Publication:
Heart failure with preserved ejection fraction-like phenotype in coronary artery disease and obstructive sleep apnea: insights from the RICCADSA cohort

dc.contributor.coauthorThunström, E.
dc.contributor.coauthorGlantz, H.
dc.contributor.coauthorPihtili, A.
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorPeker, Yüksel
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2026-07-22T13:08:26Z
dc.date.issued2026
dc.description.abstractBackground Heart failure with preserved ejection fraction (HFpEF) is closely linked to aging and cardiometabolic risk factors and frequently coexists with obstructive sleep apnea (OSA). We aimed to investigate the prevalence and clinical correlates of an HFpEF‐like phenotype in a revascularized coronary artery disease (CAD cohort), focusing on OSA and its severity. Methods A total of 435 patients with preserved left ventricular ejection fraction from the RICCADSA cohort were included. OSA was defined as apnea–hypopnea index (AHI) ≥ 15 events/h. HFpEF‐like phenotype was defined by ≥ 2 of the following: elevated filling pressures (E/e′ ≥ 15), left atrial enlargement, increased left ventricular mass index, elevated pulmonary artery systolic pressure (≥ 35 mmHg), and elevated NT‐proBNP (≥ 125 pg/mL). Multivariable logistic regression analyses included age, sex, obesity, hypertension, diabetes, and OSA status. Additional models evaluated AHI and oxygen desaturation index (ODI) as continuous variables and assessed the impact of excluding body mass index (BMI). Results Mean age was 63.6 ± 8.6 years and BMI 28.1 ± 4.1 kg/m 2 ; 69.9% met HFpEF‐like criteria. Age and obesity were independently associated with HFpEF‐like phenotype, whereas categorical OSA was not. AHI and ODI were not independently associated after adjustment; however, in models excluding BMI, both AHI (OR 1.019, 95% CI 1.005–1.033) and ODI (OR 1.030, 95% CI 1.010–1.050) were significant predictors. Conclusions HFpEF‐like phenotype is highly prevalent in CAD and primarily associated with aging and adiposity. The relationship between OSA severity and cardiac remodeling appears dependent on obesity, underscoring the interplay between cardiometabolic and sleep‐related factors. Pre‐registered Clinical Trial Number The RICCADSA trial is registered at ClinicalTrials.gov (NCT00519597) and in the Swedish national research registry (FoU i Sverige—Research and Development in Sweden; registration no. VGSKAS‐4731; April 29, 2005).
dc.description.harvestedfromManual
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.publisherscopeInternational
dc.description.readpublishN/A
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipThe authors would like to gratefully acknowledge the independent clinical event committee, Lennart Welin (MD, PhD, Associate Professor of Medicine), the data monitoring board, Marina Modin (RN, MSc), and research secretary Eija Magnusson for her professional assistance in data entry and coordinating quality control of patient records and data follow-up. During the preparation of this work, the authors used ChatGPT 5.2 in order to improve language and readability. After using this tool/service, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication. The RICCADSA trial was supported by grants from the Swedish Research Council (521-2011-537 and 521-2013-3439); the Swedish Heart-Lung Foundation (20080592, 20090708 and 20100664); the "Agreement concerning research and education of doctors" of Vastra Gotalandsregionen (ALFGBG-11538 and ALFGBG-150801), Research fund at Skaraborg Hospital (VGSKAS-4731, VGSKAS-5908, VGSKAS-9134, VGSKAS-14781, VGSKAS-40271 and VGSKAS-116431); Skaraborg Research and Development Council (VGFOUSKB-46371); the Heart Foundation of Karnsjukhuset; ResMed Foundation; and ResMed Ltd. ResMed Sweden provided some of the sleep recording devices and technical support.
dc.description.versionPublished Version
dc.identifier.ScopusPercentile72
dc.identifier.ScopusQuartileQ2
dc.identifier.WoSPercentile57.6
dc.identifier.WoSQuartileQ2
dc.identifier.doi10.1002/clc.70402
dc.identifier.eissn1932-8737
dc.identifier.embargoN/A
dc.identifier.grantno521‐2011‐537
dc.identifier.grantno521‐2013‐3439
dc.identifier.issn0160-9289
dc.identifier.issue7
dc.identifier.pubmed42370761
dc.identifier.scopus2-s2.0-105043050988
dc.identifier.urihttp://doi.org/10.1002/clc.70402
dc.identifier.urihttps://hdl.handle.net/20.500.14288/33772
dc.identifier.volume49
dc.identifier.wos001806494600001
dc.keywordsAging
dc.keywordsCoronary artery disease
dc.keywordsHFpEF
dc.keywordsObesity
dc.keywordsObstructive sleep apnea
dc.languageeng
dc.publisherWiley
dc.relation.affiliationKoç University
dc.relation.collectionKoç University Institutional Repository
dc.relation.ispartofClinical Cardiology
dc.subjectHealth sciences
dc.subjectMedicine
dc.subjectPhysiology
dc.subjectCardiology and cardiovascular medicine
dc.titleHeart failure with preserved ejection fraction-like phenotype in coronary artery disease and obstructive sleep apnea: insights from the RICCADSA cohort
dc.typeJournal Article
dspace.entity.typePublication
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