Encouraging grant 2023 'Rosa Blanckaert' for young researchers: (Bio)Medical Sciences. 01/12/2023 - 31/12/2025

Abstract

Adults with a congenital heart disease (ACHD) have a lower functional capacity, reduced quality of life and worse prognosis compared to healthy individuals. ACHD and patients with heart failure (HF) induced by other etiologies share many characteristics, incl. exercise intolerance, right ventricular (RV) dysfunction and increased inflammatory cytokine levels. Among the pathophysiological changes in HF, endothelial dysfunction is highlighted. However, the presence of endothelial dysfunction in ACHD is unknown as literature is limited and conflicting. We hypothesize that coronary microvascular dysfunction (CMD) is important in the pathophysiology of ACHD. We believe that multiple factors incl. genetics, underlying cardiac abnormality, history of cardiac surgery and RV overload, further aggravated by classical acquired risk factors (including overweight, hypertension and sedentary lifestyle), alter shear stress and promote systemic inflammation and endothelial oxidative stress in ACHD leading to a reduced nitric oxide bioavailability and endothelial dysfunction. As such we assume CMD is associated with systemic endothelial dysfunction, reflecting CMD as part of a systemic microvascular disorder. We are convinced that detecting CMD is important to allow identification of ACHD with an unfavorable prognosis and that this CMD can easily be identified with adenosine-based Doppler echocardiography. Finally, the potential therapeutic effect of exercise training will be investigated.

Researcher(s)

Research team(s)

Project type(s)

  • Research Project

Microvascular dysfunction in adults with a congenital heart disease and the effect of exercise training (MICONEX). 01/11/2021 - 31/10/2025

Abstract

Adults with a congenital heart disease (ACHD) have a lower functional capacity, reduced quality of life and worse prognosis compared to healthy individuals. ACHD and patients with heart failure (HF) induced by other aetiologies share many characteristics, incl. exercise intolerance, right ventricular (RV) dysfunction and increased inflammatory cytokine levels. Among the pathophysiological changes in HF, endothelial dysfunction is highlighted. However, the presence of endothelial dysfunction in ACHD is unknown as literature is limited and conflicting. I hypothesize that coronary microvascular dysfunction (CMD) is important in the pathophysiology of ACHD. I believe that multiple factors incl. genetics, underlying cardiac abnormality, history of cardiac surgery and RV overload, further aggravated by classical acquired risk factors (including overweight, hypertension and sedentary lifestyle), alter shear stress and promote systemic inflammation and endothelial oxidative stress in ACHD leading to a reduced nitric oxide bioavailability and endothelial dysfunction. As such I assume that CMD is associated with systemic endothelial dysfunction, reflecting CMD as part of a systemic microvascular disorder. I am convinced that detecting CMD is important to allow identification of ACHD with an unfavorable prognosis and that this CMD can easily be identified with adenosine-based Doppler echocardiography. Finally, the potential therapeutic effect of exercise training will be investigated.

Researcher(s)

Research team(s)

Project type(s)

  • Research Project

Right ventricular (dys)function in congenital heart disease: role of microvascular dysfunction and effect of exercise training. 01/11/2020 - 31/10/2021

Abstract

Exercise capacity is markedly depressed in adults with congenital heart disease (ACDH) and associated with an increased risk of hospitalization or death. Right ventricular (RV) function is of major importance in ACHD prognosis. Our group recently demonstrated reduced subclinical RV function in ACHD patients with RV overload. Moreover, in a TOF population, strain measurements could predict functional capacity. In other study populations (HFpEF and PAH patients) coronary microvascular dysfunction (CMD) has been shown to be highly prevalent and associated with worse RV strain and exercise intolerance. To the best of our knowledge, the presence of CMD has not been investigated before in ACHD. We hypothesize that multiple factors including genetics, underlying cardiac abnormality, history of cardiac surgery and RV overload, further aggravated by classical acquired risk factors that are known to induce an inflammatory state and reduce nitric oxide bioavailability promote systemic inflammation leading to endothelial dysfunction. As such we hypothesize that the presence of endothelial dysfunction can act as a prognostic and potential therapeutic marker in ACHD. In this research project, we aim to design a prospective study of CMD in ACHD. Potential correlates of reduced CFR including RV loading conditions, clinical and biochemical markers, systemic endothelial function and echocardiographic data will be investigated as well as the potential therapeutic effect of exercise training.

Researcher(s)

Research team(s)

Project type(s)

  • Research Project