Evidence map›Paper›PMID 38014658›Full record

ArticleJournal of the American Heart Association2023

Omics and Extreme Phenotyping Reveal Longitudinal Association Between Left Atrial Size and Pulmonary Vascular Resistance in Group 2 Pulmonary Hypertension.

Neil J Kelly, David Newhouse, Himal Chapagain, Ashish Patel, Yicheng Tang, Ato Howard, Anna Kirillova, Hee-Jung J Kim, Haris Rahman, Wadih El Khoury and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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

15 authors at 2 institutions in 1 country.

Neil J KellyCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.ORCID 0000-0003-0455-5348
David NewhouseCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.
Himal ChapagainDepartment of Medicine UPMC McKeesport McKeesport PA.ORCID 0009-0002-9284-5205
Ashish PatelHeart and Vascular Institute Pittsburgh PA.
Yicheng TangCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.
Ato HowardDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center Pittsburgh PA.
Anna KirillovaCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.ORCID 0000-0003-2113-5257
Hee-Jung J KimCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.
Haris RahmanCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.
Wadih El KhouryCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.ORCID 0000-0001-5635-9643
Seyed Mehdi NouraieDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center Pittsburgh PA.ORCID 0000-0001-7465-0581
Gavin HickeyHeart and Vascular Institute Pittsburgh PA.ORCID 0000-0002-0547-4921
Leyla Elif SadeHeart and Vascular Institute Pittsburgh PA.ORCID 0000-0003-3737-8595
Sandeep JainHeart and Vascular Institute Pittsburgh PA.ORCID 0000-0002-5815-370X
Stephen Y ChanCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute Pittsburgh PA.ORCID 0000-0002-9520-7527
University of Pittsburgh Medical Center · USUPMC McKeesport · US

Funding

Defining the Complex Biology of the miR-130/301 Family in Pulmonary HypertensionR01HL124021 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2014 to 2025
$4.9M
Training Program in Imaging Sciences in Translational Cardiovascular ResearchT32HL129964 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Flordeliza S Villanueva · 2016 to 2026
$4.7M
Iron-Sulfur Deficiency as a Critical Pathogenic Cause of Pulmonary HypertensionR01HL122596 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2015 to 2024
$4.5M
Genetic and hypoxic control of a lncRNA axis orchestrates endothelial reprogramming in pulmonary hypertensionR01HL151228 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Stephen Y Chan · 2023 to 2026
$2.8M
ACTN4 Binding to Functional SNP rs9277336 Controls the Genome Architecture and Endothelial Pathophenotypes in Pulmonary ArterialF30HL170649 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Anna Kirillova · 2023 to 2026
$198k
NHLBI NIH HHS F30 HL170649NHLBI NIH HHS R01 HL122596NHLBI NIH HHS R01 HL124021NHLBI NIH HHS R01 HL151228NHLBI NIH HHS T32 HL129964
6 · The paper itself

Abstract

backgroundLeft heart disease is the most common cause of pulmonary hypertension (PH) and is frequently accompanied by increases in pulmonary vascular resistance. However, the distinction between phenotypes of PH due to left heart disease with a normal or elevated pulmonary vascular resistance-isolated postcapillary PH (IpcPH) and combined pre- and postcapillary PH (CpcPH), respectively-has been incompletely defined using unbiased methods. METHODS AND

resultsPatients with extremes of IpcPH versus CpcPH were identified from a single-center record of those who underwent right heart catheterization. Individuals with left ventricular ejection fraction <40% or with potential causes of PH beyond left heart disease were excluded. Medication usage in IpcPH and CpcPH was compared across Anatomical Therapeutic Chemical classes and identified vitamin K antagonists as the only medication with pharmacome-wide significance, being more commonly used in CpcPH and for an indication of atrial fibrillation in ≈90% of instances. Accordingly, atrial fibrillation prevalence was significantly higher in CpcPH in a phenome-wide analysis. Review of echocardiographic data most proximal to right heart catheterization revealed that left atrial diameter indexed to body surface area-known to be associated with atrial fibrillation-was increased in CpcPH regardless of the presence of atrial fibrillation. An independent cohort with serial right heart catheterizations and PH-left heart disease showed a significant positive correlation between change in left atrial diameter indexed to body surface area and change in pulmonary vascular resistance.

conclusionsGuided by pharmacomic and phenomic screens in a rigorously phenotyped cohort, we identify a longitudinal association between left atrial diameter indexed to body surface area and pulmonary vascular resistance with implications for the future development of diagnostic, prognostic, and therapeutic tools.

Indexed as

Atrial FibrillationHeart FailureHypertension, PulmonaryHumansStroke VolumeVascular ResistanceVentricular Function, Leftatrial fibrillationleft atriumpulmonary hypertensionpulmonary vascular resistance

Identifiers

PMID38014658
PMCPMC10727316
OpenAlexW4389087258

What Socratic holds

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LicenceCC BY-NC-ND
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 Socratic graph.