Aircraft noise exposure induces pro-inflammatory vascular conditioning and amplifies vascular dysfunction and impairment of cardiac function after myocardial infarction

Author:

Molitor Michael123ORCID,Bayo-Jimenez Maria T1,Hahad Omar13,Witzler Claudius2,Finger Stefanie2,Garlapati Venkata S123,Rajlic Sanela4,Knopp Tanja2,Bieler Tabea K2,Aluia Melania123,Wild Johannes123,Lagrange Jeremy256,Blessing Recha1,Rapp Steffen7,Schulz Andreas7,Kleinert Hartmut8,Karbach Susanne123,Steven Sebastian123,Ruf Wolfram23ORCID,Wild Philipp1237,Daiber Andreas123,Münzel Thomas123ORCID,Wenzel Philip123

Affiliation:

1. Department of Cardiology – Cardiology I, University Medical Center Mainz , Langenbeckstraße 1, 55131 Mainz , Germany

2. Center for Thrombosis and Haemostasis, University Medical Center Mainz , Langenbeckstraße 1, 55131 Mainz , Germany

3. German Center for Cardiovascular Research (DZHK), partner site Rhine-Main

4. Department of Cardiothoracic and Vascular Surgery, University Medical Center Mainz , Langenbeckstraße 1, 55131 Mainz , Germany

5. Université de Lorraine, Inserm, DCAC , Nancy , France

6. CHRU Nancy, Vandœuvre-lès-Nancy , France

7. Department of Cardiology, Preventive Medicine, University Medical Center Mainz , Langenbeckstraße 1, 55131 Mainz , Germany

8. Department of Pharmacology, Johannes Gutenberg University Medical Center , Langenbeckstraße 1, 55131 Mainz , Germany

Abstract

Abstract Aims Traffic noise may play an important role in the development and deterioration of ischaemic heart disease. Thus, we sought to determine the mechanisms of cardiovascular dysfunction and inflammation induced by aircraft noise in a mouse model of myocardial infarction (MI) and in humans with incident MI. Methods and results C57BL/6J mice were exposed to noise alone (average sound pressure level 72 dB; peak level 85 dB) for up to 4 days, resulting in pro-inflammatory aortic gene expression in the myeloid cell adhesion/diapedesis pathways. The noise alone promoted adhesion and infiltration of inflammatory myeloid cells in vascular/cardiac tissue, paralleled by an increased percentage of leucocytes with a pro-inflammatory, reactive oxygen species (ROS)-producing phenotype and augmented expression of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase type 2 (Nox2)/phosphorylation of nuclear factor ‘kappa light chain enhancer’ of activated B-cells (phospho-NFκB) in peripheral blood. Ligation of the left anterior descending artery resulted in worsening of cardiac function, pronounced cardiac infiltration of CD11b+ myeloid cells and Ly6Chigh monocytes, and induction of interleukin (IL) 6, IL-1β, CCL-2, and Nox2, being aggravated by noise exposure prior to MI. MI induced stronger endothelial dysfunction and more pronounced increases in vascular ROS in animals preconditioned with noise. Participants of the population-based Gutenberg Health Cohort Study (median follow-up:11.4 years) with incident MI revealed elevated C-reactive protein at baseline and worse left ventricular ejection fraction (LVEF) after MI in case of a history of noise exposure and subsequent annoyance development. Conclusion Aircraft noise exposure before MI substantially amplifies subsequent cardiovascular inflammation and aggravates ischaemic heart failure, facilitated by a pro-inflammatory vascular conditioning. Our translational results suggest that measures to reduce environmental noise exposure will be helpful in improving the clinical outcome of subjects with MI. Key question Key finding Take-home-MessageAircraft noise exposure before MI substantially amplifies cardiovascular inflammation and aggravates cardiac impairment after MI.

Funder

Boehringer Ingelheim Foundation

German Federal Ministry for Education and Research

DFG Major Research Instrumentation Programme

Else-Kröner-Fresenius Foundation

Humboldt Foundation

German Research Foundation

University Medical Center Mainz

Principle Investigators

Publisher

Oxford University Press (OUP)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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