1 ed effectively by correcting the responsible valvular lesion.

2 ese enzymes, and (4) development of TAAs and valvular lesions.

3  be associated with the development of these valvular lesions.

4  therapy was halted in 1997 after reports of valvular lesions affecting almost one third of patients

5 ease remains unclear, although regression of valvular lesions after the end of treatment has been rep

6 h malignancies, autoimmune diseases, cardiac valvular lesions, and in patients on mechanical circulat

7 aortic size in control patients with matched valvular lesions (aortic regurgitation, aortic stenosis,

8                                   Many adult valvular lesions appear similar to the embryonic prolife

9 urgical treatment of stenotic or regurgitant valvular lesions can alter the natural history of the di

10 promise to offer a novel approach to correct valvular lesions, especially in this high-risk surgical

11 he primary cause of regurgitant and stenotic valvular lesion in the U.S.

12 ssociation between apoE alleles and calcific valvular lesions in 802 patients undergoing transthoraci

13  safe and durable surgical correction of the valvular lesions in up to 31% of these high-risk cases.

14                                              Valvular lesions initiated at the valve surface endothel

15 tor in the amino acid-stringent, thrombotic, valvular lesions of bacterial endocarditis.

16 idate the mechanism of "fen-phen"-associated valvular lesions, we examined the interaction of fenflur

17 ansthoracic echocardiography for significant valvular lesions within a mean of 97 days from the manuf