Non-invasive assessment of functional, cellular and molecular mechanisms linking inflammation and cardiac remodeling after acute myocardial injury.
Ischemic heart disease is a leading cause of death. The metabolic, functional, cellular and structural changes after acute myocardial injury, also termed cardiac remodeling, determine residual cardiac function, development of heart failure, and survival. Acute/chronic inflammation and reperfusion not only contribute to infarct healing but paradoxically also cause aggravation of the injury. Type, extent and timing of post injury events will determine whether they result in beneficial cardiac remodeling and healing, or an opposite effect of adverse ventricular remodeling. We will use preclinical models of acute myocardial ischemic injury with stimulated/ inhibited inflammation, using transgenic models (CLEC4E), pharmacological intervention (TDB) and pro-inflammatory condition (obesity/ diabetes) to understand the effect of immune cells on functional, cellular and metabolic mechanisms of cardiac remodeling. To understand the link between cardiac function, inflammation, metabolism and outcome, we will further develop new in vivo imaging methods to acquire cardiac/respiration gated and simultaneously acquired multi-modal and multi-parametric imaging data. This permits longitudinal monitoring of cardiac function, metabolism, inflammation and outcome in individuals immediately after ischemic injury/ intervention until end points using translational techniques. We will make use of our state-of-the-art imaging infrastructure including advance techniques that are used in the clinic.