In detail, the following questions will be answered:
1. Do distinct metabolic phenotypes (with respect to insulin secretion, insulin sensitivity, circulating free fatty acids and ectopic lipid storage, especially in the liver) determine myocardial infarct size and decline of contractile function of the remote myocardium?
2. Which factors modify the progression of the disease (insulin resistance, ectopic lipid storage, subclinical inflammation, abnormal energy metabolism)? People are thoroughly examined at baseline and one year after STEMI.
3. Can we identify risk profiles and their relevance for development of diabetes-associated complications as well as long-term progression of diabetes?
4. Can we improve risk assessment algorithms for targeted therapy in line with Precision Medicine?
