Abstract 2312: High Prevalence of Novel Amyloid Protein Deposition in Surgically Removed Heart Valves
Amyloid deposition has been described in degenerative cardiac valve failure, but the prevalence, pathophysiology, and clinical indicators have not been clarified yet. Extensive histological analysis of 150 consecutive, surgically resected heart valve specimens (aortic n = 119, mitral n ± 31; 67.4 ± 1.0 years) was performed. Amyloid deposition was graded semi-quantitatively and classified by specific antisera identifying the most common amyloid proteins. Histological findings were correlated with clinical data. 119 patients had aortic valve disease: aortic stenosis (AS; 100/119; 84%), aortic regurgitation (19/119; 16%); 31 patients had mitral valve disease: mitral stenosis (7/31; 22.6%), mitral regurgitation (24/3177.4%). Amyloid was found in 83/150 (55.3%) specimens with the highest prevalence in aortic stenosis (74/100; 74%), intermediate in mitral stenosis (n = 2/7; 28.6%) and mitral regurgitation (n = 7/24; 29.2%), and lowest in aortic regurgitation (2/19; 10.5%). Moderate to severe amyloid deposition was almost exclusively found in aortic stenosis. Similarily coarse polymorphic amyloid deposits by morphologic analysis were most abundant in aortic stenosis (n = 35/100; 35%). Filamentous cloudy amyloid patterns occurred with the same frequency in aortic stenosis (n = 29/100; 29%). A combination of both was only found in aortic stenosis (n = 7/100; 7%). By immunohistochemical staining none of the most common amyloid proteins was identified. Some of the specimens were weakly stained by the apolipoprotein-AI antibody, more markedly adjacent to the amyloid fibrils. Amyloid deposition in aortic stenosis depended on hyperlipidemia, echocardiographic valvular thickening, and - by trend - on the presence of coronary artery disease, and obesity. Dystrophic valvular amyloidosis appears to represent an underestimated local manifestation of progressive destruction and scarring with diverse deposition pattern predominantly affecting stenotic aortic valves. It appears to depend on risk factors for atheroinflammatory processes and high shear-stress hemodynamic. The underlying protein structure has to be clarified in further studies.