Research team
The pathophysiological role of physical exercise in the development of (left ventricular) myocardial fibrosis during viral myocarditis.
Abstract
Despite physical exercise being our oldest and most efficacious medicine, animal and human data suggest that excessive exercise may contribute to pathological cardiac remodelling, resulting in increased susceptibility for atrial and ventricular arrhythmias and sudden cardiac death. One hallmark of this pathological remodelling is the development of myocardial fibrosis (MF). In two types of MF in athletes, insertion point MF and right ventricular fibrosis in the context of arrhythmogenic cardiomyopathy, exercise contributes as a causal factor. We hypothesise that exercise also contributes to the development of MF in the left ventricle after (silent) myocarditis, which could explain its higher incidence in athletes. We will verify this hypothesis in a murine coxsackie B virus-induced myocarditis and exercise model. Standard histological, RT-qPCR and immunohistochemical analysis, including the use of tissue clearing, will provide further insights into (patho)physiological remodelling and molecular pathways. In addition, the modulating effect of NSAID and several exercise variables (intensity and timing relative to the onset of myocarditis) on the aforementioned interaction between myocarditis and physical exercise will be evaluated. Simultaneously, a multicentre registry (including serial cardiac magnetic resonance imaging and viral PCR on endomyocardial biopsies) is conducted to gain insight into the aetiology of MF in athletes.Researcher(s)
- Promoter: Heidbuchel Hein
- Co-promoter: Guns Pieter-Jan
- Fellow: Favere Kasper
Research team(s)
Project type(s)
- Research Project
The pathophysiological role of physical exercise in the development of (left ventricular) myocardial fibrosis during viral myocarditis.
Abstract
Despite physical exercise being our oldest and most efficacious medicine, animal and human data suggest that excessive exercise may contribute to pathological cardiac remodelling, resulting in increased susceptibility for atrial and ventricular arrhythmias and sudden cardiac death. One hallmark of this pathological remodelling is the development of myocardial fibrosis (MF). In two types of MF in athletes, insertion point MF and right ventricular fibrosis in the context of arrhythmogenic cardiomyopathy, exercise contributes as a causal factor. We hypothesise that exercise also contributes to the development of MF in the left ventricle after (silent) myocarditis, which could explain its higher incidence in athletes. We will verify this hypothesis in a murine coxsackie B virus-induced myocarditis and exercise model. Standard histological, RT-qPCR and immunohistochemical analysis, including the use of tissue clearing, will provide further insights into (patho)physiological remodelling and molecular pathways. In addition, the modulating effect of NSAID and several exercise variables (intensity and timing relative to the onset of myocarditis) on the aforementioned interaction between myocarditis and physical exercise will be evaluated. Simultaneously, a multicentre registry (including serial cardiac magnetic resonance imaging and viral PCR on endomyocardial biopsies) is conducted to gain insight into the aetiology of MF in athletes.Researcher(s)
- Promoter: Heidbuchel Hein
- Co-promoter: Guns Pieter-Jan
- Fellow: Favere Kasper
Research team(s)
Project type(s)
- Research Project
Is arterial stiffness an overlooked marker in cardio-oncology?
Abstract
Anthracyclines (such as doxorubicin, DOX) are among the most effective chemotherapeutics and are widely used in modern cancer treatment despite the advent of targeted therapies. However, dose-dependent cardiotoxicity limits the clinical use of DOX. It is well documented that DOX may provoke cardiotoxicity leading to left ventricular dysfunction and eventually congestive heart failure. Recent studies have reported that anthracyclines also interfere with arterial stiffness, an overall measure of vascular health. However, it is unclear whether vascular toxicity occurs through the same mechanisms and pathways as the cardiac toxicity. The current research proposal aims to shed light on the mechanisms and clinical relevance of DOX-induced vascular toxicity by pursuing a translational experimental research approach.Researcher(s)
- Promoter: Guns Pieter-Jan
- Fellow: Favere Kasper
Research team(s)
Project type(s)
- Research Project