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Clinical Trial
. 2023 Apr;11(4):454-464.
doi: 10.1016/j.jchf.2022.12.011. Epub 2023 Mar 1.

Effect of Training on Vascular Function and Repair in Heart Failure With Preserved Ejection Fraction

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Free article
Clinical Trial

Effect of Training on Vascular Function and Repair in Heart Failure With Preserved Ejection Fraction

Andreas B Gevaert et al. JACC Heart Fail. 2023 Apr.
Free article

Abstract

Background: Exercise training improves peak oxygen uptake (V.O2peak) in heart failure with preserved ejection fraction (HFpEF). Multiple adaptations have been addressed, but the role of circulating endothelium-repairing cells and vascular function have not been well defined.

Objectives: The authors investigated effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on vascular function and repair in HFpEF.

Methods: This study is a subanalysis of the OptimEx-Clin (Optimizing Exercise Training in Prevention and Treatment of Diastolic Heart Failure) study randomizing patients with HFpEF (n = 180) to HIIT, MICT, or guideline control. At baseline, 3, and 12 months, the authors measured peripheral arterial tonometry (valid baseline measurement in n = 109), flow-mediated dilation (n = 59), augmentation index (n = 94), and flow cytometry (n = 136) for endothelial progenitor cells and angiogenic T cells. Abnormal values were defined as outside 90% of published sex-specific reference values.

Results: At baseline, abnormal values (%) were observed for augmentation index in 66%, peripheral arterial tonometry in 17%, flow-mediated dilation in 25%, endothelial progenitor cells in 42%, and angiogenic T cells in 18%. These parameters did not change significantly after 3 or 12 months of HIIT or MICT. Results remained unchanged when confining analysis to patients with high adherence to training.

Conclusions: In patients with HFpEF, high augmentation index was common, but endothelial function and levels of endothelium-repairing cells were normal in most patients. Aerobic exercise training did not change vascular function or cellular endothelial repair. Improved vascular function did not significantly contribute to the V.O2peak improvement after different training intensities in HFpEF, contrary to previous studies in heart failure with reduced ejection fraction and coronary artery disease. (Optimizing Exercise Training in Prevention and Treatment of Diastolic Heart Failure [OptimEx-Clin]; NCT02078947).

Keywords: HFpEF; cardiac rehabilitation; endothelial function; endothelial progenitor cells; flow-mediated dilation.

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Conflict of interest statement

Funding Support and Author Disclosures This work was supported by the European Commission, Framework Program 7 (EU-FP7; Brussels, Belgium [grant number: EU 602405-2]); the Deutsche Forschungsgemeinschaft (DFG) through the TUM International Graduate School of Science and Engineering (IGSSE; Garching, Germany) (Flavia Baldassarri, Stephan Mueller, Drs Duvinage and Haykowsky); and the Flanders Research Foundation (FWO; Brussels, Belgium) (senior clinical investigator grant to Dr Van Craenenbroeck). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Dr Gevaert has received personal fees from Abbott, AstraZeneca, Boehringer Ingelheim (lectures), and Novartis (lectures, advisory board) outside the submitted work. Dr Duvinage has received grants from Novartis outside the submitted work. Dr Van De Heyning has received personal fees from Abbott, Daiichi-Sankyo, Bayer, and Edwards Lifesciences (lectures) outside the submitted work. Dr Pieske has received personal fees from AstraZeneca (lectures), Bayer (steering committee, lectures), Bristol-Myers Squibb (lectures), Medscape (lectures), Merck (steering committee, lectures), Novartis (steering committee, lectures), and Servier outside the submitted work. Dr Haykowsky has received grants from Novartis and personal fees from Abbott (advisory board), AstraZeneca, Bayer, Berlin Chemie-Menarini, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Novartis, Roche, Sanofi, and Pfizer; and serves as an advisor for Medical Park SE, Germany; outside the submitted work. Dr Van Craenenbroeck has received grants from Vifor Pharma, outside the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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