Klinik für Kardiologie
Klinik für Kardiologie / Forschung
Research Lab
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

Petra Büttner, PhD
Julia Böttner, PhD
Sarah Werner (MTA)
Angela Kricke (MTA)
Paulien Vinke, MSc
Florian Schlotter, MD
Danilo Obradovic, MD
Jelena Kornej, MD, MSc
Laura Ueberham, MD
Sophia Eisenkolb, MD
Erik Holzwirth (doctoral student)
Salmina Guivala (doctoral student)
Lisa Schulz (doctoral student)

Former group members:

Tina Fischer-Scheapmann (MTA)
Sarah Knauth (MTA)

Head of Lab: Petra Büttner

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.
  1. Arginine derivatives in atrial fibrillation progression phenotypes
  2. Myeloperoxidase in atrial fibrillation: association with progression, origin and influence of renin-angiotensin system antagonists
  3. Circulating proteomic patterns in AF related left atrial remodeling indicate involvement of coagulation and complement cascade
  4. Role of NT-proANP and NT-proBNP in patients with atrial fibrillation: Association with atrial fibrillation progression phenotypes
  5. Myeloperoxidase in Atrial Fibrillation

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.
  1. HDL-function in atrial fibrillation
  2. Atrial fibrillation is associated with alterations in HDL function, metabolism, and particle number
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.
  1. PR Interval Associated Genes, Atrial Remodeling and Rhythm Outcome of Catheter Ablation of Atrial Fibrillation-A Gene-Based Analysis of GWAS Data.
  2. Association of atrial fibrillation susceptibility genes, atrial fibrillation phenotypes and response to catheter ablation: a gene-based analysis of GWAS data.
  3. Genomic Contributors to Rhythm Outcome of Atrial Fibrillation Catheter Ablation - Pathway Enrichment Analysis of GWAS Data.
  4. Genomic contributors to atrial electroanatomical remodeling and atrial fibrillation progression: Pathway enrichment analysis of GWAS data.
  5. Identification of Central Regulators of Calcium Signaling and ECM-Receptor Interaction Genetically Associated With the Progression and Recurrence of Atrial Fibrillation.
Focus on Acute Myocardial Infarction

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.

Selenoprotein P in Myocardial Infarction with 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.

The Heart and The Gut - Examining the microbiome, intestinal permeability and TMAO under HFpEF in the ZSF1 rat animal model

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.

  1. EGF (Epidermal Growth Factor) Receptor Ligands in Atrial Fibrillation.
  2. EGF-Receptor Ligands in Atrial Fibrillation - From Genomic Evidence to the Identification of New Players

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.

Label-free Imaging of Myocardial Remodeling in Atrial Fibrillation Using Nonlinear Optical Microscopy: A Feasibility Study.
Julia Böttner
Methamphetamine Induced Heart Failure

Paulien Vinke-Schröter
Nutritional Intervention in Cardiac Cachexia and Pulmonary Arterial Hypertension

Florian Schlotter
Valvular Heart Disease Biology

Laura Ueberham
Cardiac Progenitor Cells

 18.10.2023 -
Kardiovaskulärer Bildgebungsstammtisch
Fokus chronisches Koronarsyndrom
 28.10.2023 -
31. Leipziger Notfalltag
Klinik für Kardiologie