Patient diversity in Bicuspid Aortic Valve disease.
A bicuspid aortic valve (BAV) is the most common congenital heart defect, in which the aortic valve consists of only two instead of three leaflets. People with a BAV have an increased risk of developing aortic valve stenosis and thoracic aortic aneurysms (TAA). Currently, there is no treatment option other than surgical removal of the aortic valve and/or thoracic aorta when the patient is estimated to be at a high risk of aortic rupture. There is a lack of knowledge about how the BAV and aortic aneurysms/ aortic valve calcification are related and why there is such a big variation in patient prognosis. Therefore, my research is focussed on understanding the patient variation leading to either aortic valve calcification or aortic dilation. To this end, I culture endothelial colony forming cells (ECFCs) from BAV patients and study aortic tissue samples collected from different locations in the aorta. In these, I explore the role of endothelial to mesenchymal transition, flow, inflammation, and disturbed TGFβ/BMP signalling in the development of BAV associated TAA.
I have have achieved my bachelor and master degree biomedical sciences from the Leiden University, the Netherlands. During my internship in the department of Anatomy and Embryology at the LUMC I became interested in cardiovascular diseases. In October 2014 I started my PhD in the group of professor Marie-José Goumans within the NHS-BAV consortium.
Thoracic Aortic Aneurysm
Development in Patients with Bicuspid Aortic Valve: What Is the Role of
van de Pol V, Kurakula K, DeRuiter MC, Goumans MJ.
Front Physiol. 2017 Nov 30;8:938. doi: 10.3389/fphys.2017.00938. eCollection 2017. Review. PubMed PMID: 29249976; PubMed Central PMCID: PMC5714935.
Akintola AA, van de Pol V, Bimmel D, Maan AC, van Heemst D.
Comparative Analysis of the Equivital EQ02 Lifemonitor with Holter Ambulatory ECG Device for Continuous Measurement of ECG, Heart Rate, and Heart Rate Variability: A Validation Study for Precision and Accuracy.
Front Physiol. 2016 Sep 21;7:391. eCollection 2016. PubMed PMID: 27708585; PubMed Central PMCID: PMC5030218.
Contractile Defect Caused by Mutation in MYBPC3 Revealed under Conditions
Optimized for Human PSC-Cardiomyocyte Function.
Birket MJ, Ribeiro MC, Kosmidis G, Ward D, Leitoguinho AR, van de Pol V, Dambrot C, Devalla HD, Davis RP, Mastroberardino PG, Atsma DE, Passier R, Mummery CL.
Cell Rep. 2015 Oct 27;13(4):733-745. doi: 10.1016/j.celrep.2015.09.025. Epub 2015 Oct 17. PubMed PMID: 26489474; PubMed Central PMCID: PMC4644234.
Groups: Cardiovascular Cell Biology