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1 e endocardial cushion, the primordium of the cardiac valves.
2 perspectives on transcatheter replacement of cardiac valves.
3  of pathological microfractures in calcified cardiac valves.
4 tribution were found both between and within cardiac valves.
5  as myocardial fibrosis and calcification of cardiac valves.
6 al cushions that ultimately develop into the cardiac valves.
7  and function and detailed evaluation of all cardiac valves.
8  and for its adhesion to the vessel wall and cardiac valves.
9 rt development necessary to the formation of cardiac valves.
10 ralization of the arterial blood vessels and cardiac valves.
11  potentially therapeutic regeneration of the cardiac valves.
12 cal event for the embryonic morphogenesis of cardiac valves.
13 ibomian glands, and defects in the semilunar cardiac valves.
14 e impact of potential residual CPAs on human cardiac valves.
15 Cs are a constituent of the normal aorta and cardiac valves.
16 perties, and pathobiological behavior of the cardiac valves.
17 M), predominates in the supporting tissue of cardiac valves.
18 pproaches to therapeutic regeneration of the cardiac valves.
19 ncluding the intima and media of vessels and cardiac valves.
20 tissue remodeling formed the leaflets of the cardiac valves.
21 gies to guide tissue formation in engineered cardiac valves.
22 ocardial Nfatc1 expression within developing cardiac valves.
23 scription factor required for development of cardiac valves.
24               Although patients with certain cardiac valve abnormalities have increased risk of infec
25 ents (53 of 233) met the case definition for cardiac-valve abnormalities (odds ratio, 22.6; 95 percen
26            There were no cases of idiopathic cardiac-valve abnormalities among the subjects who had n
27                        After case reports of cardiac-valve abnormalities related to the use of appeti
28                      The odds ratio for such cardiac-valve abnormalities was 12.7 (95 percent confide
29 ween the use of any appetite suppressant and cardiac-valve abnormalities was analyzed in a final matc
30                              The presence of cardiac-valve abnormalities, defined by the Food and Dru
31 was used to identify factors associated with cardiac-valve abnormalities.
32  of papillary muscles, the fibrous tissue of cardiac valve and chordae tendineae and the course of co
33 echocardiography (TEE) is used frequently in cardiac valve and proximal aortic surgical procedures, b
34 correlated with severity of disease, causing cardiac valve and septal disease in the neonate that was
35 Cs proved to be particularly abundant in the cardiac valves and aortic sinus.
36 r arrhythmias, and percutaneous placement of cardiac valves and closure devices will also be discusse
37  realistic and unique comprehensive views of cardiac valves and congenital abnormalities.
38  cells and is necessary for formation of the cardiac valves and for complete cardiac septation.
39 docardial cushions are the precursors of the cardiac valves and form by a process of epithelial-mesen
40 riable morphology, were detected in all four cardiac valves and in some tendinous cords.
41                           Hyperplasia of the cardiac valves and outflow tract septation defects indic
42 e macrophages required for the remodeling of cardiac valves and septa.
43                  Abnormal development of the cardiac valves and septae is the most frequent form of b
44 formation exists on the innervation of human cardiac valves and the relationship of nerve fibers and
45 s prevalent, such as in the formation of the cardiac valves and trabeculae.
46 ed endocardium and fail to form identifiable cardiac valves and trabeculae.
47 c surgery, including coronary artery bypass, cardiac valve, and aortic procedures, is among the most
48                                Keywords: CT, Cardiac, Valves, Aortic Stenosis (C) RSNA, 2025.
49                                              Cardiac valves are essential to direct forward blood flo
50                                              Cardiac valves arise from endocardial cushions, speciali
51 h mineralization can occur at various sites (cardiac valves, arterial intima or media, capillaries),
52 c OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4
53       Furthermore, adult mutant mice exhibit cardiac valve calcifications associated with abnormal ma
54 nges in coronary artery, thoracic aorta, and cardiac valve calcium scores and pulse wave velocity wer
55 on of the pathomorphological features of the cardiac valves compared with previously used sparse arra
56  development of the embryonic outflow tract, cardiac valves, conducting system, and the developing co
57 heumatic heart disease (RHD) with persistent cardiac valve damage.
58 -/-) embryos as well as additional semilunar cardiac valve defects and a double-outlet right ventricl
59                                              Cardiac valve defects are a common congenital heart malf
60 ogical approaches show that NS mutants cause cardiac valve defects by increasing Erk MAPK activation,
61  who presented predominantly with congenital cardiac valve defects.
62 hisms in a patient population suffering from cardiac valve defects.
63 lish the cellular and molecular signature of cardiac valve delamination in vivo and demonstrate the c
64 zebrafish atrioventricular canal (AVC) where cardiac valves develop.
65 eously suppresses elements that could hinder cardiac valve development and homeostasis.
66 ndocardium is a crucial signaling center for cardiac valve development and maturation.
67 light on the function of Nfatc1 in zebrafish cardiac valve development and reveals its role in VIC fo
68 d that many key genetic pathways involved in cardiac valve development are also implicated in disease
69                Defining molecular factors in cardiac valve development has facilitated identification
70 ulates the release of active TGF-beta during cardiac valve development in the avian heart.
71  protein) activity in the endocardium during cardiac valve development.
72 to better understand its mechanistic role in cardiac valve development.
73 ry pathways that control normal and abnormal cardiac valve development.
74 sly to play important and selective roles in cardiac valve development.
75                                Patients with cardiac valve disease (CVD) frequently have congestive h
76                          The pathogenesis of cardiac valve disease correlates with the emergence of m
77 f TNF and inflammation in the development of cardiac valve disease in man.
78      Mitral valve prolapse (MVP) is a common cardiac valve disease that affects nearly 1 in 40 indivi
79 cytopenia, 1, 1, 2, and 0, respectively; for cardiac valve disease, 0, 0, 3, and not analyzed, respec
80 r C. burnetii in antiphospholipid-associated cardiac valve disease, and performing early echocardiogr
81     In some persons, particularly those with cardiac valve disease, infection with C. burnetii can ca
82 carotid artery disease, atrial fibrillation, cardiac valve disease, obesity, dyslipidemia, hypertensi
83 aPL-positive patients with thrombocytopenia, cardiac valve disease, skin ulcer, aPL nephropathy, and/
84      Mitral valve prolapse (MVP) is a common cardiac valve disease, which affects 1 in 40 in the gene
85  etiology of both degenerative and rheumatic cardiac valve diseases.
86 trating the role of cilia function in common cardiac valve disorders, including mitral valve prolapse
87 five-year cumulative incidence of idiopathic cardiac-valve disorders was 0 per 10,000 subjects among
88 ed with an increased risk of newly diagnosed cardiac-valve disorders, particularly aortic regurgitati
89 in abundantly expressed in great vessels and cardiac valves during embryogenesis, and in many adult t
90 f cell phenotypes and matrix architecture in cardiac valves during fetal maturation and postnatal ada
91  microRNA 21 (miR-21), which is expressed in cardiac valve endothelium during development, in order t
92  E416D mutant enzymes were unable to restore cardiac valve formation and could only partially rescue
93 hese results suggest that FOG-2 functions in cardiac valve formation as an attenuator of EMT by repre
94         To gain mechanistic understanding of cardiac valve formation at single-cell resolution and in
95 h signaling pathway is crucial for primitive cardiac valve formation by epithelial-mesenchymal transi
96                                              Cardiac valve formation is a complex process that involv
97                                       During cardiac valve formation, Dll4-Notch1 signaling leads to
98 e gene expression in lymphocytes and control cardiac valve formation.
99 l-transduction processes required for normal cardiac valve formation.
100 in early cardiac morphogenesis as well as in cardiac valve formation.
101   Several gene mutations are known to affect cardiac valve formation.
102 rophages were abundant in inflamed/rheumatic cardiac valves from both mice and humans.
103                                        Human cardiac valves have distinct patterns of innervation tha
104 comitant inflammation of synovial joints and cardiac valves in disorders such as rheumatic fever and
105 alpha interaction as a key driver of chronic cardiac valve inflammation and suggest these molecules a
106 is specifically prevented the development of cardiac valve inflammation.
107  clinical sequelae, such as life-threatening cardiac valve involvement.
108 and that renal stones developed at 64 years, cardiac-valve involvement at 54 years, and coronary-arte
109 lopment of the extracellular matrix (ECM) of cardiac valves is necessary for proper heart function.
110 r, these results suggest a role of FGF-4 for cardiac valve leaflet formation through proliferative ex
111                                              Cardiac valve leaflets and large conduit arteries have b
112                                              Cardiac valve leaflets develop from rudimentary structur
113 , which confer biomechanical strength to the cardiac valve leaflets.
114 diovascular development in the maturation of cardiac valve leaflets.
115  activation may be an important mechanism in cardiac valve maintenance and function by enhancing endo
116 tor to transduce reverse signals involved in cardiac valve maturation and axon pathfinding.
117 predominantly by valvular endocardium during cardiac valve maturation, exhibited enlarged valves.
118                                   Defects in cardiac valve morphogenesis and septation of the heart c
119 ial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis.
120                PFE occurred most commonly on cardiac valves (n = 400 [78%]).
121 tations comprised of fibrin and platelets on cardiac valves, NBTE poses a diagnostic challenge due to
122                                              Cardiac valves of transgenic mice expressing human TNF d
123       This results in excess Collagen within cardiac valves of uninjured hearts.
124 ic surgery, it now is apparent that standard cardiac valve operations can be performed through very s
125 acement, or a previous operation involving a cardiac valve or ascending aorta.
126  clinical outcomes among patients undergoing cardiac valve or proximal aortic surgery with vs without
127                      Among adults undergoing cardiac valve or proximal aortic surgery, intraoperative
128 was receipt of intraoperative TEE during the cardiac valve or proximal aortic surgery.
129 (64.6%) were male, 39 (30.0%) had prosthetic cardiac valve or valve repair, 21 (16.2%) cardiac implan
130 rdiogenic emboli in patients with mechanical cardiac valves or nonvalvular atrial fibrillation.
131 es in either initial adherence of strains to cardiac valves or vegetation weights.
132                                              Cardiac valves originate from endocardial cushions (EC)
133 ighly expressed in the embryonic periosteum, cardiac valves, placenta, and periodontal ligament as we
134                                              Cardiac valve procedures are commonly performed concurre
135 an and GAS proteins triggers proinflammatory cardiac valve-reactive T cells.
136 mine is associated with an increased risk of cardiac-valve regurgitation.
137 at endocardial hematopoiesis is critical for cardiac valve remodeling as a source of tissue macrophag
138 aled that these macrophages are essential in cardiac valve remodeling.
139 e impacted by the findings of these studies: cardiac valve repair and replacement, assessment of vent
140 aving coronary artery bypass grafting and/or cardiac valve repair or replacement from 2009 to 2011.
141 ients aged at least 18 years undergoing open cardiac valve repair or replacement surgery and/or proxi
142  of US kidney transplantation patients after cardiac valve replacement and to compare associations of
143           Although some patients who require cardiac valve replacement clearly benefit more from one
144           Allograft valves have been used in cardiac valve replacement for 35 years.
145  142 women; mean age 68 years) who underwent cardiac valve replacement surgery between 1994 and 1998.
146 portion pulmonary hypertension who underwent cardiac valve replacement surgery.
147 rence in survival of dialysis patients after cardiac valve replacement with tissue versus nontissue p
148            Seventeen patients, who underwent cardiac valve replacement, completed a neuropsychologica
149  hip fracture repair, lung cancer resection, cardiac valve replacement, coronary angioplasty, pancrea
150  scheduled for coronary artery bypass graft, cardiac valve replacement, or both.
151 o underwent coronary artery bypass grafting, cardiac valve replacement, or total joint arthroplasty (
152 on patients hospitalized in 1991 to 2004 for cardiac valve replacement.
153 r findings, including abnormalities of other cardiac valves, septal defects, persistent left superior
154 lopmental defects in the endocardial-derived cardiac valve, septum, and vasculature.
155 , Pannus, Paravalvular Leak, CT Angiography, Cardiac, Valves Supplemental material is available for t
156 nd short-axis imaging readily disclosed each cardiac valve, support structures and chamber, as well a
157 nomorphic ventricular tachycardia (VT) after cardiac valve surgeries have not been studied extensivel
158                        In patients with both cardiac valve surgery and dialysis treatment (n = 197),
159 gery, percutaneous coronary intervention, or cardiac valve surgery between January 1, 2009 and Septem
160  more comorbidities and more often underwent cardiac valve surgery compared with nondialysis patients
161                                              Cardiac valve surgery has seen a rapid and ongoing evolu
162                                              Cardiac valve surgery is, consequently, becoming much mo
163 post-operative conduction disturbances after cardiac valve surgery requiring a permanent pacemaker (P
164 ing, percutaneous coronary intervention, and cardiac valve surgery were most strongly associated with
165                  Among patients referred for cardiac valve surgery, age does not appear to limit the
166 ans for percutaneous coronary interventions, cardiac valve surgery, and pediatric cardiac surgery (on
167 ong-term survival of dialysis patients after cardiac valve surgery.
168 e review the evolution of minimally invasive cardiac valve surgery.
169 oaches have become increasingly important in cardiac valve surgery.
170 laces both native cardiac ventricles and all cardiac valves, thus eliminating problems commonly seen
171 es, we developed a tissue model using rabbit cardiac valves to investigate the interaction of A. acti
172 acterial adhesion to the vessel wall and the cardiac valves under flow.
173  in zebrafish embryos leads to hypercellular cardiac valves, whereas Notch inhibition prevents valve
174              This is exemplified by EndMT in cardiac valves, which are lined with a specialized endot
175 opmental valve anomalies and have myxomatous cardiac valves with 100% penetrance.

 
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