Evidence map›Paper›PMID 42604439›Full record

Observational studyHeart (British Cardiac Society)2026

Haemodynamic response to exercise in patients with hypertrophic cardiomyopathy without left ventricular outflow tract obstruction.

Helga Lillian Gudmundsdottir, Anna Axelsson Raja, Kasper Rossing, Hanne Rasmusen, Martin Snoer, Lars Juul Andersen, Rikke Gottlieb, Alex Hørby Christensen, Henning Bundgaard, Emil Wolsk and 3 more

Abstract readObservational Study
In one paragraph

Observational study in Heart (British Cardiac Society), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Helga Lillian GudmundsdottirCardiology, Bispebjerg Hospital, Copenhagen, Denmark helga.lillian.gudmundsdottir@regionh.dk.ORCID 0000-0002-1715-1329
Anna Axelsson RajaRigshospitalet, Kobenhavn, Denmark.
Kasper RossingDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark.
Hanne RasmusenCardiac, Bispebjerg Hospital, Kobenhavn, Denmark.
Martin SnoerCardiology, Sjællands Universitetshospital Roskilde, Roskilde, Denmark.
Lars Juul AndersenCardiology, Sjællands Universitetshospital Roskilde, Roskilde, Denmark.
Rikke GottliebRigshospitalet, Kobenhavn, Denmark.
Alex Hørby ChristensenRigshospitalet, Kobenhavn, Denmark.
Henning BundgaardDepartment of Cardiology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark.
Emil WolskHerlev Hospital, Herlev, Denmark.
Christian HassagerCardiology, The University Hospital of Copenhagen, Copenhagen, Denmark.
Finn GustafssonDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark.
Jens Jakob ThuneDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDyspnoea and reduced exercise capacity are common features in hypertrophic cardiomyopathy (HCM) without left ventricular outflow tract (LVOT) obstruction, yet the haemodynamic mechanisms contributing to these symptoms are poorly described. This study aimed to characterise the haemodynamic response to exercise in patients with HCM without LVOT obstruction.

methodsIn this observational study, 121 subjects underwent right heart catheterisation with haemodynamic measurements during rest and supine incremental exercise: 59 patients with HCM without LVOT obstruction (58±12 years) and 62 healthy controls (49±17 years). Left ventricular (LV) filling pressure was assessed as pulmonary capillary wedge pressure (PCWP) and compared with diagnostic thresholds (rest: <15 mm Hg; exercise: <25 mm Hg). Group comparisons were performed using Student's t-tests or Wilcoxon rank-sum tests, as appropriate

resultsAt rest, patients had higher PCWP than controls (14±6 vs 9±2 mm Hg, p<0.001), while other haemodynamic parameters were similar. Already at mild exercise (25 W), patients showed elevated PCWP (27±7 vs 16±7 mm Hg, p<0.001), mean arterial pressure (100±18 vs 93±13 mm Hg, p=0.02), central venous pressure (12±6 vs 9±4 mm Hg, p<0.001) and mean pulmonary artery pressure (38±11 vs 26±8 mm Hg, p<0.001). At peak exercise, patients exhibited higher PCWP (32±8 vs 18±8 mm Hg, p<0.001), with lower cardiac index (6.4±1.8 vs 8.9±1.4 L/min/m², p<0.001), heart rate (114±21 vs 132±19 bpm, p<0.001) and arteriovenous oxygen difference (58±13 vs 64±6%, p=0.004). Peak exercise capacity (119±50 vs 149±40 W, p<0.001) and peak oxygen consumption (21±7 vs 35±8 mL/kg/min, p<0.001) were lower in patients. Abnormal PCWP was found in 68% of patients at mild exercise and 85% at peak, compared with 6% of controls at mild exercise and 24% at peak. PCWP at mild exercise was inversely correlated with peak oxygen consumption in patients (r=-0.61; 95% CI -0.7 to -0.4; p<0.001).

conclusionPatients with HCM without LVOT obstruction exhibited significant haemodynamic impairments during exercise. Abnormally elevated LV filling pressures were present even at low workloads and were correlated with reduced exercise capacity.

Indexed as

Cardiomyopathy, HypertrophicExerciseExercise ToleranceHemodynamicsVentricular Function, LeftAdultAgedCardiac CatheterizationCase-Control StudiesExercise TestFemaleHumansMaleMiddle AgedPulmonary Wedge PressureVentricular Outflow ObstructionCardiomyopathy, Hypertrophic

Identifiers

PMID42604439
PMCPMC13638292

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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.