Evidence map›Paper›PMID 37476571›Full record

ReviewFrontiers in cardiovascular medicine2023

Cardiovascular toxicity from therapies for light chain amyloidosis.

Paolo Morfino, Alberto Aimo, Vincenzo Castiglione, Michela Chianca, Giuseppe Vergaro, Carlo Maria Cipolla, Antonella Fedele, Michele Emdin, Iacopo Fabiani, Daniela Cardinale

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Review
  4. Review
  5. Article
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Paolo MorfinoInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Alberto AimoInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Vincenzo CastiglioneInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Michela ChiancaInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Giuseppe VergaroInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Carlo Maria CipollaCardioncology Unit, Cardioncology and Second Opinion Division, European Institute of Oncology, I.R.C.C.S., Milan, Italy.
Antonella FedeleCardioncology Unit, Cardioncology and Second Opinion Division, European Institute of Oncology, I.R.C.C.S., Milan, Italy.
Michele EmdinInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Iacopo FabianiInterdisciplinary Center for Health Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Daniela CardinaleCardioncology Unit, Cardioncology and Second Opinion Division, European Institute of Oncology, I.R.C.C.S., Milan, Italy.
Scuola Superiore Sant'Anna · ITEuropean Institute of Oncology · ITFondazione Toscana Gabriele Monasterio · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid light-chain (AL) amyloidosis is a hematological disorder characterized by abnormal proliferation of a plasma cell clone producing monoclonal free light chains that misfold and aggregate into insoluble fibrils in various tissues. Cardiac involvement is a common feature leading to restrictive cardiomyopathy and poor prognosis. Current first-line treatments aim at achieving hematological response by targeting the plasma cell clones, and these have been adapted from multiple myeloma therapy. Patients with AL amyloidosis often exhibit multiorgan involvement, making them susceptible to cancer therapy-related cardiovascular toxicity. Managing AL amyloidosis is a complex issue that requires enhanced knowledge of the cardio-oncological implications of hematological treatments. Future research should focus on implementing and validating primary and secondary prevention strategies and understanding the biochemical basis of oncological therapy-related damage to mitigate cardiovascular toxicity.

Indexed as

AL amyloidosiscardiac amyloidosiscardiovascular toxicitychemotherapytreatment

Identifiers

PMID37476571
PMCPMC10354454
OpenAlexW4383198715

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.