Abstract
The roles that aortitis plays in the development of annuloaortic ectasia (AAE) remain uncertain, while clinical features of AAE in arteritis are largely unknown. This study was designed to highlight the clinical features of AAE, the treatments of choice, and the causative relations between aortitis and AAE. The morphology of the aortic valve leaflets was normal in half of the patients, while the valves were thin and overstretched in the other half. Most patients had an aortic aneurysm. Half of the patients had severe aortic valve insufficiency, and one-quarter of them had dilation of the sinuses of Valsalva. Takayasu arteritis was prone to develop coronary artery lesions, whereas giant cell arteritis were not. Aortic branch lesions in Takayasu arteritis were stenotic or occlusive in 92.9% of the patients, while in giant cell arteritis, they were all dilated lesions. Most patients (94.7%) required surgical treatment with steroid therapy. However, long-term follow-up results showed a higher anastomotic dehiscence rate, particularly in patients with Takayasu arteritis. Further morphometric and pathological research on AAE in arteritis should be undertaken, and more feasible measures should be warranted for preventing postoperative anastomotic dehiscence.
Highlights
In 1961, Ellis et al.[1] proposed the concept of annuloaortic ectasia (AAE) representing an entity of dilation of the proximal ascending aorta, sinuses of Valsalva, and aortic annulus with poor coaptation of the valvular leaflets and aortic regurgitation
The etiological evaluations suggested that cystic medial necrosis is the most frequent etiology of AAE[5], and less common etiologies may include atherosclerosis, luetic aortits, chronic aortic dissection, and syphilitic aortic aneurysm[6]
This study aims to highlight the clinical features of AAE in patients with arteritis, the treatments of choice, and the causative relations between aortitis and AAE
Summary
In 1961, Ellis et al.[1] proposed the concept of annuloaortic ectasia (AAE) representing an entity of dilation of the proximal ascending aorta, sinuses of Valsalva, and aortic annulus with poor coaptation of the valvular leaflets and aortic regurgitation. In the cohort of AAE, patients may have aortic dissection, aneurysm, or rupture[2,3]. The etiological evaluations suggested that cystic medial necrosis is the most frequent etiology of AAE[5], and less common etiologies may include atherosclerosis, luetic aortits, chronic aortic dissection, and syphilitic aortic aneurysm[6].
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