Evidence map›Paper›PMID 27669015›Full record

ArticlePloS one

Adrenergic Receptor Polymorphism and Maximal Exercise Capacity after Orthotopic Heart Transplantation.

Mélanie Métrich, Fortesa Mehmeti, Helene Feliciano, David Martin, Julien Regamey, Piergiorgio Tozzi, Philippe Meyer, Roger Hullin, Swiss Transplant Cohort Study

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. VOCurrent cardiology reports · 2025
    Review
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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

9 authors at 2 institutions in 1 country.

Mélanie MétrichCardiology, Cardiovascular Department, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0003-2528-9317
Fortesa MehmetiCardiology, University Hospital Geneva, University of Geneva, Geneva, Switzerland.
Helene FelicianoDepartment of Radiology, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
David MartinCardiology, Cardiovascular Department, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Julien RegameyCardiology, Cardiovascular Department, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Piergiorgio TozziCardiac Surgery, Cardiovascular Department, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Philippe MeyerCardiology, University Hospital Geneva, University of Geneva, Geneva, Switzerland.
Roger HullinCardiology, Cardiovascular Department, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Swiss Transplant Cohort Study
University of Lausanne · CHUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaximal exercise capacity after heart transplantion (HTx) is reduced to the 50-70% level of healthy controls when assessed by cardiopulmonary exercise testing (CPET) despite of normal left ventricular function of the donor heart. This study investigates the role of donor heart β1 and β2- adrenergic receptor (AR) polymorphisms for maximal exercise capacity after orthotopic HTx.

methodsCPET measured peak VO2 as outcome parameter for maximal exercise in HTx recipients ≥9 months and ≤4 years post-transplant (n = 41; mean peak VO2: 57±15% of predicted value). Donor hearts were genotyped for polymorphisms of the β1-AR (Ser49Gly, Arg389Gly) and the β2-AR (Arg16Gly, Gln27Glu). Circumferential shortening of the left ventricle was measured using magnetic resonance based CSPAMM tagging.

resultsPeak VO2 was higher in donor hearts expressing the β1-Ser49Ser alleles when compared with β1-Gly49 carriers (60±15% vs. 47±10% of the predicted value; p = 0.015), and by trend in cardiac allografts with the β1-AR Gly389Gly vs. β1-Arg389 (61±15% vs. 54±14%, p = 0.093). Peak VO2 was highest for the haplotype Ser49Ser-Gly389, and decreased progressively for Ser49Ser-Arg389Arg > 49Gly-389Gly > 49Gly-Arg389Arg (adjusted R2 = 0.56, p = 0.003). Peak VO2 was not different for the tested β2-AR polymorphisms. Independent predictors of peak VO2 (adjusted R2 = 0.55) were β1-AR Ser49Gly SNP (p = 0.005), heart rate increase (p = 0.016), and peak systolic blood pressure (p = 0.031). Left ventricular (LV) motion kinetics as measured by cardiac MRI CSPAMM tagging at rest was not different between carriers and non-carriers of the β1-AR Gly49allele.

conclusionSimilar LV cardiac motion kinetics at rest in donor hearts carrying either β1-AR Gly49 or β1-Ser49Ser variant suggests exercise-induced desensitization and down-regulation of the β1-AR Gly49 variant as relevant pathomechanism for reduced peak VO2 in β1-AR Gly49 carriers.

Identifiers

PMID27669015
PMCPMC5036840
OpenAlexW2526242253

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.