Evidence map›Paper›PMID 34339454›Full record

ArticlePloS one2021

The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation.

Stamatia Pagoulatou, Dionysios Adamopoulos, Georgios Rovas, Vasiliki Bikia, Nikolaos Stergiopulos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. A spectral machine learning approach to derive central aortic pressure waveforms from a brachial cuff.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Arterial pulse wave modeling and analysis for vascular-age studies: a review from VascAgeNet.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

5 authors at 2 institutions in 1 country.

Stamatia PagoulatouLaboratory of Hemodynamics and Cardiovascular Technology (LHTC), Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.ORCID 0000-0003-0347-3754
Dionysios AdamopoulosCardiology Department, Geneva University Hospitals (HUG), Geneva, Switzerland.
Georgios RovasLaboratory of Hemodynamics and Cardiovascular Technology (LHTC), Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.ORCID 0000-0002-4020-6826
Vasiliki BikiaLaboratory of Hemodynamics and Cardiovascular Technology (LHTC), Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.ORCID 0000-0002-4660-1560
Nikolaos StergiopulosLaboratory of Hemodynamics and Cardiovascular Technology (LHTC), Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
École Polytechnique Fédérale de Lausanne · CHUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ventricular-arterial coupling is a major determinant of cardiovascular performance, however, there are still inherent difficulties in distinguishing ventricular from vascular effects on arterial pulse phenotypes. In the present study, we employed an extensive mathematical model of the cardiovascular system to investigate how sole changes in cardiac contractility might affect hemodynamics. We simulated two physiologically relevant cases of high and low contractility by altering the end-systolic elastance, Ees, (3 versus 1 mmHg/mL) under constant cardiac output and afterload, and subsequently performed pulse wave analysis and wave separation. The aortic forward pressure wave component was steeper for high Ees, which led to the change of the total pressure waveform from the characteristic Type A phenotype to Type C, and the decrease in augmentation index, AIx (-2.4% versus +18.1%). Additionally, the increase in Ees caused the pulse pressure amplification from the aorta to the radial artery to rise drastically (1.86 versus 1.39). Our results show that an increase in cardiac contractility alone, with no concomitant change in arterial properties, alters the shape of the forward pressure wave, which, consequently, changes central and peripheral pulse phenotypes. Indices based on the pressure waveform, like AIx, cannot be assumed to reflect only arterial properties.

Indexed as

HemodynamicsModels, CardiovascularModels, TheoreticalMyocardial ContractionAortaArteriesBlood PressureHumansPulse Wave AnalysisVentricular Function, Left

Identifiers

PMID34339454
PMCPMC8328319
OpenAlexW3187965654

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.