Research Caroline Van De Heyning

Abstract

Acute myocarditis (AM) is an inflammatory disease of the heart that can be caused by infectious agents, autoimmune disorders, and drug hypersensitivity reactions. The diagnosis of AM is based on symptoms, biomarkers and non-invasive imaging. Cardiovascular magnetic resonance imaging (CRM) can accurately diagnose AM by detection of oedema and inflammation in the acute setting, as well as demonstration of residual scar after recovery. In virus-triggered AM, it is assumed that myocardial injury mainly results from autoimmunity. Although there is a rationale for immunosuppressive therapy, no trial has tested this hypothesis in the acute phase. The multicentre MYTHS trial will evaluate the efficacy of pulsed intravenous corticosteroids on top of standard therapy in patients with fulminant AM (left ventricular ejection fraction (LVEF) <41%). The first aim of this project proposal is to evaluate the treatment with corticosteroids in patients with complicated, non-fulminant AM (LVEF 41-50%) regarding outcome (cardiac death and life-threatening arrhythmias) and myocardial scar formation on CMR, as these patients have an increased risk of adverse events, but will not be included in the main MYTHS trial. Second, we want to improve risk stratification in patients with AM by identifying prognostic markers related to myocardial scar on baseline and follow-up CMR, to estimate sudden cardiac death risk and the need for a prophylactic implantable cardioverter-defibrillator.

Researcher(s)

• Promoter: Van De Heyning Caroline

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Mitral valve prolapse (MVP) is a valvular disorder with a prevalence of 2-3% in the general population. MVP can be associated with mitral regurgitation (MR), congestive heart failure, ventricular arrhythmias and sudden cardiac death. Barlow's Disease (BD) and Fibro-Elastic deficiency (FED) present the 2 most common MVP phenotypes. In recent years, several genetic mutations have been identified which might play a role in the pathophysiology of MVP, but the exact genotype-phenotype correlation remains largely unknown. Furthermore, recent evidence points to the existence of a concomitant cardiomyopathy in BD, regardless of MR severity. We hypothesise that BD and FED are determined by different genetic mutations and pathophysiological processes, which result in more severe left ventricular remodelling in BD as compared with FED. A better understanding of the genetic and phenotypic differences between BD and FED is crucial to improve patient's risk stratification, diagnostic and therapeutic management. The aim of this project is to prospectively assess the differences in genotype and phenotype between BD versus FED with a focus on left ventricular remodelling, myocardial fibrosis and arrhythmias and its evolution with or without mitral valve surgery. We will recruit 100 patients with FED and BD at 2 large volume centres (Antwerp University Hospital and Maastricht Medical University Center) for genetic analysis and an in-depth phenotyping with 3D-echocardiography and cardiovascular magnetic resonance scan.

Researcher(s)

• Promoter: Van De Heyning Caroline
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Pype Lobke

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Mitral valve prolapse (MVP) is a valvular disorder with a prevalence of 2-3% in the general population. MVP can be associated with mitral regurgitation (MR), congestive heart failure, ventricular arrhythmias and sudden cardiac death. Barlow's Disease (BD) and Fibro-Elastic deficiency (FED) present the 2 most common MVP phenotypes. Recently, several genetic mutations have been identified, however the exact genotype-phenotype correlation remains largely unknown. Furthermore, recent evidence points to the existence of a concomitant cardiomyopathy in BD, regardless of MR severity. We hypothesise that BD and FED are determined by different genetic mutations and pathophysiological processes, resulting in more severe left ventricular (LV) remodelling, more myocardial fibrosis and a higher arrhythmogenic risk in BD as compared with FED. The aim of this project is to prospectively assess the differences in genotype and phenotype between BD and FED with a focus on LV remodelling, myocardial fibrosis and arrhythmias and its evolution with or without mitral valve surgery. We will recruit 170 patients, 110 with FED and 60 with BD, at 2 large volume centres (Antwerp University Hospital and Maastricht Medical University Center) for genetic analysis and an in-depth phenotyping with 3D-echocardiography, cardiovascular magnetic resonance scan and 24h-Holter. Follow-up exams will be performed after 1-year in all included patients.

Researcher(s)

• Promoter: Van De Heyning Caroline
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Pype Lobke

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project