Caroline Van De Heyning assistant professor

Research Caroline Van De Heyning

Research team

Expertise

Valvular heart disease Mitral regurgitation Cardiac imaging Exercise hemodynamics Cardiac fibrosis

Cardiopulmonary exercise testing with echocardiography for early diagnosis and deep phenotyping of heart failure with preserved ejection fraction 01/11/2024 - 31/10/2026

Abstract

Heart failure with preserved ejection fraction (HFpEF) is the most common form of heart failure, with limited therapeutic options and a poor prognosis. Challenges in HFpEF diagnosis, undifferentiated treatment of HFpEF patients despite phenotypical differences, and ignoring non-cardiac contribution to this multisystem disorder underly the unfavorable prognosis. Although exercise intolerance is the primary symptom among HFpEF patients, and current guidelines recommend exercise training, the responsible mechanisms remain unclear. Combined echocardiography and cardiopulmonary exercise testing (CPETecho) is a non-invasive method that can characterize physiological limits to exercise, including in HFpEF patients. In this study, we aim to (1) evaluate whether routine use of CPETecho can improve the accuracy of HFpEF diagnosis, (2) identify subgroups of HFpEF patients with different exercise limitations (exercise phenotypes), and (3) characterize in detail a "muscle phenotype" of HFpEF, limited mostly by peripheral muscle oxygenation instead of cardiac limits. We will recruit HFpEF patients from third-line hospitals and perform CPETecho, apply machine learning algorithms to define HFpEF phenotypes, and combine near-infrared-spectroscopy and muscle biopsies to assess peripheral oxygen extraction. Our study aims to address the clinical need for improved efficiency in HFpEF diagnosis and to identify HFpEF exercise phenotypes, contributing to the precision of HFpEF treatment.

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Project type(s)

  • Research Project

Cardiopulmonary exercise testing with echocardiography (CPETecho) in diagnosis, phenotyping, and treatment of heart failure with preserved ejection fraction. 01/10/2024 - 30/09/2028

Abstract

Heart failure with preserved ejection fraction (HFpEF) is currently the most prevalent type of heart failure, with poor prognosis and few therapeutic options. Possible explanations for the poor prognosis include often late diagnosis of HFpEF when intervention is not feasible anymore, that HFpEF includes phenotypically different patients while all HFpEF patients are treated equally, and the underuse of exercise training as a part of treatment. Exercise intolerance is a universal symptom among HFpEF patients, and this can be objectively measured by peak oxygen uptake (peakVO2). Guidelines currently recommend exercise training to improve peakVO2, but the underlying pathophysiological mechanisms remain unclear. Combined echocardiography and cardiopulmonary exercise testing (CPETecho) can therefore serve as a non-invasive tool to fully characterize all the different physiologic abnormalities limiting exercise capacity. In this project, we will (1) test whether CPETecho can improve diagnosis of HFpEF, (2)prospectively identify HFpEF exercise phenotypes using comprehensive CPETecho measurements, and (3) assess the influence of exercise training on these HFpEF exercise phenotypes. To achieve this, highly detailed CPETecho analysis will be prospectively performed in HFpEF patients from 7 different referral hospitals including Antwerp University Hospital (UZA). Also, retrospectively we will analyze the OptimEx and Priority databases to determine the influence of exercise training. The outcomes of this research will contribute to the clinical need to improve efficiency in HFpEF diagnosis and thereby quality of life and will facilitate personalized treatment. The latter will result from defining HFpEF exercise phenotypes-subgroups more amenable to therapy, but also by unraveling the benefits of exercise training in these HFpEF phenotypes.

Researcher(s)

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  • Research Project

Improvement of risk stratification and treatment in acute myocarditis. 01/01/2022 - 31/12/2025

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.

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  • Research Project

Mechanistic insights in mitral valve prolapse and associated left ventricular remodelling: Barlow's Disease versus Fibroelastic Deficiency. 01/10/2021 - 30/09/2025

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.

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  • Research Project

Mitral valve prolapse and associated cardiomyopathy: impact of mitral valve prolapse subtype and genetics. 01/11/2020 - 31/10/2021

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)

Research team(s)

Project type(s)

  • Research Project