Evidence map›Paper›PMID 31187875›Full record

ArticleThe Journal of physiology2019

The natural matching of harmonic responses in the pulmonary circulation.

Candelas Pérez Del Villar, Pablo Martínez-Legazpi, Teresa Mombiela, Christian Chazo, Mar Desco, Daniel Rodríguez-Pérez, Yolanda Benito, Alicia Barrio, Enrique Gutiérrez-Ibañes, Juan C Del Álamo and 5 more

Abstract read
In one paragraph

Article in The Journal of physiology, 2019. 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
–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

2 citing papers in PubMed.

  1. Article
  2. The Biological Bases of Group 2 Pulmonary Hypertension.International journal of molecular sciences · 2019
    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

15 authors.

Candelas Pérez Del VillarDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Pablo Martínez-LegazpiDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.ORCID 0000-0003-0511-7120
Teresa MombielaDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Christian ChazoDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.ORCID 0000-0002-5109-6378
Mar DescoDepartment of Mathematical Physics and Fluids, Facultad de Ciencias, Universidad Nacional de Educación a Distancia, Madrid, Spain.
Daniel Rodríguez-PérezDepartment of Mathematical Physics and Fluids, Facultad de Ciencias, Universidad Nacional de Educación a Distancia, Madrid, Spain.
Yolanda BenitoDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Alicia BarrioDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Enrique Gutiérrez-IbañesDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Juan C Del ÁlamoMechanical and Aerospace Engineering Department, University of California San Diego, and the Institute for Engineering in Medicine, University of California San Diego, La Jolla, CA, USA.
Jaime ElízagaDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
José Carlos AntoranzDepartment of Mathematical Physics and Fluids, Facultad de Ciencias, Universidad Nacional de Educación a Distancia, Madrid, Spain.
Francisco Fernández-AvilésDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.ORCID 0000-0001-5501-5275
Raquel YottiDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Javier BermejoDepartment of Cardiology, Hospital General Universitario Gregorio Marañón; Facultad de Medicina, Universidad Complutense de Madrid; Instituto de Investigación Sanitaria Gregorio Marañón; and CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.ORCID 0000-0002-5241-2758

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsThe right ventricle of the mammal heart is highly sensitive to the afterload imposed by a combination of the pulmonary circulation and the retrograde contribution of the left heart. Right ventricular afterload can be analysed in terms of pulmonary artery input impedance, which we were able to decompose as the result of the harmonic frequency responses of the pulmonary vessels and the left heart attached in series. Using spectral methods, we found a natural matching between the pulmonary vasculature and the left chambers of the heart. This coupling implies that the upstream transmission of the left heart frequency-response has favourable effects on the pulmonary tree. This physiological mechanism protects the right ventricle against acute changes in preload, and its impairment may be a relevant contribution to right ventricle dysfunction in pulmonary hypertension. ABSTRACT: The right ventricle (RV) of the mammal heart is highly sensitive to the afterload imposed by the pulmonary circulation, and the left heart (LH) retrogradely contributes significantly to this vascular load. Transmission-line theory anticipates that the degree of matching between the frequency responses of the pulmonary vasculature and the LH should modulate the global right haemodynamic burden. We measured simultaneous high-fidelity flow (pulmonary artery) and pressure (pulmonary artery and left atrium) in 18 healthy minipigs under acute haemodynamic interventions. From these data, we decomposed the impedance spectra of the total right-circulation system into the impedance of the pulmonary vessels and the harmonic response of the LH. For frequencies above the first harmonic, total impedance was below the pulmonary impedance during all phases (P < 0.001; pooled phases), demonstrating a favourable effect of the LH harmonic response on RV pulsatile load: the LH harmonic response was responsible for a 20% reduction of pulse pulmonary artery pressure (P < 0.001 vs. a theoretical purely-resistive response) and a 15% increase of pulmonary compliance (P = 0.009). This effect on compliance was highest during acute volume overload. In the normal right circulation, the longitudinal impedance of the pulmonary vasculature is matched to the harmonic response of the LH in a way that efficiently reduces the pulmonary pulsatile vascular load. This source of interaction between the right and left circulations of mammals protects the RV against excessive afterload during acute volume transients and its disruption may be an important contributor to pulmonary hypertension.

Indexed as

HemodynamicsModels, CardiovascularPulmonary CirculationAnimalsAtrial FunctionFemaleMalePulmonary ArterySwineSwine, MiniatureVentricular Functionhemodynamicsimpedancepulmonary circulationvascular function

Identifiers

PMID31187875
PMCPMC9328395

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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.