Evidence map›Paper›PMID 39068288›Full record

ArticleScientific reports2024

Left ventricular dysfunction in pulmonary arterial hypertension is attributed to underfilling rather than intrinsic myocardial disease: a CMR 2D phase contrast study.

Ashwin Venkateshvaran, Jessica Bohlin, Barbro Kjellström, Elsa Bergström, Anders Nelsson, Anna Werther Evaldsson, Göran Rådegran, Håkan Arheden, Ellen Ostenfeld

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Ejection fraction quantification from ungated chest CT by AI.medRxiv : the preprint server for health sciences · 2025
    Article
  7. Article
  8. 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

9 authors.

Ashwin VenkateshvaranClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Jessica BohlinDepartment of Cardiology, Skåne University Hospital, Malmö, Sweden.
Barbro KjellströmClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Elsa BergströmClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Anders NelssonClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Anna Werther EvaldssonDepartment of Clinical Sciences Lund, Cardiology, and the Section for Heart Failure and Valvular Disease, Skåne University Hospital, Lund University, Lund, Sweden.
Göran RådegranDepartment of Clinical Sciences Lund, Cardiology, and the Section for Heart Failure and Valvular Disease, Skåne University Hospital, Lund University, Lund, Sweden.
Håkan ArhedenClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Ellen OstenfeldClinical Physiology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden. ellen.ostenfeld@med.lu.se.

Funding

Crafoord Foundation, Lund, Sweden 200681Crafoord Foundation, Lund, Sweden 20230611Swedish Heart and Lung Foundation, Stockholm, Sweden 20190576Swedish Heart and Lung Foundation, Stockholm, Sweden 20210337Swedish Heart and Lung Foundation, Stockholm, Sweden 20220449Swedish Heart and Lung Foundation, Stockholm, Sweden 20230550Swedish Research Council, Stockholm, Sweden 2021-02779Swedish Society of Medicine, Stockholm, Sweden SLS-961558
6 · The paper itself

Abstract

The pathophysiology underlying impaired LV function in PAH remains unclear, with some studies implicating intrinsic myocardial dysfunction and others pointing to LV underfilling. Evaluation of pulmonary vein area (PVA) and flow may offer novel, mechanistic insight by distinguishing elevated LV filling pressure common in myocardial dysfunction from LV underfilling. This study aimed to elucidate LV filling physiology in PAH by assessing PVA and flow using cardiac magnetic resonance (CMR) and compare pulmonary vein flow in PAH with HFrEF as a model representing elevated filling pressures, in addition to healthy controls. Patients with PAH or heart failure with reduced ejection fraction (HFrEF) referred for CMR were retrospectively reviewed, and healthy controls were included as reference. Pulmonary vein S, D and A-wave were compared between groups. Associations between pulmonary vein area (PVA) by CMR and echocardiographic indices of LV filling pressure were evaluated. Nineteen patients with PAH, 25 with HFrEF and 24 controls were included. Both PAH and HFrEF had lower ejection fraction and S-wave velocity than controls. PAH displayed smaller LV end-diastolic volumes than controls, while HFrEF demonstrated larger PVA and higher A-wave reversal. PVA was associated with mitral E/e' ratio (r

Indexed as

Pulmonary Arterial HypertensionVentricular Dysfunction, LeftAdultAgedEchocardiographyFemaleHeart FailureHumansMagnetic Resonance ImagingMaleMiddle AgedPulmonary VeinsRetrospective StudiesStroke VolumeVentricular Function, LeftCardiac magnetic resonance imagingHeart failurePulmonary arterial hypertension

Identifiers

PMID39068288
PMCPMC11283488

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.