A key research focus at the DZHK partner site Munich is the identification of gene and environmental factors that are associated with cardiovascular disease. Here the aim is to identify molecular markers that predispose for the disease and its associated symptoms and, in conjunction with lifestyle factors, influence the development and course of the disease. More on:

Research Projects:

Early Clinical Trials with Focus Arrhythmia

Duration: 2011 to 2018; Budget: € 638.105,71

PI: Stefan Kääb

Clinical Platelet Therapy Research

Duration: 2013 to 2018; Budget: € 1.567.485,72                                  

PI: Steffen Massberg

Platelets are central mediators of arterial thrombosis and the main target of treatment as well as prophylaxis of coronary heart disease. However, despite improvements in antiplatelet therapy thrombotic disorders a still a leading cause of mortality worldwide. Therefore, the central aim of this project is to pave the way for innovative therapeutic approaches targeting the prothrombotic functions of platelets. This is based on an improved understanding of the interactions of platelets with the coagulation as well as the immune system using state-of-the-art basic science approaches and reaching to clinical evaluation. The results of this project will provide valuable insight into the mechanisms of thrombotic disorders and will break new ground for the treatment of coronary heart disease.

Gender Medicine

Duration: 2012 to 2018; Budget: € 581.646,43 

PI: Julinda Mehili

gender-related analyses from different registries and ongoing randomized trials focused on clinical outcomes after trans-catheter aortic valve repair, after heart transplantation as well as after implantation of bioresorbable vascular scaffolds

Preclinical Research:

Generation and functional characterization of macrophage cell lines from yolk sac precursors                                   

Duration: 2017 to 2018; Budget: € 256.655 

PI: Christian Schulz

Summary and objectives: The project aims at establishing macrophage cell lines from yolk sac progenitors of mice and humans. Existing macrophage cell lines mostly derive from peripheral blood mononuclear cells or leukemic cells. However, many macrophages in adult organs, including cardiovascular tissues, originate from embryonic precursors located in the yolk sac. Thus, available cell lines do not adequately represent macrophages located in tissues and are insufficient to study tissue macrophage functions under culture conditions. The project therefore aims to generate cell lines of bona fide yolk sac-derived macrophage progenitors, which can be expanded and differentiated into tissue macrophages as needed. This will allow scientists to conduct high throughput screening in disease-relevant cell culture models. Further, using mouse cardiovascular injury models we will characterize and compare the potential of murine macrophages of different developmental origins to contribute to tissue remodelling and healing. These experiments could lay the basis for future regenerative therapies using bona fide macrophages expanded in culture.

PostDoc Start-up Grant: Myocardial HMGB1 as mediator of increased atherosclerosis and thrombosis in the post-myocardial infarction period                                  

Duration: 2016 to 2018; Budget: € 60.000 

PI: Konstantin Stark

Patients suffering from myocardial infarction (MI) have an increased risk of cardiovascular events after the acute event despite optimal medical treatment and dual antiplatelet therapy. These can be related to the affected vascular bed such as reinfarction due to thrombosis of a coronary artery, but can also occur in unrelated vascular areas resulting in stroke, venous thrombosis, and pulmonary embolism. Although it has been demonstrated that MI leads to accelerated atherosclerosis due to mobilization of hematopoietic stem and progenitor cells from bone marrow niches, it is unclear if factors released from the damaged myocardium might contribute the increased risk of cardiovascular events.
High-mobility group box 1 protein (HMGB1) is danger-associated molecular pattern which is mainly associated with DNA during resting conditions, but becomes a major mediator of sterile inflammation once released into the extracellular space during necrosis or tissue injury. High amounts of the HMGB1 are released from the myocardium after STEMI/NSTEMI and HMGB1 has been associated with an increased risk of cardiovascular events in clinical studies. Therefore, we will investigate the contribution of myocardial HMGB1 to accelerated atherosclerosis and increased risk of arterial as well as venous thrombosis after MI.

Clinical Studies:

APPROACH-ACS-AF-DZHK7: Apixaban versus Phenprocoumon: Orale Antikoagulation plus antithrombozytäre Therapie bei Patienten mit akuten Koronarsyndrom und Vorhofflimmern Identifier: NCT02789917

Duration: 2016 to 2018; Budget: € 530.965,56

PI: Reza Wakili

SMART-MI-DZHK9: Implantierte Monitorinstrumente zur Überwachung von Hochrisikopatienten nach Herzinfarkt und reduzierter linksventrikulärer Auswurffraktion Identifier: NCT02594488

Duration: 2016 to 2018; Budget: € 1.420.958,52

PI: Axel Bauer