Abstract
Aortic stenosis is the most common valvular heart disease affecting up to 4% of the elderly population. It can be associated with dilatation of the ascending aorta and subsequent dissection. Post-stenotic dilatation is seen in patients with AS and/or aortic regurgitation, patients with a haemodynamically normal bicuspid aortic valve and following aortic valve replacement. Controversy exists as to whether to replace the aortic root and ascending aorta at the time of aortic valve replacement, an operation that potentially carries a higher morbidity and mortality.The aetiology of post-stenotic aortic dilatation remains controversial. It may be due to haemodynamic factors caused by a stenotic valve, involving high velocity and turbulent flow downstream of the stenosis, or due to intrinsic pathology of the aortic wall. This may involve an abnormality in the process of extracellular matrix remodelling in the aortic wall including inadequate synthesis, degradation and transport of extracellular matrix proteins.This article reviews the aetiology, pathology and management of patients with post-stenotic aortic dilatation.
Highlights
The aetiology of post-stenotic aortic dilatation remains controversial
This study showed that aortic valve replacement (AVR) could not prevent progressive aortic dilatation in bicuspid aortic valve (BAV)
Post-stenotic aortic dilatation is most commonly seen in patients with a BAV
Summary
An English literature search using Pubmed-Medline database between 1960 and today was carried out. The study group consisted of 26 patients, undergoing surgery for AS, AR, ascending aortic aneurysm or type A dissection (BAV n = 10, TAV n = 16, controls n = 4) They showed that MMP-9 expression was significantly higher in BAV compared to normal and diseased TAV. The pulmonary and aortic roots share a common embryological origin and it has been proposed that the dilatation of the pulmonary autograft may occur as a result of an intrinsic abnormality within the wall, as seen in the aorta of patients with congenital AV disease [57] This theory is supported by the findings of de Sa et al [46], that the degenerative changes in the ascending aorta and pulmonary trunk of patients with BAV were more severe than those with TAV. Synthetic inhibitors of MMPs have been investigated in other disease processes, including the use of minocycline in rheumatoid arthritis, and several are currently under investigation for the use in cardiovascular disease [35]
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