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1 ary mitral regurgitation (MR) is a prevalent valvular lesion.
2 ed effectively by correcting the responsible valvular lesion.
3  be associated with the development of these valvular lesions.
4 ese enzymes, and (4) development of TAAs and valvular lesions.
5 dex, and renal function were associated with valvular lesions.
6 s known about the long-term outcomes of mild valvular lesions.
7  overload that may result from hypertension, valvular lesions, acute, or chronic ischemic injuries.
8  therapy was halted in 1997 after reports of valvular lesions affecting almost one third of patients
9 ease remains unclear, although regression of valvular lesions after the end of treatment has been rep
10 e the independent associations between the 3 valvular lesions and these outcomes.
11 h malignancies, autoimmune diseases, cardiac valvular lesions, and in patients on mechanical circulat
12 aortic size in control patients with matched valvular lesions (aortic regurgitation, aortic stenosis,
13                                   Many adult valvular lesions appear similar to the embryonic prolife
14 urgical treatment of stenotic or regurgitant valvular lesions can alter the natural history of the di
15 promise to offer a novel approach to correct valvular lesions, especially in this high-risk surgical
16 f this study indicate an association between valvular lesions, even at mild stage, and a long-term ri
17                          The total number of valvular lesions had graded associations with all cardio
18 he primary cause of regurgitant and stenotic valvular lesion in the U.S.
19 ssociation between apoE alleles and calcific valvular lesions in 802 patients undergoing transthoraci
20  safe and durable surgical correction of the valvular lesions in up to 31% of these high-risk cases.
21 ar findings were observed for stages of each valvular lesion individually.
22                                              Valvular lesions initiated at the valve surface endothel
23 thoracic echocardiography (TTE) identified a valvular lesion of acute Q fever endocarditis without un
24 tor in the amino acid-stringent, thrombotic, valvular lesions of bacterial endocarditis.
25 tity, acute Q fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: veget
26                                         Each valvular lesion was significantly associated with at lea
27 idate the mechanism of "fen-phen"-associated valvular lesions, we examined the interaction of fenflur
28                                        Three valvular lesions were analyzed: aortic sclerosis, aortic
29 ansthoracic echocardiography for significant valvular lesions within a mean of 97 days from the manuf