Inflammation and Fibrosis in Sleep-Disordered Breathing after Acute Myocardial Infarction

Author:

Pec Jan1ORCID,Buchner Stefan2,Fox Henrik3ORCID,Oldenburg Olaf4,Stadler Stefan1,Maier Lars S.1,Arzt Michael1,Wagner Stefan1ORCID

Affiliation:

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

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.

Funder

ResMed Foundation

Resmed Germany

Faculty of Medicine of the University of Regensburg

Philips Home Healthcare Solutions

Publisher

MDPI AG

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