It is known today that inflammatory processes play a big role in the development of coronary arthery disease (CAD). However, standard medication still just focusses on lowering cholesterol, leaving most patients with low-grade chronic inflammation. This may lead to critical events like recurring heart attacks or strokes in these patients. Attamps to treat inflammation in CAD patients systemically resulted in elevated risk for severe infection, thus there is a need to identify more selective targets for treatment.
In my PhD thesis I focus on investigating the impact of different immune cells, e.g. neutrophils, monocytes and regulatory T cells, on chronic inflammation in CAD patients. There is a need to understand inflammatory processes in patients in greater detail in order to find a way to lower inflammation accompanied by less severe adverse effects.
