Dr Larissa Fabritz


Senior Clinical Lecturer in Acute Medicine

Cardiovascular and Respiratory Sciences


Contact details

Centre for Cardiovascular Sciences
School of Clinical and Experimental Medicine
College of Medical and Dental Sciences
University of Birmingham
B15 2TT


Dr Larissa Fabritz studies novel mechanisms of heart disease and performs translational research towards mechanism-based therapies of cardiovascular diseases.   She joined the SWBH NHS trust as a Consultant in Acute Medicine with a special interest in the cardiovascular system.

Dr Larissa  Fabritz continues research on molecular cardiovascular imaging as well as molecular mechanisms of cardiomyopathies amd arrhythmias with her working group and collaborations at the University of Muenster, Germany.


2010 Board Certification in Medicine

1997 Graduation from Medical School 


Froese A, Breher SS, Waldeyer C, Schindler RFR, 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, Mueller TD, Neumann J, Stieber J, Ludwig A, Maier SK, Decher N, Arnold HH, Kirchhof P, Fabritz L*, Brand T*. Popeye domain containing proteins are essential for stress-mediated modulation of cardiac pacemaking in mice. J Clin Invest. 2012; in press.

Kahr PC*, Piccini I*, Fabritz L, Greber B, Schöler H, Scheld HH, Hoffmeier A, Brown NA, Kirchhof P Systematic Analysis of Gene Expression Differences between Left and Right Atria in Different Mouse Strains and in Human Atrial Tissue. PLOS One 2001: published 19 Oct 2011 10.1371/journal.pone.0026389

Kirchhof P*, Marijon E*, Fabritz L*, Li N, Wang W, Schulte K, Hanstein J, Schulte JS, Vogel M, Mougenot N, Laakmann S, Fortmueller L, Eckstein J, Verheule S, Kaese S, Staab C, Grote-Wessels S, Schotten U, Moubarak H, Wehrens XH, Schmitz W, Hatem S, Muller F. Overexpression of cAMP-response element modulator causes abnormal growth and development of the atrial myocardium resulting in a substrate for sustained atrial fibrillation in mice. Int J Cardiol. 2011; in press: (PK ME LF contributed equally)

Lemoine MD, Duverger JE, Naud P, Chartier D, Qi XY, Comtois P, Fabritz L, Kirchhof P, Nattel S. Arrhythmogenic left atrial cellular electrophysiology in a murine genetic long QT syndrome model. Cardiovasc Res 2011; PMID: 21672931

Fabritz L*, Hoogendijk M*, Scicluna BP, Van Amersfoorth SC, Fortmueller L, Wolf S, Laakmann S, Kreienkamp N, Piccini I, Breithardt G, Ruiz P, Witt H, Ebnet K, Wichter T, Levkau B, Franke WW, Pieperhoff S, de Bakker J, Coronel R, Kirchhof P. Preload-Reducing therapy prevents expression of arrhythmogenic right ventricular cardiomyopathy in plakoglobin-deficient mice. J Am Coll Cardiol; 2011;57:740-50.

Kirchhof P*, Kahr PC*, Kaese S, Piccini I, Vokshi I, Scheld HH, Rotering H, Fortmueller L, Laakmann, Verheule S, Schotten U, Fabritz L, Brown NA. PTIX2c is expressed in the adult left atrium, and reducing Pitx2c expression promotes atrial fibrillation inducibility and complex changes in gene expression. Circ Cardiovasc Genet 2011;(CIRCCVG/2010/958058).

Herrmann S, Fabritz L, Layh B, Kirchhof P, Ludwig A. Insights into sick sinus syndrome by an inducible mouse model. Cardiovascular Research 2010; (doi:10.1093/cvr/cvq390).

Blana A, Kaese S, Fortmüller L, Laakmann S, Damke D, van Bragt K, Eckstein J, Piccini I, Kirchhefer U, Nattel S, Breithardt G, Carmeliet P, Carmeliet E, Schotten U, Verheule S, Kirchhof P, Fabritz L. A knock-in gain-of-function sodium channel mutation prolongs atrial action potentials and alters atrial vulnerability. Heart Rhythm 2010; 7:1862-9

Fabritz L, Damke D, Emmerich M, Kaufmann SG, Theis K, Blana A, Fortmüller L, Laakmann S, Hermann S, Aleynichenko E, Steinfurt J, Volkery D, Riemann B, Kirchhefer U, Franz MR, Breithardt G, Carmeliet E, Schäfers M, Maier SKG, Carmeliet P, Kirchhof P. Autonomic modulation and antiarrhythmic therapy in a model of long QT syndrome type 3. Cardiovascular Research 2010; 87:60-72.

Wittköpper K, Fabritz L, Neef S, Ort KR, Grefe C, Unsöld B, Kirchhof P, Maier LS, Hasenfuss G, Dobrev D, Eschenhagen T, El-Armouche A Constitutively active phosphatase inhibitor-1 improves cardiac contractility in young mice but is deleterious after catecholaminergic stress and with aging. J Clin Invest 2010; 120:617-26.

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