We hypothesize that mechanisms of LV remodelling in BD include a larger prolapse volume and underlying genetic substrate, beyond volume overload related to MR, resulting in more severe LV remodelling and dysfunction compared to FED.
ID
Bron
Verkorte titel
Aandoening
Heart valve disease: mitral valve prolapse
Ondersteuning
Onderzoeksproduct en/of interventie
Uitkomstmaten
Primaire uitkomstmaten
1) Difference in LV volume, prolapse volume and MR volume in patients with BD versus FED, measured by echocardiography and CMR.
Achtergrond van het onderzoek
Mitral valve prolapse (MVP) is a frequent valvular disorder with a prevalence of 2-3% in the general population, which can be associated with mitral regurgitation (MR), heart failure, ventricular arrhythmias and sudden cardiac death. Barlow's Disease (BD) and fibroelastic deficiency (FED) present the 2 most common MVP subtypes. Interestingly, recent evidence points to the existence of a concomitant cardiomyopathy in BD, regardless of MR severity. This hypothesis is supported by the recent association of MVP with mutations in cardiomyopathy genes, suggesting a genetic predisposition for concomitant myocardial disease. Furthermore, disproportionate left ventricular (LV) remodelling in BD might also be explained by the total volume load, i.e. the sum of the transvalvular MR volume and the prolapse volume.
We hypothesize that mechanisms of LV remodelling in BD include a larger prolapse volume and underlying genetic substrate, beyond volume overload related to MR, resulting in more severe LV remodelling and dysfunction compared to FED.
The main aim of this project is to unravel the underlying mechanisms of LV remodelling in the different MVP subtypes. Furthermore, we will assess the arrhythmogenic potential of BD versus FED, and its relationship with the severity of MR, the degree of LV remodelling and the presence of myocardial fibrosis. We will perform an observational multicentre study where we will recruit 200 patients over 2 large centers, University Hospital Antwerp (UZA, BE) and Maastricht University Medical centre (MUMC+, NL). We aim to include 100 patients with BD and 100 with FED. After inclusion, patients will be scheduled for a 3D echocardiography, cardiac magnetic resonance, 24h holter monitoring and genetic testing.
Doel van het onderzoek
We hypothesize that mechanisms of LV remodelling in BD include a larger prolapse volume and underlying genetic substrate, beyond volume overload related to MR, resulting in more severe LV remodelling and dysfunction compared to FED.
Onderzoeksopzet
One timepoint: baseline
Onderzoeksproduct en/of interventie
Observational study with minimal amount of investigations, only once:
- 3D echocardiography (usually in clinical routine)
- Cardiac magnetic resonance scan
- 24h holter monitoring
- Blood sample for genetic testing
Publiek
Wetenschappelijk
Belangrijkste voorwaarden om deel te mogen nemen (Inclusiecriteria)
* Non-syndromic mitral valve prolapse (e.g. no Marfan syndrome)
* Age 18-80 years old
Belangrijkste redenen om niet deel te kunnen nemen (Exclusiecriteria)
* History of cardiac surgery
* Concomitant valve disease (grade ‘moderate’ or ‘severe’)
* Ischaemic heart disease
* Hypertrophic cardiomyopathy
* Intra-cardiac device
* History of myocarditis
* Left bundle branch block
* Chronic kidney disease stage 4-5
* Pregnancy
Opzet
Deelname
Voornemen beschikbaar stellen Individuele Patiënten Data (IPD)
Toelichting
Opgevolgd door onderstaande (mogelijk meer actuele) registratie
Geen registraties gevonden.
Andere (mogelijk minder actuele) registraties in dit register
Geen registraties gevonden.
In overige registers
| Register | ID |
|---|---|
| NTR-new | NL9677 |
| Ander register | METC AZM/UM : METC068 |