Dr. Constanze Schmidt

Senior physician and scientific group leader
Department of Cardiology

Im Neuenheimer Feld 410, 69120 Heidelberg

+49-6221-56-36779

constanze.schmidt@med.uni-heidelberg.de

  • Cardiac ion channels, atrial cardiomyopathy, atrial fibrillation, arrhythmias, action potentials, ion channel remodeling, large animal models for cardiac diseases

  • 2022 Else Kröner Fresenius Foundation Clinician Scientist professorship, for “Atrial Arrhythmopathy”, University Heidelberg

    2021 Call to University Professor W3 position for experimental cardiology, University Münster

    2021 DZHK PI of the German Center of Cardiovascular Research (DZHK) partner site Heidelberg/Mannheim

    2020 PI of the SFB 1425 (P16)

    2018 Scientists of Tomorrow of the European Society of Cardiology, ESC

    2017 Wilhelm und Liselotte Becht Research Award, German Heart Foundation

    2016 Oskar-Lapp Research Award, German Society of Cardiology

    2016 German Center of Cardiovascular Research Postdoc Excellence Grant

    2014 Olympia Morata Advanced Research Program of Heidelberg University

    2001 Winner of the national scientific youth competition Jugend forscht, 1st prize with Award of the German President for an outstanding work

  • 1) Wiedmann F, Beyersdorf C, Zhou XB, Kraft M, Paasche A, Jávorszky N, Rinné S, Sutanto H, Büscher A, Foerster KI, Blank A, El-Battrawy I, Li X, Lang S, Tochtermann U, Kremer J, Arif R, Karck M, Decher N, van Loon G, Akin I, Borggrefe M, Kallenberger S, Heijman J, Haefeli WE, Katus HA, Schmidt C. Treatment of atrial fibrillation with doxapram: TASK-1 potassium channel inhibition as a novel pharmacological strategy. Cardiovasc Res 24:cvab177, 2021

    2) Wiedmann F, Beyersdorf C, Zhou XB, Büscher A, Kraft M, Nietfeld J, Walz T, Unger L, Loewe A, Schmack B, Ruhparwar A, Karck M, Thomas D, Borggrefe M, Seemann G, Katus H, Schmidt C. The pharmacological TASK-1 potassium channel inhibitor A293 facilitates acute cardioversion of paroxysmal atrial fibrillation in a porcine large animal model. JAHA 9:e015751, 2020

    3) Wiedmann F, Schulte JS, Gomes B, Zafeiriou M-P, Ratte A, Rathjens F, Fehrmann E, Scholz B, Voigt N, Müller FU, Thomas D, Katus HA, Schmidt C. Atrial fibrillation and heart failure-associated remodeling of two-pore-domain potassium (K2P) channels in murine disease models: focus on TASK 1. Basic Res Cardiol 113:27, 2018

    4) Schmidt C, Wiedmann F, Zhou XB, Heijman J, Voigt N, Ratte A, Lang S, Kallenberger SM, Campana C, Wey-mann A, De Simone R, Szabo G, Ruhparwar A, Kallenbach K, Karck M, Ehrlich JR, Baczkó I, Borggrefe M, Ravens U, Dobrev D, Katus HA, Thomas D. Inverse remodelling of K2P3.1 K+ channel expression and action potential duration in left ventricular dysfunction and atrial fibrillation: implications for patient-specific antiarrhythmic drug therapy. Eur Heart Journal 38:1764-1774, 2017

    5) Schmidt C, Wiedmann F, Voigt N, Zhou XB, Heijman J, Lang S, Albert V, Kallenberger S, Ruhparwar A, Szabó G, Kallenbach K, Karck M, Borggrefe M, Biliczki P, Ehrlich JR, Baczkó I, Lugenbiel P, Schweizer PA, Donner BC, Katus HA, Dobrev D*, Thomas D*. Upregulation of K2P3.1 K+ Current Causes Action Potential Shortening in Patients with Chronic Atrial Fibrillation. Circulation 132:82-92, 2015 model of atrial fibrillation and heart failure. Heart Rhythm 11:1798-805, 2014