Abstract
Central MessageDysregulated endothelial nitric oxide synthase is a primary feature in unicuspid valve disease-related aortopathy.See Article page 157. Dysregulated endothelial nitric oxide synthase is a primary feature in unicuspid valve disease-related aortopathy. See Article page 157. In a carefully conducted study, Balint and colleagues1Balint B. Kollmann C. Gauer S. Federspiel J.M. Schäfers H.-J. Endothelial nitric oxide synthase alterations are independent of turbulence in the aorta of patients with a unicuspid aortic valve.J Thorac Cardiovasc Surg Open. 2021; 8: 157-169Scopus (4) Google Scholar demonstrate that dysregulated endothelial nitric oxide (eNOS) is a cause and not a consequence in unicuspid aortic valve aortopathy.1Balint B. Kollmann C. Gauer S. Federspiel J.M. Schäfers H.-J. Endothelial nitric oxide synthase alterations are independent of turbulence in the aorta of patients with a unicuspid aortic valve.J Thorac Cardiovasc Surg Open. 2021; 8: 157-169Scopus (4) Google Scholar These findings mirror patterns of dysregulated eNOS in closely related conditions, including bicuspid aortic valve disease related aortopathy.2Gauer S. Balint B. Kollmann C. Federspiel J.M. Henn D. Bandner-Risch D. et al.Dysregulation of endothelial nitric oxide synthase does not depend on hemodynamic alterations in bicuspid aortic valve aortopathy.J Am Heart Assoc. 2020; 9: e016471https://doi.org/10.1161/JAHA.120.016471Crossref PubMed Scopus (6) Google Scholar,3Kotlarczyk M.P. Billaud M. Green B.R. Hill J.C. Shiva S. Kelley E.E. et al.Regional disruptions in endothelial nitric oxide pathway associated with bicuspid aortic valve.Ann Thorac Surg. 2016; 102: 1274-1281https://doi.org/10.1016/j.athoracsur.2016.04.001Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar Thoracic aortic aneurysm disease is common and represents a significant risk in those with congenital malformations of the aortic valve.4Sidloff D. Choke E. Stather P. Bown M. Thompson J. Sayers R. Mortality from thoracic aortic diseases and associations with cardiovascular risk factors.Circulation. 2014; 130: 2287-2294https://doi.org/10.1161/CIRCULATIONAHA.114.010890Crossref PubMed Scopus (45) Google Scholar Although the risks that aortic aneurysms pose to patients with bicuspid and unicuspid aortic valve disease are clear, the precise molecular mechanisms underpinning these complex valvular-aortic traits remain poorly understood. Whether or not aortic dilation in this population is a product of altered valve hemodynamic parameters, a consequence of an embryologic event, or a combination of both remains unknown. Understanding the precise mechanism is important because it could potentially alter surgical strategy for replacement of mildly aneurysmal ascending aorta during surgery for bicuspid or unicuspid aortic valve disease as well as extent of aortic replacement. One can argue that aneurysmal changes are secondary to altered valve hemodynamic status and a valve replacement only would suffice. The study by Balint and colleagues1Balint B. Kollmann C. Gauer S. Federspiel J.M. Schäfers H.-J. Endothelial nitric oxide synthase alterations are independent of turbulence in the aorta of patients with a unicuspid aortic valve.J Thorac Cardiovasc Surg Open. 2021; 8: 157-169Scopus (4) Google Scholar represents a significant advance by demonstrating that dysregulation of eNOS in the aortic wall of patients with a unicuspid aortic valve is not a consequence of altered valve hemodynamic status. Although a role for eNOS in unicuspid aortic valve aortopathy is evident at the molecular level, more work is needed to clearly define the genetic underpinnings of this phenomenon and how that translates to clinical practice and surgical strategy for patients with aortopathy. Endothelial nitric oxide synthase alterations are independent of turbulence in the aorta of patients with a unicuspid aortic valveJTCVS OpenVol. 8PreviewCertain aortic valve malformations predispose to ascending aortic aneurysm, although the mechanisms are incompletely understood. The aim of this study was to determine whether turbulence across the unicuspid aortic valve (UAV) contributes to regional differences in endothelial nitric oxide (eNOS) signaling in the ascending aortic wall. Full-Text PDF Open Access
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