ArticleJACC. Basic to translational science2025
Myocardium From Patients With ATTR Amyloidosis Produces Less Force Secondary to Increased Fibrosis.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- The CabioRxiv : the preprint server for biology · 2026Article
- Development of Human iPSC-based Microphysiogical Models of Transthyretin Amyloid Cardiomyopathy.Research square · 2026Article
- Human atrial skinned muscle fibers exhibit reduced length-dependent activation but show faster force development kinetics than ventricular muscle.Journal of molecular and cellular cardiology · 2026Article
- Biomolecular mechanisms of cardiac amyloidosis and its cardiovascular pathological basis.Frontiers in immunology · 2026Review
- Pharmacological considerations for next-generation protein therapeutics in cardiovascular disease.The Journal of pharmacology and experimental therapeutics · 2025Review
- Profibrotic Biomarkers Correlate with Clinical Presentation and Outcome in Cardiac Transthyretin Amyloidosis.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid transthyretin cardiac amyloidosis is one of the most common infiltrative cardiomyopathies. Contractile, biochemical, and histological assays were performed on myocardium from patients with and without amyloid transthyretin amyloidosis. Force was reduced in amyloidosis, but calcium sensitivity was increased. The change in calcium sensitivity may reflect dephosphorylation of troponin I. The proportion of stiffness attributable to the extracellular matrix was larger in amyloidosis. Septal fibrosis and amyloid burden correlated with measurements from LV samples. Technetium pyrophosphate scans may detect increased microcalcifications in amyloidosis myocardium. Replacement of myocytes with extracellular matrix is the most important factor depressing contractile force in amyloidosis myocardium.
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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 Socratic graph.