Background: Heart failure resulting from acute myocardial infarction (AMI), is a leading cause of morbidity and mortality worldwide. The initial inflammatory response crucially contributes to the remodeling process after AMI. Recent clinical studies indicate that environmental factors like traffic noise or air pollution play an important hitherto underestimated role in the development of cardiovascular disease (CVD). Our study investigated the impact of the acute environmental stressor aircraft noise on cardiac remodeling, inflammation and survival after AMI.

Methods+ Results: 8-12 week old male C57BL/6-J mice were initially subjected to a four days-period of aircraft noise at an average volume of 72dB and a peak volume of 85dB, followed by an operative induction of a myocardial infarction by permanent LAD ligation. Cardiac function and infiltration of immune cells were investigated 7 days later. After 4-days aircraft noise exposure mice showed an increased number of circulating myeloid cells especially monocytes and neutrophils in full blood. Flow cytometric analyzation of the bone marrow simultaneously demonstrated augmented myeloid hematopoiesis. Isolation of circulating PBMC in the blood was performed. Western blot analysis showed an increased expression of NADPH oxidase 2 and phosphorylated NFkB on myeloid cells reflecting a proinflammatory phenotype. After AMI noise-exposed animals had a decreased survival and an impaired left ventricular function investigated by small animal echocardiography. Cardiac tissue demonstrated an increased infiltration of CD11b⁺ myeloid cells especially neutrophils and Ly6C⁺ inflammatory monocytes. In line heart tissue expressed higher levels of proinflammatory cytokines like interleukin 6 or 1 beta and adhesion molecules like Vcam-1 or MCP assed by qualitative Realtime PCR.

Furthermore, we could detect significant difference in vascular function assessed by isometric tension studies on isolated aortic rings in mice with AMI and aircraft noise exposure in comparison to MI only. Systemic and vascular reactive oxygen species (ROS) production assessed by L-012 enhanced chemiluminescence and dihydroethidiumbromid staining were augmented by the additional environmental stressor noise.

Conclusion: Environmental exposure to traffic noise reflect a novel and often neglected risk factor for cardiovascular diseases. Acute exposure to aircraft noise leads to a systemic proinflammatory phenotype driven by myeloid cells. Noise exposure before AMI results in a worsening of survival and cardiac remodeling due to amplified cardiac inflammation.