Acute Effects of Myeloperoxidase Inhibition on Exercise Hemodynamics in Heart Failure With Preserved Ejection Fraction: A Randomized Clinical Trial

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F25%3A00085833" target="_blank" >RIV/00023001:_____/25:00085833 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/abs/pii/S0025619625001594?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/abs/pii/S0025619625001594?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.mayocp.2025.02.022" target="_blank" >10.1016/j.mayocp.2025.02.022</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Acute Effects of Myeloperoxidase Inhibition on Exercise Hemodynamics in Heart Failure With Preserved Ejection Fraction: A Randomized Clinical Trial

Popis výsledku v původním jazyce

Objective: Myeloperoxidase (MPO) is a heme peroxidase that scavenges nitric oxide and contributes to microvascular dysfunction. Patients with heart failure and preserved ejection fraction (HFpEF) have microvascular dysfunction that leads to increased pulmonary capillary wedge pressure (PCWP). We sought to investigate whether acute MPO inhibition can reduce exertional PCWP in patients with Patients and Methods: Between July 1, 2018, and February 24, 2022, participants with HFpEF were recruited. They underwent baseline invasive hemodynamic exercise evaluation and were then randomized, double-blind, to a single dose of the MPO inhibitor mitiperstat at 30 mg or matching placebo, after which they underwent repeated invasive hemodynamic exercise testing. The primary end point was PCWP during 20-W exercise workload. Results: Patients with HFpEF (N1/430; mean +/- SD age, 70 +/- 9 years; 11 female [37%]; body mass index, 34.0 kg/m2) displayed typical hemodynamic responses to exercise prior to treatment, with PCWP increasing from 17 +/- 5 to 32 +/- 6 mm Hg with exercise and mean pulmonary artery pressure increasing from 28 +/- 9 to 49 +/- 11 mm Hg. Contrary to our hypothesis, as compared with placebo, mitiperstat treatment resulted in a higher PCWP during the second bout of exercise (-1 +/- 3 vs -4 +/- 5 mm Hg; P1/4.04). There was a trend for less reduction in mean pulmonary artery pressure and lower pulmonary artery compliance during exercise with mitiperstat as compared with placebo. There was no effect of mitiperstat on arterial, coronary sinus, or transcardiac uptake/release of O2, CO2, and lactate compared with placebo. Conclusion: Acute MPO inhibition with mitiperstat did not reduce exertional hemodynamic congestion in patients with HFpEF. (c) 2025 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights are reserved, including those for text and data

Název v anglickém jazyce

Acute Effects of Myeloperoxidase Inhibition on Exercise Hemodynamics in Heart Failure With Preserved Ejection Fraction: A Randomized Clinical Trial

Popis výsledku anglicky

Objective: Myeloperoxidase (MPO) is a heme peroxidase that scavenges nitric oxide and contributes to microvascular dysfunction. Patients with heart failure and preserved ejection fraction (HFpEF) have microvascular dysfunction that leads to increased pulmonary capillary wedge pressure (PCWP). We sought to investigate whether acute MPO inhibition can reduce exertional PCWP in patients with Patients and Methods: Between July 1, 2018, and February 24, 2022, participants with HFpEF were recruited. They underwent baseline invasive hemodynamic exercise evaluation and were then randomized, double-blind, to a single dose of the MPO inhibitor mitiperstat at 30 mg or matching placebo, after which they underwent repeated invasive hemodynamic exercise testing. The primary end point was PCWP during 20-W exercise workload. Results: Patients with HFpEF (N1/430; mean +/- SD age, 70 +/- 9 years; 11 female [37%]; body mass index, 34.0 kg/m2) displayed typical hemodynamic responses to exercise prior to treatment, with PCWP increasing from 17 +/- 5 to 32 +/- 6 mm Hg with exercise and mean pulmonary artery pressure increasing from 28 +/- 9 to 49 +/- 11 mm Hg. Contrary to our hypothesis, as compared with placebo, mitiperstat treatment resulted in a higher PCWP during the second bout of exercise (-1 +/- 3 vs -4 +/- 5 mm Hg; P1/4.04). There was a trend for less reduction in mean pulmonary artery pressure and lower pulmonary artery compliance during exercise with mitiperstat as compared with placebo. There was no effect of mitiperstat on arterial, coronary sinus, or transcardiac uptake/release of O2, CO2, and lactate compared with placebo. Conclusion: Acute MPO inhibition with mitiperstat did not reduce exertional hemodynamic congestion in patients with HFpEF. (c) 2025 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights are reserved, including those for text and data

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30201 - Cardiac and Cardiovascular systems

Projekt

—

Návaznosti

N - Vyzkumna aktivita podporovana z neverejnych zdroju

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Mayo Clinic proceedings

ISSN

0025-6196

e-ISSN

1942-5546

Svazek periodika

100

Číslo periodika v rámci svazku

9

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

1495-1505

Kód UT WoS článku

001568826100005

EID výsledku v databázi Scopus

2-s2.0-105012746434