Evidence map›Paper›PMID 40976551›Full record

ArticleJournal of cardiac failure2026

Antibody-independent Microvascular Inflammation Impacts Long-term Risk in Heart Transplantation.

Shi Huang, Nelson Chow, Kyle Saysana, Eric Farber-Eger, Quinn S Wells, David W Bearl, Joann Lindenfeld, Kelly H Schlendorf, Kaushik Amancherla

Abstract read
In one paragraph

Article in Journal of cardiac failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Shi HuangDepartment of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Nelson ChowDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Kyle SaysanaDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Eric Farber-EgerVanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University School of Medicine, Nashville, Tennessee.
Quinn S WellsDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University School of Medicine, Nashville, Tennessee.
David W BearlDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee.
Joann LindenfeldDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Kelly H SchlendorfDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Kaushik AmancherlaDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University School of Medicine, Nashville, Tennessee. Electronic address: kaushik.amancherla@vumc.org.

Funding

Cell-Specific Transcriptional Programs in Cardiac Allograft VasculopathyK23HL166960 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kaushik Amancherla · 2024 to 2026
$556k
NHLBI NIH HHS K23 HL166960NHLBI NIH HHS L30 HL165555
6 · The paper itself

Abstract

backgroundMicrovascular inflammation (MVI) after heart transplantation (HT) can occur with or without circulating anti-human leukocyte antigen donor-specific antibodies (DSAs). We sought to characterize the relationship between MVI, with or without accompanying DSA, and post-transplant outcomes. METHODS AND

resultsWe analyzed 8305 endomyocardial biopsies from 832 adult and pediatric HT recipients between July 1, 2013, and October 31, 2023. Endomyocardial biopsies were graded by consensus guidelines, with MVI defined as histological evidence of AMR grade ≥1. Rejection phenotypes were classified as no rejection, isolated cellular rejection, DSA-negative MVI, and DSA-positive MVI. Cox models with time-varying covariates were constructed to evaluate associations with incident cardiac allograft vasculopathy (CAV) and mortality, adjusting for donor and recipient age. Among 832 HT recipients, 238 developed CAV and 121 died over a median follow-up of 4 years (interquartile range 2.3-6.4 years). Compared with individuals who never experienced biopsy-proven rejection, DSA-negative MVI was independently associated with CAV (hazard ratio [HR] 1.47, 95% confidence interval [CI] 1.00-2.16, P = 0.047). DSA-positive MVI was associated with mortality (HR 1.97, 95% CI 1.07-3.64) with DSA-negative MVI demonstrating directional concordance (HR 1.50, 95% CI 0.87-2.57), independent of CAV (HR 1.71, 95% CI 1.13-2.58). These associations remained consistent when stratified by adult and pediatric subgroups and in a 6-month landmark sensitivity analysis.

conclusionsMVI, with or without DSA, may be harmful in HT, extending recent renal findings to thoracic transplantation. Understanding the mechanistic basis for these results will be essential for identifying novel targets for therapeutic modulation and prolonging graft survival.

Indexed as

Graft RejectionHeart TransplantationHLA AntigensInflammationIsoantibodiesMicrovesselsAdultChildFemaleFollow-Up StudiesHumansMaleMiddle AgedRetrospective StudiesRisk FactorsTime FactorsHLA AntigensIsoantibodiesAMRCAVDSAHeart transplantmicrovascular inflammation

Identifiers

PMID40976551
PMCPMC13040508

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Registered trials

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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.