Evidence map›Paper›PMID 39941618›Full record

ReviewJournal of clinical medicine2025

Autoimmunity in Cardiomyopathy-Induced Heart Failure and Cardiac Autoantibody Removal by Immunoadsorption.

Michael Dandel

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. 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

1 author.

Michael DandelGerman Centre for Heart and Circulatory Research (DZHK), Potsdamer Str. 58, 10785 Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is increasing evidence that β1-adrenoreceptor autoantibody (β1AR-AAb) elimination can break the vicious circle induced by certain pathological conditions associated with alteration of the physiological self-tolerance, followed by generation of such AAbs and activation of cell-mediated immune processes directed against the myocardium. Concerning this, the present narrative review article provides an updated overview of the state of knowledge about the role of auto-immunity in the etiopathogenesis of cardiomyopathies, with a particular focus on immunoadsorption (IA) therapy for β1AR-AAb-positive adult patients with a dilated cardiomyopathy (DCM)-associated refractory heart failure (HF). Among many relevant findings, the increasing prevalence (up to 97%) of β1AR-AAb-positive patients related to the aggravation of HF, the high prevalence (between 84% and 91%) of HF patients in which IA can reduce to a minimum any increased β1AR-AAb level, as well as the high prevalence (about 80%) of responders to the IA-induced normalization of β1AR-AAb levels by long-term improvement in LV ejection fraction with increase in LV stroke volume and cardiac output, are of particular relevance. Given that after the elimination of β1AR-AAbs in potential candidates for heart transplantation (HTx), the post-IA 3- and 5-year HTx-/mechanical support-free survival probability reached 80% and 63-69%, respectively, the good tolerability of IA and the possibility to repeat that therapy also in elderly persons strongly suggest that in appropriately selected patients, this therapy deserves much more attention in the future.

Indexed as

autoimmunitycardiac autoantibodiesdilative cardiomyopathyheart failureimmunoadsorptionmyocardial recovery

Identifiers

PMID39941618
PMCPMC11818089

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.