Robert H. G. Schwinger1, Kathryn Yan2
1Kardiologie, Nephrologie/Hypertonie, Pneumologie, Internistische Intensivmedizin, Medizinische Klinik II, Klinikum Weiden, Weiden, Germany; 2CDT Editorial Office, AME Publishing Company
Correspondence to: Kathryn Yan. CDT Editorial Office, AME Publishing Company. Email: editor@thecdt.org
This interview can be cited as: Schwinger RHG, Yan K. Meeting the Editorial Board Member of CDT: Dr. Robert H. G. Schwinger. Cardiovasc Diagn Ther. 2025. Available from: https://cdt.amegroups.org/post/view/meeting-the-editorial-board-member-of-cdt-dr-robert-h-g-schwinger
Expert introduction
Currently, Dr. Robert H. G. Schwinger (Figure 1) is the head of the Clinic II of Internal Medicine, Cardiology and Intensive Care Treatment, at the Klinikum Weiden, teaching hospital of the University Regensburg, Bavaria, Germany. Following residence at University Munich and University of Cologne, Dr. Schwinger built up the Laboratory of Muscle Research and Molecular Cardiology at the Clinic III of Internal medicine, University of Cologne. He is interested in pathophysiology and treatment of heart failure. As a clinician, he experienced in heart catherization, implantation of biventricular pacing sytems, interventional treatment of mitral / tricuspidal regurgitation by TEER as well as on treatment of atrial fibrillation using single device ablation technics (PFA, Kryoablation). In addition, he focuses on the treatment of acute heart failure and cardiac shock using mechanical assist devices (ECMO, mAFP).
Figure 1 Dr. Robert H. G. Schwinger
Interview
CDT: What inspired you to specialize in cardiology and heart failure research?
Dr. Schwinger: At the medical university I was fascinated by the experiments performed in physiology e.g. using frog hearts. Later on contraction behavior of the human heart, I found my interest.
CDT: Can you share some of the key milestones in your career that have shaped your research focus?
Dr. Schwinger: I focused on cardiac contraction coupling during a grant by the DFG (German Research Foundation). On human cardiac muscle strips (heart transplants , human nonfailing donor hearts – cooperation with Prof. Bruno Reichart and Prof. Erland Erdmann, Munich) frequency-induced force generation as well as tension-induced force (Frank Starling mechanism) was measured. In addition the effect of inotropic compounds on force development as well as on frequency-induced force generation was analysed as well. Thereafter additional studies were conducted in close collaboration with Harvard Medical Center (Roger Hajjar M.D.), with The Heart Institute, The Hospital of the Good Samaritan, Los Angeles (L. Kedes M.D, L. Kloner M.D.), with the Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, Los Angeles (Alicia Mc Donough M.D.), with the Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine (E.G.Kranias M.D.) and others cooperating institutions. When I moved to the University of Cologne I founded the Laboratory of Muscle Research and Molecular Cardiology, Clinic III for Internal Medicine, University of Cologne, Germany. In addition to my interest on basic cardiology research I developed myself in clinical cardiology and was trained in interventional cardiology as well. Thereafter I moved to the teaching hospital of the university of Regensburg, and serves as the head of the department of cardiology. My special focus lies in the treatment of heart failure and in teaching students and physicians in cardiology especially in treatment of heart failure patients.
CDT: What are some of the most significant advancements in cardiology that you have witnessed during your career?
Dr. Schwinger: Frequency-induced force generation and tension-induced force in human failing and nonfailing myocardium and the effect of SERCA found my interest. We found unchanged levels of SERCA protein and concluded that changes in regulation i.e. phospholamban phosphorylation may be relevant. In clinical cardiology I focused on medical treatment of the heart failure with reduced ejection fraction using the “big five for HFrEF” i.e. ACE-I, MRA, BB, SGLT2-I and diuretics. Also interventional treatments became relevant like TEER of mitral valve regurgitation, TAVI to treat aortic stenosis, ablation techniques for atrial fibrillation as well as mechanical circulation supports (ECMO, mAFP/Impella). These interventions help the heart to pump more adequately.
CDT: Your article, "Pathophysiology of heart failure,"(1) has received a high readership. What do you think it is about your article that resonates most with the cardiology community?
Dr. Schwinger: The main attraction is the combination of basic research findings in the context of clinical heart failure symptoms. Thus research gives the opportunity to understand principles of heart failure treatments i.e. contractility, preload, afterload, frequency.
CDT: You demonstrate in the article that heart failure symptoms may be present in patients with reduced and preserved ejection fraction. Could you share more about the clinical implications of this finding?
Dr. Schwinger: HFpEF is characterised by structural and cellular alterations leading to an inability of the left ventricle to relax properly, e.g., cardiomyocyte hypertrophy, intercellular fibrosis, altered cardiomyocyte relaxation and inflammation. HFpEF is often connected with chronic comorbidities, such as arterial hypertension, type 2 diabetes mellitus (T2DM), obesity, renal insufficiency, pulmonary disease, liver disease, sleep apnoea, gout, and cancer. The inflammatory process in HFpEF is often linked to these comorbidities e.g., diabetes which also exert activation of inflammation. To understand that relaxation abnormalities may lead to failure of the heart with similar clinical findings as seen in patients with reduced ejection fraction is a fascinating finding. This demonstrates that a lot of future research is needed to understand contraction and relaxation of the human heart. And this may be the prerequisite to find new treatment options for heart failure, for HFrEF, HFmrEF and HFpEF. Overall I think that in future we will only have heart failure patients with reduced ejection fraction and with normal ejection fraction; so HFmrEF will move in the “reduced” part!
CDT: Your research has contributed to the understanding heart failure pathophysiology. In your opinion, what are the biggest knowledge gaps that remain in this field?
Dr. Schwinger: When you look at the basics for contraction coupling, and the limitations still being present to understand this mechanism. One can imagine how important basic research still is. For the implication of treatments in the clinical setting controlled clinical studies remain the gold standard and most important. Not the changes of surrogate parameters e.g. laboratory parameters as NTproBNP but the outcome i.e. cardiovascular or overall death has to be relevant.
CDT: What advice would you give to young researchers who are interested in cardiovascular disease research?
Dr. Schwinger: The heart is most important. And to treat patients with heart attack or heart failure has improved life expectancy significantly. To understand the mechanisms of treatment e.g. for heart failure or coronary interventions and to use this knowledge in daily practice is fascinating! The understanding of the underlying pathophysiology of heart failure is essential to initiate the adequate therapeutic option individually for each patient.
Reference
- 1. Schwinger RHG. Pathophysiology of heart failure. Cardiovasc Diagn Ther 2021;11(1):263-276. doi: 10.21037/cdt-20-302