Dataset related to the article "Isolated Valve Amyloid Deposition in Aortic Stenosis: Potential Clinical and Pathophysiological Relevance"

<p>This record contains raw data related to the article "Isolated Valve Amyloid Deposition in Aortic Stenosis: Potential Clinical and Pathophysiological Relevance"</p> <p>Abstract: Amyloid deposition within stenotic aortic valves (AVs) also appears frequent in the absence&nbsp;of cardiac amyloidosis, but its clinical and pathophysiological relevance has not been investigated.&nbsp;We will elucidate the rate of isolated AV amyloid deposition and its potential clinical and pathophysiological&nbsp;significance in aortic stenosis (AS). In 130 patients without systemic and/or cardiac&nbsp;amyloidosis, we collected the explanted AVs during cardiac surgery: 57 patients with calcific AS<br>and 73 patients with AV insufficiency (41 with AV sclerosis and 32 without, who were used as&nbsp;controls). Amyloid deposition was found in 21 AS valves (37%), 4 sclerotic AVs (10%), and none&nbsp;of the controls. Patients with and without isolated AV amyloid deposition had similar clinical and&nbsp;echocardiographic characteristics and survival rates. Isolated AV amyloid deposition was associated&nbsp;with higher degrees of AV fibrosis (p = 0.0082) and calcification (p &lt; 0.0001). Immunohistochemistry&nbsp;analysis suggested serum amyloid A1 (SAA1), in addition to transthyretin (TTR), as the protein&nbsp;possibly involved in AV amyloid deposition. Circulating SAA1 levels were within the normal range<br>in all groups, and no difference was observed in AS patients with and without AV amyloid deposition.&nbsp;In vitro, AV interstitial cells (VICs) were stimulated with interleukin (IL)-1&beta; which induced increased&nbsp;SAA1-mRNA both in the control VICs (+6.4 &plusmn; 0.5, p = 0.02) and the AS VICs (+7.6 &plusmn; 0.5, p = 0.008).&nbsp;In conclusion, isolated AV amyloid deposition is frequent in the context of AS, but it does not appear&nbsp;to have potential clinical relevance. Conversely, amyloid deposition within AV leaflets, probably&nbsp;promoted by local inflammation, could play a role in AS pathophysiology.</p>