Evidence map›Paper›PMID 41702982›Full record

ArticleScientific reports2026

Non-invasive stroke volume assessment during cardiopulmonary exercise testing provides additional insight beyond O

Massimo Mapelli, Nikita Baracchini, Nicola Campana, Teresa Maria Capovilla, Alessandro Nava, Elisabetta Salvioni, Carlo Vignati, Filippo Maria Rubbo, Damiano Magrì, Beatrice Pezzuto and 12 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. RoMa Classification: When the Parts Do Not Equal the Sum.Journal of the American Heart Association · 2026
    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

22 authors.

Massimo MapelliCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138. massimo.mapelli@cardiologicomonzino.it.
Nikita BaracchiniCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Nicola CampanaCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Teresa Maria CapovillaCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Alessandro NavaAzienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Trieste, Italy.
Elisabetta SalvioniCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Carlo VignatiCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Filippo Maria RubboCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Damiano MagrìDepartment of Clinical and Molecular Medicine, Azienda Ospedaliera Sant'Andrea, 'Sapienza' Università Degli Studi Di Roma, Rome, Italy.
Beatrice PezzutoCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Irene MattavelliCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Nicolò CapraCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Simona CostantinoCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Fiorella PuttiniCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Cosimo CarriereCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Irena TavčarCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Maddalena RossiCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Christian Cadeddu DessalviDepartment of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Robin WillixhoferCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.
Marco MerloCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Gianfranco SinagraCenter for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste, Via P. Valdoni 7, Trieste, 34100, Italy.
Piergiuseppe AgostoniCentro Cardiologico Monzino, IRCCS, Milan, Italy, via Parea 4, 20138.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In hypertrophic cardiomyopathy (HCM), cardiopulmonary exercise testing (CPET) is considered the gold standard for assessing exercise tolerance, with O2-pulse commonly used as a surrogate for stroke volume (SV). However, because SV reduction can be masked by increased oxygen extraction, direct non-invasive measurement of SV is valuable. This study involved 102 HCM patients (mean age 53 ± 16 years, 78% male), predominantly with a non-obstructive phenotype (74%), who underwent CPET with SV measurement using Physioflow (PF). Abnormal O2-pulse kinetics were observed in 12 patients, all confirmed by abnormal SV trends with PF. Additionally, PF identified another 28 patients with altered SV kinetics. Abnormal SV trends were associated with higher peak VE/VO2 ratios (42.6 [37.4–47.5] vs. 38.0 [33.6–41.3]) and lower end-tidal CO2 values (31.8 ± 4.9 vs. 34.3 ± 5.6 mmHg, p < 0.05). Patients with greater SV growth during the final 25% of exercise showed improved anaerobic threshold VO2 (49.8 ± 12.3% vs. 43.9 ± 15.2% predicted peak VO2), VO2/work slope (10.2 ± 2.0 vs. 9.3 ± 1.3 mL/min/Watt), and peak PetCO2 (34.5 ± 5.6 vs. 32.3 ± 5.2 mmHg), alongside a lower VE/VCO2 slope (28.7 [24.9–31.0] vs. 31.3 [27.3–34.2], p < 0.05). Integrating PF and CPET may enhance the detection of abnormal SV kinetics, which are associated with reduced functional capacity in HCM patients.

Indexed as

Cardiomyopathy, HypertrophicExercise TestOxygenStroke VolumeAdultAgedExercise ToleranceFemaleHumansMaleMiddle AgedOxygen ConsumptionOxygenCardiopulmonary exercise testingHypertrophic cardiomyopathyPhysioflowStroke volume evaluation

Identifiers

PMID41702982
PMCPMC13004987

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Registered trials

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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.