ReviewHeart international2024
Evolution of Disease-modifying Therapy for Transthyretin Cardiac Amyloidosis.
Review in Heart international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
9 citing papers in PubMed.
- Disease-Modifying Therapies for Hereditary Transthyretin Amyloidosis with Polyneuropathy: Current Status and Future Perspectives.Neurology and therapy · 2026Review
- Survival in a Contemporary, Real-World, Matched Cohort of Patients with Transthyretin Amyloid Cardiomyopathy Treated vs Not Treated with Tafamidis.Cardiology and therapy · 2026Article
- Article
- Multimodal Diagnosis of Cardiac Amyloidosis: Integrating Imaging, Histochemistry, and Proteomics of Precise Typing.International journal of molecular sciences · 2026Review
- The Weight of Comorbidities in the Specific Treatment of ATTR-Related Amyloid Cardiomyopathy.Current cardiology reports · 2025Review
- The Last Decade in Cardiac Amyloidosis: Advances in Understanding Pathophysiology, Diagnosis and Quantification, Prognosis, Treatment Strategies, and Monitoring Response.JACC. Cardiovascular imaging · 2025Review
- Monitoring Disease Progression in Transthyretin Amyloid Cardiomyopathy.Heart international · 2025Review
- A Snapshot of the Most Recent Transthyretin Stabilizers.International journal of molecular sciences · 2024Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transthyretin cardiac amyloidosis (ATTR-CA) represents an inexorably progressive and fatal cardiomyopathy. Increased understanding of the underlying pathogenesis responsible for the misfolding of transthyretin and the subsequent accumulation of amyloid fibrils within the myocardium has led to the development of several disease-modifying therapies that act on different stages of the disease pathway. Tafamidis is the first, and to date remains the only, therapy approved for the treatment of ATTR-CA, which, alongside acoramidis, stabilizes the transthyretin tetramer, preventing disaggregation, misfolding and formation of amyloid fibrils. Gene-silencing agents, such as patisiran, vutrisian and eplontersen, and novel gene-editing therapies, such as NTLA-2001, act to reduce the hepatic synthesis of transthyretin. Anti-amyloid therapies represent another strategy in the treatment of ATTR-CA and are designed to bind amyloid fibril epitopes and stimulate macrophage-mediated removal of amyloid fibrils from the myocardium. Many of these treatments are at an early investigational stage but represent an important area of unmet clinical need and could potentially reverse disease and restore cardiac functions even in patients with advanced disease.
Indexed as
Identifiers
What OpenQuestion holds
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.