Evidence map›Paper›PMID 23426022›Full record

ArticleEuropean journal of heart failure2013

Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction.

Muaz M Abudiab, Margaret M Redfield, Vojtech Melenovsky, Thomas P Olson, David A Kass, Bruce D Johnson, Barry A Borlaug

Registry-linked trialOpen access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of heart failure, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03111017 (Mechanisms and Management of Exercise Intolerance in Older Heart Failure Patients With Preserved Ejection Fraction), which is not on this map. Cited by 151 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 8 pooled it
16.0field-weighted citation impact, top 1% 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.

NCT03111017 nacompletednot on this mapstarted 2017, after this paper: background citation

Mechanisms and Management of Exercise Intolerance in Older Heart Failure Patients With Preserved Ejection Fraction

TypeinterventionalSponsorThe University of Texas at ArlingtonRan2017 to 2019Enrolled12ConditionsHeart Failure, DiastolicArmsExercise Training
3 · Its place in the literature

Who cites it

151 citing papers in PubMed, 8 syntheses or guidelines pooled it, 323 citations in OpenAlex.

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  13. The pathophysiology of wild-type transthyretin amyloidosis: implications for exercise intolerance.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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91 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Muaz M AbudiabDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA.
Margaret M Redfield
Vojtech Melenovsky
Thomas P Olson
David A Kass
Bruce D Johnson
Barry A Borlaug
Mayo Clinic in Arizona · USMayo Clinic · USJohns Hopkins University · USMayo Clinic in Florida · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
NCRR NIH HHS UL RR024150
6 · The paper itself

Abstract

aimsExercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. METHODS AND

resultsPatients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non-invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial-venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial-venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually.

conclusionWhile diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.

Indexed as

AgedCardiac OutputExercise TestExercise ToleranceFemaleFollow-Up StudiesHeart FailureHumansMaleMiddle AgedOxygenOxygen ConsumptionPrognosisRetrospective StudiesStroke VolumeVentricular Function, LeftOxygenCardiac outputDiastolic heart failureExerciseHeart rateOxygen consumptionStroke volume

Identifiers

PMID23426022
PMCPMC3857919
OpenAlexW1966518108

What OpenQuestion holds

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Registered trials

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.