Evidence map›Paper›PMID 25550438›Full record

ArticleCirculation. Heart failure2015

Central cardiac limit to aerobic capacity in patients with exertional pulmonary venous hypertension: implications for heart failure with preserved ejection fraction.

Mário Santos, Alexander R Opotowsky, Amil M Shah, Julie Tracy, Aaron B Waxman, David M Systrom

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

Article in Circulation. Heart failure, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 3 pooled it
8.0field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 3 syntheses or guidelines pooled it, 61 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Mário SantosFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
Alexander R OpotowskyFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
Amil M ShahFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
Julie TracyFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
Aaron B WaxmanFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
David M SystromFrom the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.). dsystrom@partners.org.
Universidade do Porto · PT

Funding

Systolic & diastolic dysfunction in heart failure and preserved ejection fractionK08HL116792 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SHAH, AMIL M · 2013 to 2017
$735k
NHLBI NIH HHS 1K08HL116792-01A1NHLBI NIH HHS K08 HL116792
6 · The paper itself

Abstract

backgroundThe mechanism of functional limitation in heart failure with preserved ejection fraction remains controversial. We examined the contributions of central cardiac and peripheral mechanisms and hypothesized that the pulmonary vascular response to exercise is an important determinant of aerobic capacity among patients with exertional pulmonary venous hypertension (ePVH). METHODS AND

resultsWe compared 31 ePVH patients (peak VO2<80% of predicted and peak pulmonary arterial wedge pressure≥20 mm Hg) with 31 age- and sex-matched controls (peak VO2>80% predicted) who underwent invasive cardiopulmonary exercise testing for unexplained exertional intolerance. ePVH patients had lower peak cardiac output (73±14% versus 103±18% predicted; P<0.001) compared with controls, related both to impaired chronotropic response (peak heart rate 111±25 beats per minute versus 136±24 beats per minute; P<0.001) and to reduced peak stroke volume index (47±10 mL/min per m(2) versus 54±15 mL/min per m(2); P=0.03). Peak systemic O2 extraction was not different between groups (arterial-mixed venous oxygen content difference: 13.0±2.1 mL/dL versus 13.4±2.4 mL/dL; P=0.46). ePVH patients had higher resting (150±74 versus 106±50 dyne/s per cm(-5); P=0.009), peak (124±74 dyne/s per cm(-5) versus 70±41 dyne/s per cm(-5); P<0.001), and isoflow pulmonary vascular resistance (124±74 dyne/s per cm(-5) versus 91±33 dyne/s per cm(-5) at cardiac output≈10.6 L/min; P=0.04). Pulmonary vascular resistance decreased with exercise in all control subjects but increased in 36% (n=11) of ePVH patients. Abnormal pulmonary vascular response was not associated with peak VO2.

conclusionsReduced cardiac output response, rather than impaired peripheral O2 extraction, constrains oxygen delivery and aerobic capacity in ePVH. Pulmonary vascular dysfunction is common in patients with ePVH at rest and during exercise.

Indexed as

Vascular ResistanceAdrenergic beta-AntagonistsAgedCardiac OutputExerciseExercise ToleranceFemaleHeart FailureHemodynamicsHumansHypertension, PulmonaryMaleMiddle AgedPhysical ExertionPulmonary CirculationPulmonary Gas ExchangeAdrenergic beta-Antagonistsexerciseheart failurehemodynamicspulmonary vascular resistance

Identifiers

PMID25550438
PMCPMC4936392
OpenAlexW2136090099

What OpenQuestion holds

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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.