ReviewEuropean heart journal2026
Transthyretin amyloid cardiomyopathy: from cause to novel treatments.
Review in European heart journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Neurohormonal Therapy in Patients With Transthyretin Cardiac Amyloidosis: Is it an Option?JACC. Case reports · 2026Article
- Rationale and Design of ACO-REAL: A Real-World Non-Interventional Study of Acoramidis in Routine Clinical Practice.Cardiology and therapy · 2026Article
- ACO-SWITCH: Rationale and Design of a Phase 4 Study Evaluating Serum Transthyretin in ATTR-CM After Switching from Tafamidis to Acoramidis.Cardiology and therapy · 2026Article
- Bidirectional impact between cardiovascular comorbidities and heart failure: an updated position paper from the Italian society of cardiology (SIC) working group on heart failure.Heart failure reviews · 2026Article
- Vutrisiran Treatment and Changes in Cardiac Parameters and Amyloid Burden Assessed by Cardiovascular MRI.JAMA cardiology · 2026Article
- Frailty status, clinical and functional outcomes in cardiac amyloidosis: a systematic review and meta-analysis.EClinicalMedicine · 2026Article
- Prognostic impact of chronotropic incompetence in transthyretin cardiac amyloidosis: a multicentre study.ESC heart failure · 2026Article
- Better Outcomes After Initiation of Disease-Modifying Therapy in Patients with Transthyretin Cardiac Amyloidosis.Journal of clinical medicine · 2026Article
- Transthyretin Amyloidosis-From Peculiar Neuropathy to a Treatable Chronic Multisystemic Disease.Genes · 2026Review
- Article
- Therapy of amyloidosis: stabilizers and silencers.European heart journal supplements : journal of the European Society of Cardiology · 2026Article
- Baroreflex Activation Therapy in a Patient With Transthyretin Amyloid Cardiomyopathy.JACC. Case reports · 2026Article
- Endomyocardial Biopsy Revisited: Diagnostic Value and Expanding Roles in Cardiac Amyloidosis.Current heart failure reports · 2026Review
- Emerging Pharmacological Strategies for Cardiac Amyloidosis: A Qualitative Analysis of Interventional Clinical Trials Registered on ClinicalTrials.Gov.Journal of clinical medicine · 2026Review
- Review
- Expanding the scope of SGLT inhibitors in underrepresented cardiac populations: from pathophysiology to clinical evidence.Frontiers in cardiovascular medicine · 2026Review
- Targeting transthyretin deposition in lumbar spinal stenosis: a mechanistic rationale for tafamidis.Frontiers in surgery · 2026Article
- Transthyretin Cardiac Amyloidosis and Heart Failure: State-of-the-Art Review and Practice Guidance.Reviews in cardiovascular medicine · 2025Review
- Navigating the emerging landscape of asymptomatic ATTR-CM: challenges, opportunities and the path ahead.Future cardiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive disorder marked by amyloid deposition in the heart, ultimately impairing cardiac function. Recent treatment advances have paralleled an evolving understanding of ATTR-CM pathophysiology. One emerging hypothesis suggests that an imbalance between in vivo amyloid production and natural clearance may drive disease progression, a conceptual framework that still requires validation. Transthyretin (TTR) stabilizers, such as tafamidis and acoramidis, mitigate amyloid formation by promoting the native tetrameric conformation of circulating TTR, thereby slowing functional decline and prolonging survival. Similarly, TTR gene silencers inhibit hepatic TTR synthesis, and gene-editing therapy with nexiguran ziclumeran offers an additional strategy to reduce amyloid production. However, these approaches do not enhance the body's limited capacity to clear existing amyloid deposits, underscoring the need for novel agents that accelerate amyloid removal. Promisingly, monoclonal antibodies targeting TTR amyloid are under development, with early clinical trials suggesting that this passive immunotherapy may reverse disease progression and improve heart function. Ultimately, optimal management of ATTR-CM will require further elucidation of the complex interplay between amyloid formation, its structural and functional impacts, its clearance mechanisms, and the potential for myocardial reverse remodelling.
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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.