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1              The most common MR etiology was myxomatous (61%), followed by functional (9%), infective
2 s were used to measure gene expression in 11 myxomatous and 11 nonmyxomatous human mitral valves.
3  genes were differentially expressed between myxomatous and nonmyxomatous valves.
4 atients with intrinsic mitral valve disease (myxomatous, calcific, or ischemic MR).
5  from developmental valve anomalies and have myxomatous cardiac valves with 100% penetrance.
6                                              Myxomatous cerebral (oncotic) aneurysms following atrial
7 tnatal Wt1(Cre);Alk3(fl/fl) specimens showed myxomatous changes in the leaflets of the mitral valve.
8 lapse of the anterior leaflet, the degree of myxomatous changes in the MV, lack of mitral annuloplast
9 genesis of MFS, including the development of myxomatous changes of the atrioventricular valves.
10 ovel, genetically engineered murine model of myxomatous changes of the mitral valve and provide criti
11              The GAG classes elevated in the myxomatous chordae are associated with matrix microstruc
12  and more extensible than normal valves, and myxomatous chordae are more mechanically compromised tha
13 lated to the reported mechanical weakness of myxomatous chordae.
14   Fibro-elastic deficiency (FED) and diffuse myxomatous degeneration (DMD) are phenotypes of degenera
15                    The molecular disorder of myxomatous degeneration appears to consist of a connecti
16                                              Myxomatous degeneration appears to have genetic etiology
17  mediate extracellular matrix degradation in myxomatous degeneration by excessive secretion of catabo
18 titial cells in 14 mitral valves removed for myxomatous degeneration from patients with mitral regurg
19 ibited morphological changes consistent with myxomatous degeneration in the walls of knockout hearts.
20                              The genetics of myxomatous degeneration is complex and not fully worked
21                                              Myxomatous degeneration is the most common cause of mitr
22 Little is known about the pathophysiology of myxomatous degeneration of the mitral valve, the patholo
23 without annuloplasty ring, and the degree of myxomatous degeneration of the MV to be associated with
24 c examination of excised allografts revealed myxomatous degeneration without immunologic reaction.
25     Sarcomas were frequently associated with myxomatous differentiation.
26 tient, usually female, with mostly bileaflet myxomatous disease, mid-systolic click, repolarization a
27  no early death occurred among patients with myxomatous disease.
28   The repair rate was 62% overall and 80% in myxomatous disease.
29 show that FED and DMD, although both labeled myxomatous, display considerable physiological phenotypi
30 nts, myxomatous in 19, combined ischemic and myxomatous in 16, rheumatic in 5, infective in 3, and un
31  the MV disease was ischemic in 33 patients, myxomatous in 19, combined ischemic and myxomatous in 16
32 athogenesis was functional in 54% (n=22) and myxomatous in 46% (n=19).
33                                              Myxomatous leaflets and chordae had 3% to 9% more water
34 ral valve prolapse (MVP) is characterized by myxomatous leaflets and left ventricular (LV) fibrosis o
35 United States and Europe, and progression of myxomatous mitral prolapse is the most common cause of m
36 itral regurgitation (9.98 +/- 155 cm(2)) and myxomatous mitral regurgitation annuli (13.29 +/- 3.05 c
37                                  Significant myxomatous mitral regurgitation leads to progressive lef
38       In patients with grade III+ or greater myxomatous mitral regurgitation undergoing exercise echo
39 4 years; 67% men) with grade III+ or greater myxomatous mitral regurgitation who underwent exercise e
40    In both ischemic mitral regurgitation and myxomatous mitral regurgitation, annular dynamics and an
41                                           In myxomatous mitral regurgitation, annular dynamics were a
42 mpaired in ischemic mitral regurgitation and myxomatous mitral regurgitation.
43 ic mitral regurgitation and 11 patients with myxomatous mitral regurgitation.
44            Pathological processes underlying myxomatous mitral valve degeneration (MMVD) remain poorl
45 egulate matrix degradation and remodeling in myxomatous mitral valve degeneration.
46 o define the cellular mechanisms involved in myxomatous mitral valve disease and calcific aortic valv
47 ls undergo dramatic changes in the course of myxomatous mitral valve disease in both dogs and humans.
48 rs with dilated cardiomyopathy, 10 dogs with myxomatous mitral valve disease, and 7 healthy non-Boxer
49                                              Myxomatous mitral valve with prolapse are classically se
50 m with subsequent echocardiography revealing myxomatous mitral valve with prolapse.
51           We examined human diseased valves: myxomatous mitral valves (n = 23), calcified tricuspid a
52                                              Myxomatous mitral valves are weaker and more extensible
53  receptor, and osteocalcin were increased in myxomatous mitral valves by protein and gene expression
54 rganization in healthy and lesional areas of myxomatous mitral valves of dogs, using synchrotron smal
55 acellular matrix of normal mitral valves and myxomatous mitral valves with either unileaflet prolapse
56                                   Normal and myxomatous mitral valves, both human and canine, were ha
57  calcified aortic valves and negative in the myxomatous mitral valves.
58 y was 4.5% overall but 2.3% in patients with myxomatous MR (1.8% isolated, 3.1% combined).
59           Although numerous articles on MVP (myxomatous or myxoid degeneration, billowing or floppy m
60                                    Ischemic, myxomatous, rheumatic, or infective MV dysfunction may d
61 ts (62%; Group A), the valve was found to be myxomatous, thickened, and redundant.
62 ted soft tissue (including edema, mucin, and myxomatous tissue) have typical MR imaging properties, a
63 itral valve was acquired in 32 patients with myxomatous valve disease (MVD) and moderate to severe re
64 cumulation of proteoglycans is a hallmark of myxomatous valve disease, based on these data we hypothe
65 lopment may be a potential etiology of adult myxomatous valve disease.
66 ion and survival and plausibly contribute to myxomatous valve disease.
67  likely to develop SAM/LVOTO after MVRep for myxomatous valve disease.
68                    Leaflets and chordae from myxomatous valves (n = 41 ULP, 31 BLP) and normal valves
69 tin, but not alpha-actin or desmin, cells in myxomatous valves contained both vimentin and alpha-acti
70                                              Myxomatous valves demonstrated activation of canonical b
71 ular abnormality but the pathogenic cause of myxomatous valves has not been elucidated.
72                        Interstitial cells in myxomatous valves have features of activated myofibrobla
73                           Moreover, cells in myxomatous valves strongly expressed SMemb, MMPs, cathep
74 that glycosaminoglycans (GAGs) accumulate in myxomatous valves, previous biochemical analyses have no
75 n concentration was slightly elevated in the myxomatous valves.
76  preserved ability to synthesize collagen in myxomatous valves.
77 of extracellular matrix changes accompanying myxomatous valvular degeneration are uncertain.