosis (ATTRv) Neuropathy.Current neuropharmacology · 2023Article
- Role of Diphosphonates Bone Scintigraphy in Correlation with Biomarkers for a Personalized Approach to ATTR Cardiac Amyloidosis in North-Eastern Romania.Diagnostics (Basel, Switzerland) · 2022Article
- Article
- Filamin C Cardiomyopathy Variants Cause Protein and Lysosome Accumulation.Circulation research · 2021Article
- Transthyretin cardiac amyloidosis: a review of the nuclear imaging findings with emphasis on the radiotracers mechanisms.Annals of nuclear medicine · 2021Review
- Cardiac Amyloidosis-Challenging Diagnosis and Unclear Clinical Picture.Medicina (Kaunas, Lithuania) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac amyloidosis (CA) is an infiltrative restrictive cardiomyopathy caused by accumulation in the heart interstitium of amyloid fibrils formed by misfolded proteins. Most common CA types are light chain amyloidosis (AL) caused by monoclonal immunoglobulin light chains and transthyretin amyloidosis (ATTR) caused by either mutated or wild-type transthyretin aggregates. Previously considered a rare disease, CA is increasingly recognized among patients who may be misdiagnosed as undifferentiated heart failure with preserved ejection fraction (HFPEF), paradoxical low-flow/low-gradient aortic stenosis, or otherwise unexplained left ventricular hypertrophy. Progress in diagnosis has been due to the refinement of cardiac echocardiographic techniques (speckle tracking imaging) and magnetic resonance (T1 mapping) and mostly due to the advent of bone scintigraphy that has enabled noninvasive diagnosis of ATTR, limiting the need for endomyocardial biopsy. Importantly, proper management of CA starts from early recognition of suspected cases among high prevalence populations, followed by advanced diagnostic evaluation to confirm diagnosis and typing, preferentially in experienced amyloidosis centers. Differentiating ATTR from other types of amyloidosis, especially AL, is critical. Emerging targeted ATTR therapies offer the potential to improve outcomes of these patients previously treated only palliatively.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.