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Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction
by Jan Pec
1,* [ORCID] , Stefan Buchner
2, Henrik Fox
3 [ORCID] , Olaf Oldenburg
4, Stefan Stadler
1, Lars S. Maier
1, Michael Arzt
1 and Stefan Wagner
1 [ORCID]
1
Department of Internal Medicine II, University Hospital Regensburg, ...
Zusammenfassung
first_page
settings
Order Article Reprints
Open AccessArticle
Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction
by Jan Pec
1,* [ORCID] , Stefan Buchner
2, Henrik Fox
3 [ORCID] , Olaf Oldenburg
4, Stefan Stadler
1, Lars S. Maier
1, Michael Arzt
1 and Stefan Wagner
1 [ORCID]
1
Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany
2
Department of Internal Medicine, Cham Hospital, 93413 Cham, Germany
3
Clinic for General and Interventional Cardiology/Angiology, Heart and Diabetes Center NRW, Ruhr University Bochum, 32545 Bad Oeynhausen, Germany
4
Center for Cardiology, Ludgerus-Kliniken, 48153 Münster, Germany
*
Author to whom correspondence should be addressed.
Biomedicines 2024, 12(1), 154; https://doi.org/10.3390/biomedicines12010154 [Titel anhand dieser DOI in Citavi-Projekt übernehmen]
Submission received: 30 November 2023 / Revised: 13 December 2023 / Accepted: 8 January 2024 / Published: 11 January 2024
(This article belongs to the Special Issue Sleep-Disordered Breathing and Cardiovascular Diseases)
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Abstract
Background: After acute myocardial infarction (AMI), inflammatory processes promote tissue remodeling at the infarct site. Procollagen III amino-terminal propeptide (PIIINP) is a circulating biomarker of type III collagen synthesis that has been shown to be associated with changes in left ventricular ejection fraction (LVEF) and predicts the occurrence of heart failure after AMI. We hypothesize that sleep-disordered breathing (SDB) promotes inflammation and myocardial fibrosis, leading to reduced myocardial salvage. Therefore, in patients with first-time AMI successfully treated with percutaneous coronary intervention (PCI), we aimed to investigate whether circulating levels of high-sensitivity C-reactive protein (hs-CRP) and PIIINP are elevated in patients with SDB compared to patients without SDB. Methods and Results: This cross-sectional analysis included a total of 88 eligible patients with first AMI and PCI pooled from two prospective studies and stratified according to the apnea–hypopnea index (AHI, with SDB: AHI ≥ 15 h−1). We analyzed circulating levels of hs-CRP and PIIINP 3–5 days after PCI. Patients with SDB had significantly higher levels of hs-CRP (18.3 mg/L [95% CI, 8.0–42.6] vs. 5.8 mg/L [95% CI, 4.2–19.8], p = 0.002) and PIIINP (0.49 U/mL [95% CI, 0.40–0.60] vs. 0.33 U/mL [95% CI, 0.28–0.43], p < 0.001). In a multivariable linear regression model accounting for important clinical confounders, SDB significantly predicted circulating levels of hs-CRP (p = 0.028). Similarly, only SDB was independently associated with PIIINP (p < 0.001). Only obstructive but not central AHI correlated with circulating levels of hs-CRP (p = 0.012) and PIIINP (p = 0.006) levels. Conclusions: The presence of obstructive SDB after AMI was independently associated with increased circulating levels of hs-CRP and PIIINP. Our results emphasize the important role of SDB as a common comorbidity and indicate increased inflammation and myocardial fibrosis in these patients.
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