This article outlines the key research contribution to bicuspid aortic valve (BAV) aortopathy over the past 18 months.
Investigators have further defined the current gaps in knowledge and the scope of the clinical problem of BAV aortopathy. Support for aggressive resection strategies is waning as evidence mounts to suggest that BAV is not similar to genetic connective tissue disorders with respect to aortic risks. The role of cusp fusion patterns and valve-mediated hemodynamics in disease progression is a major area of discovery. Molecular and cellular mechanisms remain elusive and contradictory.
BAV aortopathy is a major public health problem that remains poorly understood. New insights on valve-mediated hemodynamics using novel imaging modalities may lead to more individualized resection strategies and improved clinical guidelines.
aDepartment of Cardiac Sciences, Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary
bDivision of Cardiac Surgery, Li Ka Shing Knowledge Institute of St Michael's Hospital, University of Toronto, Toronto, Canada
cDepartment of Radiology, Northwestern University
dDivision of Surgery – Cardiac Surgery, Bluhm Cardiovascular Institute, Chicago, USA
Correspondence to Paul W.M. Fedak, MD, PhD, FRCSC FAHA, Department of Cardiac Science, University of Calgary, Libin Cardiovascular Institute of Alberta, C880, 1403-29 Street NW, Calgary, AB T2N 2T9, Canada. Tel: +1 403 944 5931; fax: +1 403 270 3715; e-mail: firstname.lastname@example.org