Evidence map›Paper›PMID 38956982›Full record

ArticleEuropean journal of heart failure2024

Haemodynamic contributors to pulmonary hypertension across the spectrum of adult congenital heart disease.

Yogesh N V Reddy, William R Miranda, Christopher C Jain, Barry A Borlaug, Alexander C Egbe

Abstract read
In one paragraph

Article in European journal of heart failure, 2024. 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

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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

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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. Observational
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4 · The record

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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

5 authors.

Yogesh N V ReddyDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
William R MirandaDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Christopher C JainDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Barry A BorlaugDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Alexander C EgbeDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.

Funding

Mechanisms of Clinical and Hemodynamic Response to Pulmonary Vasodilator Therapy in Fontan physiologyR01HL160761 · NHLBI · MAYO CLINIC ROCHESTER · PI Alexander Egbe · 2022 to 2026
$3.1M
Pathophysiologic Mechanism for Arrhythmias and Impaired Aerobic Capacity in Tetralogy of FallotR01HL158517 · NHLBI · MAYO CLINIC ROCHESTER · PI EGBE, ALEXANDER · 2021 to 2025
$2.9M
Clinical benefits and mechanism of action of angiotensin-II receptor blocker on Cardiovascular remodeling in patients with repaired coarctation of aortaR01HL162830 · NHLBI · MAYO CLINIC ROCHESTER · PI Alexander Egbe · 2023 to 2026
$2.7M
Peripheral Limitations in Pulmonary Hypertension and Effects of Muscle TrainingK23HL164901 · NHLBI · MAYO CLINIC ROCHESTER · PI Yogesh Nellore Vilambi Reddy · 2023 to 2026
$671k
NHLBI Division of Intramural Research K23HL164901NHLBI NIH HHS K23 HL164901NHLBI NIH HHS R01 HL158517NHLBI NIH HHS R01 HL160761NHLBI NIH HHS R01 HL162830
6 · The paper itself

Abstract

aimsAdult congenital heart disease (ACHD) includes multiple disease states that predispose to pulmonary hypertension (PH). Haemodynamically, PH depends on abnormalities in three components: pulmonary blood flow (Qp), pulmonary vascular resistance (PVR) and pulmonary venous pressure (PVP). We sought to evaluate the prevalence and prognostic impact of individual haemodynamic abnormalities in ACHD. METHODS AND

resultsRetrospective study of ACHD patients undergoing cardiac catheterization at Mayo Clinic between 1999 and 2022 who were followed for the combined endpoint of death/heart transplantation. Among 1005 patients, 37% had mean pulmonary artery pressure (mPAP) ≥25 mmHg with more systemic ventricular disease, cyanotic disease and shunt lesions, highest N-terminal pro-B-type natriuretic peptide and worse right heart remodelling/dysfunction. Among those with biventricular circulation, elevated PVP, PVR and mPAP were associated with prognosis, but not increased Qp >8 L/min. However, risk of death/transplant increased for PVR only at ≥3 Wood units (hazard ratio [HR] 3.00, 95% confidence interval [CI] 2.17-4.15; p < 0.0001) and for mPAP only at ≥25 mmHg (HR 3.15, 95% CI 2.17-4.58; p < 0.0001), not at current recommended lower cutpoints. Combined abnormalities in PVP and PVR were associated with worst outcome (HR 5.20, 95% CI 3.55-7.63; p < 0.0001) with intermediate risk with either abnormality (HR 2.11, 95% CI 1.46-3.04; p < 0.0001). Findings were consistent across type of biventricular ACHD. Only with the Fontan (univentricular) circulation was a lower mPAP threshold (20 mmHg) associated with adverse outcomes.

conclusionsElevation of mPAP ≥25 mmHg in ACHD with a biventricular circulation is prognostically important regardless of disease phenotype, but milder PH of 21-25 mmHg is not associated with adverse outcome unless associated with Fontan circulation. Elevation in PVP >15 mmHg and PVR ≥3 Wood units were each individually associated with mortality with combined abnormalities associated with greatest risk. Categorizing PH in ACHD by haemodynamic mechanism (PVR, PVP or Qp) allows meaningful prognostication, and may allow more unified study of targeted therapies across heterogeneous disease states in ACHD.

Indexed as

Cardiac CatheterizationHeart Defects, CongenitalHemodynamicsHypertension, PulmonaryVascular ResistanceAdultFemaleHeart TransplantationHumansMaleMiddle AgedPrognosisPulmonary CirculationRetrospective StudiesCongenital heart diseaseHaemodynamicsPulmonary hypertensionRight heart catheterization

Identifiers

PMID38956982
PMCPMC11795213

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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.