Heart failure, sudden death, and atrial fibrillation are often manifestations of cardiomyopathies. We study the effects of genetic factors for the development of heart failure and the arrhythmia syndromes sudden death and atrial fibrillation.
These syndromes can be expression of common disease mechanisms in the heart. We use molecular biology, imaging and physiological techniques to identify such mechanisms, and test interventions to prevent heart failure and arrhythmias in experimental models and in clinical trials.
Our research group
We have only begun our work here in Birmingham at the end of 2011, and we still cooperate closely with University of Münster. The group uses physiological measurements, molecular biology, and imaging techniques to characterise heart function in transgenic models. These allow us to identify molecular mechanisms of cardiomyopathies and help to delineate new therapeutic targets for the treatment of heart failure and arrhythmias.
Together with colleagues in Birmingham and beyond, we explore possibilities to translate these insights into hypotheses that can be tested in clinical trials, with the final goal to improve treatment of patients suffering from heart failure, atrial fibrillation, an/or at risk for sudden death. We are members of international research networks.
Molecular mechanisms of atrial fibrillation due to genetic defects
Sodium channel dysfunction and their contribution to heart failure and arrhythmias
The left atrium as a driver for thrombosis
Understanding the relevance of desmosomal proteins for right heart function and failure
Testing the value of early rhythm control therapy in atrial fibrillation
Froese A, Breher SS, Waldeyer C, Schindler RF, Nikolaev VO, Rinne S, Wischmeyer E, Schlueter J, Becher J, Simrick S, Vauti F, Kuhtz J, Meister P, Kreissl S, Torlopp A, Liebig SK, Laakmann S, Muller TD, Neumann J, Stieber J, Ludwig A, Maier SK, Decher N, Arnold HH, Kirchhof P, Fabritz L and Brand T (2012) Popeye domain containing proteins are essential for stress-mediated modulation of cardiac pacemaking in mice. J Clin Invest 122:1119-30
Kirchhof P, Andresen D, Bosch R, Borggrefe M, Meinertz T, Parade U, Ravens U, Samol A, Steinbeck G, Treszl A, Wegscheider K and Breithardt G (2012) Short-term versus long-term antiarrhythmic drug treatment after cardioversion of atrial fibrillation (Flec-SL): a prospective, randomised, open-label, blinded endpoint assessment trial. Lancet 380:238-46
Fabritz L, Hoogendijk MG, Scicluna BP, van Amersfoorth SC, Fortmueller L, Wolf S, Laakmann S, Kreienkamp N, Piccini I, Breithardt G, Noppinger PR, Witt H, Ebnet K, Wichter T, Levkau B, Franke WW, Pieperhoff S, de Bakker JM, Coronel R and Kirchhof P (2011) Load-reducing therapy prevents development of arrhythmogenic right ventricular cardiomyopathy in plakoglobin-deficient mice. J Am Coll Cardiol 57:740-50
Kirchhof P, Kahr PC, Kaese S, Piccini I, Vokshi I, Scheld HH, Rotering H, Fortmueller L, Laakmann S, Verheule S, Schotten U, Fabritz L and Brown NA (2011) PITX2c is expressed in the adult left atrium, and reducing Pitx2c expression promotes atrial fibrillation inducibility and complex changes in gene expression. Circ Cardiovasc Genet 4:123-33
For full publication lists see:
Professor Paulus Kirchhof - School of Clinical and Experimental Medicine
Dr Larissa Fabritz - School of Clinical and Experimental Medicine
Dr Genna Riley - School of Clinical and Experimental Medicine
Dr Fahima Syeda - School of Clinical and Experimental Medicine
Stavros Apostolakis (part time) - School of Clinical and Experimental Medicine
Ting Yu Yue