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1 ho have exhibited early onset or accelerated cardiac allograft vasculopathy.
2  the association of mode of brain death with cardiac allograft vasculopathy.
3 arly and more severe allograft rejection and cardiac allograft vasculopathy.
4 ntrast with the known suppression by iNOS of cardiac allograft vasculopathy.
5 nhibitors protect against the development of cardiac allograft vasculopathy.
6 finitively link indirect allorecognition and cardiac allograft vasculopathy.
7 onary endothelial dysfunction contributes to cardiac allograft vasculopathy.
8 accelerated form of arteriosclerosis, termed cardiac allograft vasculopathy.
9  not STAT6, contribute to the development of cardiac allograft vasculopathy.
10  type of graft modification does not prevent cardiac allograft vasculopathy.
11 days and all long-surviving hearts developed cardiac allograft vasculopathy.
12 fter intracoronary stenting in patients with cardiac allograft vasculopathy.
13 giographic success in selected patients with cardiac allograft vasculopathy.
14 cularly immunosuppression, in these forms of cardiac allograft vasculopathy.
15 n coronary function in patients with diffuse cardiac allograft vasculopathy.
16 ms of angioscopically heterogeneous forms of cardiac allograft vasculopathy.
17 ely correlates with SMAD3 phosphorylation in cardiac allograft vasculopathy.
18 is a major contributor to the development of cardiac allograft vasculopathy.
19  coronary vascular changes may precede overt cardiac allograft vasculopathy.
20 y T cells and may have beneficial effects on cardiac allograft vasculopathy.
21 ttransplant lymphoproliferative disease, and cardiac allograft vasculopathy.
22 ting cellular trafficking, alloimmunity, and cardiac allograft vasculopathy.
23 eactive T cell activation and development of cardiac allograft vasculopathy.
24 pharmacotherapies to halt the progression of cardiac allograft vasculopathy.
25     No difference was found in deaths due to cardiac allograft vasculopathy.
26 modeling, may be an important determinant of cardiac allograft vasculopathy.
27 on and is associated with the development of cardiac allograft vasculopathy.
28 levels, which may in turn reduce the risk of cardiac allograft vasculopathy.
29 gnificant risk factor for the development of cardiac allograft vasculopathy.
30 n therapy would attenuate the development of cardiac allograft vasculopathy.
31  well as to suppress the late development of cardiac allograft vasculopathy.
32 or and immunosuppressive agent, may suppress cardiac-allograft vasculopathy.
33 o be beneficial in preventing development of cardiac allograft vasculopathy, a long-term nemesis in c
34 -segment-elevation myocardial infarction and cardiac allograft vasculopathy after heart transplantati
35 se include a higher risk of acute rejection, cardiac allograft vasculopathy after heart transplantati
36 er transplantation, may increase the risk of cardiac allograft vasculopathy and allograft loss, but n
37 cant determinant for the late development of cardiac allograft vasculopathy and influences long-term
38  Understanding of the mechanisms surrounding cardiac allograft vasculopathy and insight into the poss
39 F may provide long-term benefits in reducing cardiac allograft vasculopathy and those evaluating the
40 ated by cohort for time until graft failure, cardiac allograft vasculopathy, and hospitalization for
41     ET-1 may also play a significant role in cardiac allograft vasculopathy, and in animal models, ER
42 antation and reflects diastolic dysfunction, cardiac allograft vasculopathy, and poor late outcome.
43  delayed alloantibody production, suppressed cardiac allograft vasculopathy, and tended to further pr
44 hogenesis, natural history, and diagnosis of cardiac allograft vasculopathy, and to outline new preve
45 ion and risk stratification of patients with cardiac allograft vasculopathy are problematic.
46 tion during the first year, or likelihood of cardiac allograft vasculopathy at 1 year after transplan
47 oronary IVUS data show that H+LTx attenuates cardiac allograft vasculopathy by decreasing the rate of
48 TAT4-mediated signaling pathways may promote cardiac allograft vasculopathy by directing Th1-specific
49     Moreover, imatinib mesylate enhanced rat cardiac allograft vasculopathy, cardiac fibrosis, and la
50 letion to modulate alloimmunity or attenuate cardiac allograft vasculopathy (CAV) (classic chronic re
51 e novo donor-specific antibodies (DSAs), and cardiac allograft vasculopathy (CAV) after heart transpl
52  acute antibody-mediated rejection (AMR) and cardiac allograft vasculopathy (CAV) after human heart t
53 s to describe prevalence and impact of RR on cardiac allograft vasculopathy (CAV) and graft loss afte
54 tion is a risk factor for the development of cardiac allograft vasculopathy (CAV) and is associated w
55 ual targets suggest their important roles in cardiac allograft vasculopathy (CAV) and rejection.
56                    Group 1 animals developed cardiac allograft vasculopathy (CAV) and rejection.
57 hort course of cyclosporine developed florid cardiac allograft vasculopathy (CAV) and were rejected w
58 e evaluated the association between Lp-PLA2, cardiac allograft vasculopathy (CAV) assessed by 3D intr
59 as associated with an increased incidence of cardiac allograft vasculopathy (CAV) at 1 year postcardi
60 ulted in prolonged graft survival and marked cardiac allograft vasculopathy (CAV) by histology (mean
61                                              Cardiac allograft vasculopathy (CAV) causes impaired blo
62                                              Cardiac allograft vasculopathy (CAV) causes impaired blo
63                                              Cardiac allograft vasculopathy (CAV) causes late graft f
64 oronary angiography is the gold standard for cardiac allograft vasculopathy (CAV) diagnosis, but it u
65                                              Cardiac allograft vasculopathy (CAV) has a high prevalen
66                                              Cardiac allograft vasculopathy (CAV) has an incidence of
67                                              Cardiac allograft vasculopathy (CAV) has become a major
68 eous coronary intervention (PCI) to palliate cardiac allograft vasculopathy (CAV) has been associated
69 sessed clinical predictors of the process of cardiac allograft vasculopathy (CAV) in 39 consecutive p
70  tomography angiography (CCTA) for detecting cardiac allograft vasculopathy (CAV) in comparison with
71 ial intima termed transplant vasculopathy or cardiac allograft vasculopathy (CAV) in heart transplant
72 elial dysfunction may be an early marker for cardiac allograft vasculopathy (CAV) in orthotopic heart
73 aluable tool for noninvasive surveillance of cardiac allograft vasculopathy (CAV) in patients with he
74 o play a central role in the pathogenesis of cardiac allograft vasculopathy (CAV) in patients with he
75 ls (APCs) do not reject acutely, but develop cardiac allograft vasculopathy (CAV) in untreated recipi
76                                              Cardiac allograft vasculopathy (CAV) is a challenging co
77                                              Cardiac allograft vasculopathy (CAV) is a common cause o
78 eful model that has evolved for the study of cardiac allograft vasculopathy (CAV) is a heterotopic (a
79                                              Cardiac allograft vasculopathy (CAV) is a leading cause
80                                              Cardiac allograft vasculopathy (CAV) is a leading cause
81                                              Cardiac allograft vasculopathy (CAV) is a leading contri
82                                              Cardiac allograft vasculopathy (CAV) is a major cause of
83                                              Cardiac allograft vasculopathy (CAV) is a major contribu
84                                              Cardiac allograft vasculopathy (CAV) is a major impedime
85                                              Cardiac allograft vasculopathy (CAV) is a major limitati
86                                              Cardiac allograft vasculopathy (CAV) is an increasingly
87                                              Cardiac allograft vasculopathy (CAV) is an obliterative
88                                              Cardiac allograft vasculopathy (CAV) is associated with
89                                              Cardiac allograft vasculopathy (CAV) is one of the leadi
90                                              Cardiac allograft vasculopathy (CAV) is the leading caus
91  Chronic rejection in transplanted hearts or cardiac allograft vasculopathy (CAV) is the leading caus
92                                              Cardiac allograft vasculopathy (CAV) is the main cause o
93                                      Because cardiac allograft vasculopathy (CAV) is the major cause
94                                              Cardiac allograft vasculopathy (CAV) is the preeminent c
95                                              Cardiac allograft vasculopathy (CAV) is the principal ca
96                                     Although cardiac allograft vasculopathy (CAV) is typically charac
97 hy has been clearly established, its role in cardiac allograft vasculopathy (CAV) is unclear.
98                                              Cardiac allograft vasculopathy (CAV) leads to impaired m
99                                              Cardiac allograft vasculopathy (CAV) limits the long-ter
100                                              Cardiac allograft vasculopathy (CAV) limits the long-ter
101                                        Early cardiac allograft vasculopathy (CAV) prognostication is
102 el wall inflammation and its significance in cardiac allograft vasculopathy (CAV) progression.
103 of concomitant in-stent restenosis (ISR) and cardiac allograft vasculopathy (CAV) progression.
104              The mechanisms and treatment of cardiac allograft vasculopathy (CAV) remain elusive.
105                                              Cardiac allograft vasculopathy (CAV) remains a leading c
106                                              Cardiac allograft vasculopathy (CAV) remains a major cau
107                                              Cardiac allograft vasculopathy (CAV) remains a significa
108                                              Cardiac allograft vasculopathy (CAV) remains the Achille
109                                              Cardiac allograft vasculopathy (CAV) remains the leading
110                                              Cardiac allograft vasculopathy (CAV) remains the leading
111 cular magnetic resonance (CMR) for detecting cardiac allograft vasculopathy (CAV) using contemporary
112                                              Cardiac allograft vasculopathy (CAV) was graduated in ac
113      A role for natural killer (NK) cells in cardiac allograft vasculopathy (CAV) was suggested by ou
114  between cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on p
115  between cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on p
116 l-free DNA level within 1 y and incidence of cardiac allograft vasculopathy (CAV) within 3 y post-HT.
117               Progressive arterial stenosis (cardiac allograft vasculopathy (CAV)) is a leading cause
118  graft arteriosclerosis (AGA), also known as cardiac allograft vasculopathy (CAV), after cardiac tran
119                                              Cardiac allograft vasculopathy (CAV), an unusually accel
120  on the initial TTE for recipient mortality, cardiac allograft vasculopathy (CAV), and primary graft
121 everolimus may reduce the risk of rejection, cardiac allograft vasculopathy (CAV), chronic kidney dis
122 ages of this approach include attenuation of cardiac allograft vasculopathy (CAV), improvement in glo
123  of CD8 lymphocytes, in chronic rejection or cardiac allograft vasculopathy (CAV), is incompletely un
124 and acute cellular rejection, CMV infection, cardiac allograft vasculopathy (CAV), malignancies, and
125 ival, 10-year survival, 10-year freedom from cardiac allograft vasculopathy (CAV), non-fatal major ad
126                        Chronic rejection, or cardiac allograft vasculopathy (CAV), remains the leadin
127  chronic rejection of transplanted hearts or cardiac allograft vasculopathy (CAV).
128 n the pathophysiologic mechanisms underlying cardiac allograft vasculopathy (CAV).
129  efficacy of immunotherapy or development of cardiac allograft vasculopathy (CAV).
130 chronic rejection of transplanted hearts, or cardiac allograft vasculopathy (CAV).
131 f TSP-1 in allografts and the development of cardiac allograft vasculopathy (CAV).
132 ecruitment and precede intimal thickening in cardiac allograft vasculopathy (CAV).
133 rosis play a major role in the occurrence of cardiac allograft vasculopathy (CAV).
134 es of AR, graft survival, and development of cardiac allograft vasculopathy (CAV).
135 owth factors are postulated to contribute to cardiac allograft vasculopathy (CAV).
136 helium is associated with the development of cardiac allograft vasculopathy (CAV).
137 plantation (CTx) in patients with or without cardiac allograft vasculopathy (CAV).
138 ACR), antibody-mediated rejection (AMR), and cardiac allograft vasculopathy (CAV).
139 t 1 year after HTx and future development of cardiac allograft vasculopathy (CAV).
140 l homeostasis may prevent the development of cardiac allograft vasculopathy (CAV).
141 art is a central event in the development of cardiac allograft vasculopathy (CAV).
142 pressures to augment angiographic grading of cardiac allograft vasculopathy (CAV); however, no data e
143                Finally, in a murine model of cardiac allograft vasculopathy, depletion of donor CD4 n
144 gic risk factors with the different forms of cardiac allograft vasculopathy detected angioscopically.
145 icacy to prolong graft survival and to delay cardiac allograft vasculopathy development and antidonor
146 ngation of graft survival and suppression of cardiac allograft vasculopathy development.
147 nset CAV from disease controls (Histological Cardiac Allograft Vasculopathy Diagnostic Model [HistoCA
148 munologic risk factors to the development of cardiac allograft vasculopathy distinguished angioscopic
149 hibition to lower cholesterol and to prevent cardiac allograft vasculopathy early after HT are not we
150 ly events influence the later development of cardiac allograft vasculopathy following heart transplan
151 e incidence of primary graft dysfunction and cardiac allograft vasculopathy-free survival did not sig
152 arly posttransplant bleeding, rejection, and cardiac allograft vasculopathy-free survival.
153 ed into STAT6 -/- (n=11), the development of cardiac allograft vasculopathy (frequency 62+/-8%, sever
154 ts prevalence was positively associated with cardiac allograft vasculopathy grade.
155 splantation, indication for transplantation, cardiac allograft vasculopathy, history of rejection, an
156 CI, 1.59-5.23; P<0.001) after adjustment for cardiac allograft vasculopathy, history of rejection, ti
157 myocardial fibrosis variables to models with cardiac allograft vasculopathy, history of rejection, ti
158 al, and prevents alloantibody production and cardiac allograft vasculopathy in a stringent preclinica
159                            4C T cells caused cardiac allograft vasculopathy in the absence of other T
160 y, we sought to examine the heterogeneity of cardiac allograft vasculopathy in vivo using coronary an
161                                              Cardiac allograft vasculopathy is a complicated interpla
162                 These findings indicate that cardiac allograft vasculopathy is a heterogeneous diseas
163                                              Cardiac allograft vasculopathy is a key prognostic deter
164                                              Cardiac allograft vasculopathy is a major cause of death
165                                              Cardiac allograft vasculopathy is a major challenge to l
166                                              Cardiac allograft vasculopathy is a multifactorial proce
167                                              Cardiac allograft vasculopathy is an important cause of
168                                              Cardiac allograft vasculopathy is an important risk fact
169 s to treat discrete lesions in patients with cardiac allograft vasculopathy is associated with higher
170                                              Cardiac allograft vasculopathy is the major cause of lat
171                                              Cardiac allograft vasculopathy is the major limiting fac
172 cacy in reducing restenosis in patients with cardiac allograft vasculopathy is unknown.
173 rferon-gamma--producing T cells and enhanced cardiac allograft vasculopathy lesion formation.
174                                              Cardiac allograft vasculopathy lesions contain alloreact
175 , and to minimize late complications such as cardiac allograft vasculopathy, malignancy, and renal dy
176 e no significant differences in incidence of cardiac allograft vasculopathy (odds ratio 1.59, P = .21
177 on, but similar 5-year survival and rates of cardiac allograft vasculopathy or graft dysfunction.
178 associated with intermediate-term mortality, cardiac allograft vasculopathy, or primary graft failure
179  clinical model (Clinical Risk Factor Future Cardiac Allograft Vasculopathy Prediction Model [ClinCAV
180 ant EMBs were developed (Histological Future Cardiac Allograft Vasculopathy Prediction Model [HistoCA
181 ted Histological/Clinical Risk Factor Future Cardiac Allograft Vasculopathy Prediction Model [iCAV-Pr
182 imary immunosuppressant attenuates long-term cardiac allograft vasculopathy progression and may impro
183 ucing calcineurin inhibitor use, attenuating cardiac allograft vasculopathy progression and reducing
184 osuppressant in the long-term attenuation of cardiac allograft vasculopathy progression and the effec
185 hat is not fully explained by attenuation of cardiac allograft vasculopathy progression.
186  SRL as primary immunosuppression attenuates cardiac allograft vasculopathy progression.
187 s a primary immunosuppressant in attenuating cardiac allograft vasculopathy progression.
188 rular filtration rate, previously documented cardiac allograft vasculopathy), relative perfusion defe
189                                              Cardiac allograft vasculopathy remains a major limiting
190       Cardiac transplant arteriosclerosis or cardiac allograft vasculopathy remains the leading cause
191  particular, by chronic rejection leading to cardiac allograft vasculopathy, remains a major cause of
192                            Immunostaining of cardiac allograft vasculopathy samples revealed that p30
193 man SMC, and human arteriovenous fistula and cardiac allograft vasculopathy samples to assess the rol
194 timal hyperplastic arteriovenous fistula and cardiac allograft vasculopathy samples, and inversely co
195 ile coronary angiography is the standard for cardiac allograft vasculopathy screening and diagnosis,
196           IDEC-131-treated grafts had higher cardiac allograft vasculopathy severity scores during tr
197                                              Cardiac allograft vasculopathy severity varied with time
198 reased graft survival and the development of cardiac allograft vasculopathy, suggesting a contributio
199 ne in reducing the severity and incidence of cardiac-allograft vasculopathy, suggesting that everolim
200                                              Cardiac allograft vasculopathy, the leading cause of gra
201                                              Cardiac allograft vasculopathy, the nature of the inflam
202 study a mouse model of autoantibody-mediated cardiac allograft vasculopathy to clarify the alloimmune
203 tter understanding of the pathophysiology of cardiac allograft vasculopathy to direct interventions f
204     Secondary outcomes included incidence of cardiac allograft vasculopathy, treated rejection, renal
205                                   Similarly, cardiac allograft vasculopathy up to 5 years and primary
206 tect the heart graft from the development of cardiac allograft vasculopathy using coronary three-dime
207                               (Prevention of Cardiac Allograft Vasculopathy Using Rituximab [Rituxan]
208                   The CTOT-11 (Prevention of Cardiac Allograft Vasculopathy Using Rituximab Therapy i
209 ted tomography angiography (CTA) to rule out cardiac allograft vasculopathy versus 16 patients withou
210                        Freedom from moderate cardiac allograft vasculopathy was 94% at 5 y.
211  a clinically relevant large animal model of cardiac allograft vasculopathy, we immunized MHC inbred
212 ption factor signaling pathways that mediate cardiac allograft vasculopathy, we used mice with target

 
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