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Studies on Aortic and Aortic Valve Diseases | OMICS International | Abstract
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Review Article

Studies on Aortic and Aortic Valve Diseases

Salah A. Mohamed*, Johnson J Yan and Hans H Sievers
Department of Cardiac and Thoracic Vascular Surgery, Universitaetsklinikum Schleswig-Holstein, Campus Luebeck, Germany
Corresponding Author : Salah A. Mohamed
Department of Cardiac and Thoracic Vascular Surgery
University Clinic of Schleswig-Holstein Campus Luebeck
Ratzeburger Allee 160, 23538 Luebeck, Germany
Tel: +49-451-5006425
Fax: +49-451-5002051
E-mail: [email protected]
Received July 06, 2013; Accepted August 16, 2013; Published August 19, 2013
Citation: Mohamed SA, Yan JJ, Sievers HH (2013) Studies on Aortic and Aortic Valve Diseases. J Clin Exp Cardiolog 4:265. doi:10.4172/2155-9880.1000265
Copyright: © 2013 Mohamed SA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Bicuspid aortic valve (BAV) is the most common congenital cardiac malformation, with an estimated incidence of 1%–2% in the general population. Patients with BAV are predisposed to early and frequent stenosis, regurgitation, and endocarditis, often accompanied by aneurysm and dissection. A family-based genome-wide analysis found that BAV was linked to chromosomal regions 5q, 13q, and 18q, with autosomal dominant inheritance, reduced penetrance and a non-Mendelian inheritance pattern. Mutations in the transmembrane receptor-encoding gene NOTCH1 have been detected in familial and sporadic BAV cases. Mutations in the vascular smooth muscle cell alpha actin gene (ACTA2) have also been identified in BAV patients. Expression of UFD1L, a gene that is highly expressed in the outflow tract during embryogenesis, was downregulated in the cusps of BAV patients compared with those of controls. BAV is associated with left ventricular outflow tract abnormality, including aortic coarctation, arch hypoplasia, and supravalvular and mitral valve stenosis. A male predominance of more than 3:1 has been reported for BAV. This anomaly is very frequent in X0 Turner’s syndrome. Many studies have observed similarities between the histology of aortic aneurysmal tissue in the connective tissue disorder Marfan syndrome (MFS) and the histology of the corresponding tissue in BAV. In this lecture, we review our present understanding of BAV malformation and ascending thoracic aortic aneurysm pathogenesis. We discuss the genetic basis and the basic pathology underlying BAV and aortopathy and compare these with known mechanisms underlying MFS.

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