ReviewJournal of clinical medicine2024
Diagnostic Modalities in the Detection of Cardiac Amyloidosis.
Review in Journal of clinical medicine, 2024. 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.
- Artificial Intelligence in Cardiac Amyloidosis: A State-of-the-Art Review.Journal of clinical medicine · 2026Review
- Article
- Transthyretin Cardiac Amyloidosis and Heart Failure: State-of-the-Art Review and Practice Guidance.Reviews in cardiovascular medicine · 2025Review
- Cardiac Amyloidosis Suggested byKorean circulation journal · 2025Article
- Emerging Insights into Granulomatous and Amyloidogenic Cardiomyopathies.Journal of clinical medicine · 2025Review
- Monoclonal gammopathy progressing to systemic amyloidosis with cardiac involvement. A case report.Archivos peruanos de cardiologia y cirugia cardiovascularArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac amyloidosis (CA) results mainly from the infiltration of the myocardium by either immunoglobulin light-chain fibrils (AL) or transthyretin fibrils (ATTR), causing restrictive cardiomyopathy and eventually death if untreated. AL derives from monoclonal immunoglobulin light chains produced by plasma cell clones in the bone marrow, while ATTR is the misfolded form of hepatically derived transthyretin (TTR) protein and can be hereditary (ATTRv) or wild-type (ATTRwt). Over the last decade, improvements in diagnostic imaging and better clinical awareness have unleashed a notable presence of CA in the community, especially ATTR in the elderly population. These multimodality imaging modalities include echocardiography, cardiac magnetic resonance, and radionuclide scintigraphy with bone-avid tracers. There has been remarkable progress in the therapeutic landscape as well, and there are disease-modifying therapies available now that can alter the course of the disease and improve survival if initiated at an early stage of the disease. There remains an unmet need for detecting this disease accurately and early so that these patients can benefit the most from newly emerging therapies.
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.