Mechanism of reduction of aortic valvular stenosis by percutaneous transluminal balloon valvuloplasty: report of five cases and review of literature

Among five patients (69 to 93 years of age) in whom percutaneous transluminal balloon valvuloplasty was performed for severe aortic stenosis, fractures of cuspid calcium were observed in three, fractures and a cuspid tear in one, and no gross alterations in one. Aortic stenosis resulted from degener...

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Published inMayo Clinic proceedings Vol. 63; no. 8; p. 769
Main Authors Kennedy, K D, Hauck, A J, Edwards, W D, Holmes, Jr, D R, Reeder, G S, Nishimura, R A
Format Journal Article
LanguageEnglish
Published England 01.08.1988
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Summary:Among five patients (69 to 93 years of age) in whom percutaneous transluminal balloon valvuloplasty was performed for severe aortic stenosis, fractures of cuspid calcium were observed in three, fractures and a cuspid tear in one, and no gross alterations in one. Aortic stenosis resulted from degenerative (senile) calcification of tricuspid aortic valves in two patients, calcification of congenitally bicuspid aortic valves in two, and postinflammatory (presumably rheumatic) fibrocalcific disease in one. Fractures of calcific lesions, by allowing hingelike motion along their sites, seemed to facilitate cuspid mobility and thereby provided the apparent morphologic substrate for reduction in functional stenosis. Among three cases with fused commissures (two bicuspid and one postinflammatory), however, mobility of the conjoined cusps was not achieved after valvuloplasty, despite fracture of calcific nodules in the adjacent valve pocket of one case, because the fused and calcified commissures were not split or fractured and therefore continued to act as rigid struts that impeded cuspid motion. In the current autopsy evaluation of the effects of aortic balloon valvuloplasty, greater cuspid mobility seemed to be achieved in subjects with degenerative calcific stenosis than in those with calcified bicuspid valves or distortion by postinflammatory disease.
ISSN:0025-6196
DOI:10.1016/S0025-6196(12)62356-8