The Heart Center Leipzig has a strong expertise in clinical research and is committed to the continuous improvement of patient
care and intervention.
The knowledge on pathomechanisms that underpin the development of heart diseases is still limited. We therefore carry out various
projects in the area of basic research and clinical research in order to make a contribution to scientific progress.
Members of the group and associated physicians and scientists
Research interests: biology of cardiomyocytes, heart failure, atrial fibrillation, HDL-dysfunction, biomarkers in acute myocardial infarction with
cardiogenic shock, biomarkers in atrial fibrillation
Focus on Atrial fibrillation
Atrial fibrillation is the most common sustained arrhythmia and is associated with increased mortality and morbidity. AF is a progressive disease
underpinned by pro-fibrotic atrial remodeling. Advanced atrial fibrillation progression associates with worse therapy outcome and recurrence of
atrial fibrillation. The contribution of genetic background and pathomechanisms that underpin atrial fibrillation progression are incompletely
understood and the lack of suitable surrogate markers impedes individual therapeutic stratification and monitoring.
Biomarkers of atrial fibrillation progression
The identification and characterization of atrial fibrillation progression surrogate markers has the potential to significantly improve the suitability
of established clinical risk scores for atrial fibrillation recurrence prediction. We hope that in the future combined use of clinical scores and
biomarkers will be used for therapeutic stratification and monitoring in atrial fibrillation. This project is in close collaboration with PD Dr. med.
MSc Jelena Kornej from the Department of Electrophysiology.
HDL-dysfunction in Atrial Fibrillation
Increased morbidity and mortality in atrial fibrillation (AF) are related to the pro-fibrotic, pro-thrombotic and pro-inflammatory processes that underpin
the disease. High-density lipoproteins (HDL) have anti-inflammatory, anti-oxidative, and anti-thrombotic properties. Functional impairment of HDL may
therefore associate with AF initiation or progression. This research project is done in collaboration with the research group of Prof. Gunther Marsche at
Otto Loewi Research Center, Medical University of Graz, Austria.
Genetic background of atrial fibrillation
This project is part of the Lichtenberg-Professorship of Prof. Dr. Daniela Husser-Bollmann, MD (Department of Electrophysiology).
Hundreds or thousands of common genetic variants may modulate atrial fibrillation progression and while each single variant has an almost unmeasurable
effect, several single variant effects might sum up and finally have an impact on regulators in the atrial fibrillation pathomechanisms. This hypothesis
can be used to identify candidate genes that are associated with AF onset and progression.
From Genetics to Function: Bioinformatical tools give us the opportunity to identify potential new regulators based on the analysis of common genetic
variants in the encoding genes for an association with atrial fibrillation phenotypes. The basic assumption is that disease related-genes may be more
often than non-related genes affected by genetic variants.
Biomarkers in acute myocardial infarction
Coronary artery disease is the single most frequent cause of death accounting for 13% of all deaths. Every sixth man and every seventh woman in Europe will
die from myocardial infarction. Despite ongoing improvement of therapeutically reperfusion approaches mortality remains substantial with approximately 12%
of patients dead within 6 months. These facts justify continuous efforts to improve quality of care, adherence to guidelines and research. The pathomechanisms
that underpin the decay of the myocardium in acute myocardial infarction include ischemia reperfusion injury following characterized by increased oxidative
stress, inflammation and ultimately death of myocardial tissue which may be of particular importance in infarct-related cardiogenic shock.
Focus on Heart Failure with Preserved Ejection Fraction
Heart failure with preserved ejection fraction (HFpEF) accounts for 50% of all heart failure cases. No effective treatment exists and consequently the
long-term prognosis is poor and the mortality high. Unfortunately classical heart failure pharmacotherapy is not or only insufficiently effective in
patients with HFpEF. We use an animal model to elucidate the pathomechanisms that underpin HFpEF and hope to identify novel targets for intervention.
We aim for the ongoing implementation of novel technologies and methods to broaden our scientific spectrum. This enables interesting new insights into
cardiovascular pathomechanisms.
We identified an association of circulating EGF-receptor ligands (HB-EGF and EGF) with atrial fibrillation based on genetic evidence.
Nonlinear optical microscopy (NLOM) is an immediate, non-destructive method to visualize and characterize in detail AF associated remodeling. For this purpose, we
applied coherent anti-Stokes Raman scattering (CARS), endogenous two-photon excited fluorescence (TPEF) and second harmonic generation (SHG) to inspect unstained
human atrial appendage myocardium ex vivo. As such, ambitious development of in vivo application of the NLOM technique may represent a revolutionary approach in
characterizing myocardial tissue characteristics. This study was done in cooperation with Dr. Roberta Galli form the research group Clinical Sensoring and Monitoring
at the TU Dresden.
