Atherosclerosis; Cardiopulmonary Resuscitation; Dyslipidemias; Inflammation; Lipoprotein(a); Monocytes; Myocardial Reperfusion Injury; Systemic Inflammatory Response Syndrome
- Group Walter Speidl
Head: Walter Speidl
- Research group Johann Wojta
Head: Johann Wojta
My main research focus is the role of inflammatory mediators in both chronic and acute diseases, such as stable atherosclerotic disease but also critical illness and myocardial infarction with subsequent reperfusion injury. Within the immune system, our focus lies on the innate immune system with the monocyte-macrophage axis as our primary target.
Currently, the role of innate immune mechanisms in acute critical illness with a focus on the cardiovascular critically ill patients with cardiogenic shock or after surviving a cardiac arrest is one major research focus. This includes the search for a biomarker for intestinal complications in critically ill patients, an often devastating clinical situation with no existing biomarkers. A novel topic we are currently working on are the immunogenic properties of mitochondrial particles and especially mitochondrial DNA in critical cardiovascular care.
Within our clinical work at the newly founded cardiovascular lipid outpatients clinic we focus on the identification of patients with severe lipid disorders and atherosclerotic cardiovascular disease including patients with familial hypercholesterolemia and strongly elevated Lipoprotein(a). Here, the role of the innate immune system in disease initiation and progression is being studied.
Techniques, methods & infrastructure
Routinely used techniques in our laboratory are cell culture of cells primarily of cardiovascular origin including endothelial cells from various origin, human cardiomyocytes and smooth muscle cells (HUVEC, HAEC, HHMEC, HCAEC, HACM, HSMC,...). A broad array of techniques is being used (ELISA, PCR, western blotting, flow cytometry, adhesion and chemotactic assays, reporter gene assays, basic histology,...) Furthermore, for the study of immune mediators in chronic atherosclerosis, a mouse model of atherosclerosis is set-up. We have a longstanding experience in flow cytometry due to our ongoing work on monocyte and macrophage subsets. Due to our excellent location within the Anna-Spiegel-Forschungsgebäude, we have easy access to the wide spectrum offered by the core facilities (http://corefacilities.meduniwien.ac.at/?L=1).
- Immuno-Activation in Familial Hypercholesterolemia (2018)
Source of Funding: Österreichischer Herzfonds, Österreichischer Herzfonds
- Association of circulating microRNAs and coronary plaque composition assessed by coronary CT angiography (2017)
Source of Funding: Austrian Society of Cardiology, Research Scholarship
- Proteomic Profiling to Reveal Novel Diagnostic Markers for Intestinal Complications in Critical Ill Patients (2016)
Source of Funding: Medical Scientific Fund of the Mayor of the City of Vienna,
- Krychtiuk, K.A. et al., 2015. Mitochondrial DNA and Toll-Like Receptor-9 Are Associated With Mortality in Critically Ill Patients. Critical Care Medicine, p.1. Available at: http://dx.doi.org/10.1097/CCM.0000000000001311.
- Krychtiuk, K.A. et al., 2014. Levosimendan exerts anti-inflammatory effects on cardiac myocytes and endothelial cells in vitro. Thrombosis and Haemostasis, 113(2), pp.350-362. Available at: http://dx.doi.org/10.1160/TH14-06-0549.
- Krychtiuk, K.A. et al., 2014. Small high-density lipoprotein is associated with monocyte subsets in stable coronary artery disease. Atherosclerosis, 237(2), pp.589-596. Available at: http://dx.doi.org/10.1016/j.atherosclerosis.2014.10.015.
- Krychtiuk, K.A. et al., 2015. Monocyte subset distribution in patients with stable atherosclerosis and elevated levels of lipoprotein(a). Journal of Clinical Lipidology, 9(4), pp.533-541. Available at: http://dx.doi.org/10.1016/j.jacl.2015.04.005.
- Krychtiuk, K.A. et al., 2016. Monocyte subset distribution is associated with mortality in critically ill patients. Thrombosis and Haemostasis, 116(5), pp.949-957. Available at: http://dx.doi.org/10.1160/TH16-05-0405.