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1 peutically, GM-CSF blockade markedly reduces cardiac disease.
2 e child had a history of difficult airway or cardiac disease.
3 ic DNA modification associated recently with cardiac disease.
4 ic risk is crucial for guiding management of cardiac disease.
5 well as its any potential therapeutic use in cardiac disease.
6 maller and they developed microphthalmia and cardiac disease.
7  play important roles in the pathogenesis of cardiac disease.
8  excluding patients with clinically manifest cardiac disease.
9 ibrillation occurs in patients without known cardiac disease.
10 role for Mbnl1 loss in the initiation of DM1 cardiac disease.
11 sion associated with PTWI were predictive of cardiac disease.
12  select patients with congenital or acquired cardiac disease.
13 ill patients, specifically in the setting of cardiac disease.
14 ac T1 mapping in 62 subjects with or without cardiac disease.
15 ergetic remodeling during the progression of cardiac disease.
16 ents of advanced age and/or with preexisting cardiac disease.
17 ealing and smooth muscle cell dysfunction in cardiac disease.
18 ditions related to age, such as diabetes and cardiac disease.
19  of a road traffic accident and pre-existing cardiac disease.
20 potential novel therapeutic targets to treat cardiac disease.
21 y in these mice fully prevented the onset of cardiac disease.
22 relevant to novel redox-related therapies in cardiac disease.
23 ncluding neurological, ocular, skeletal, and cardiac disease.
24 d as therapeutic agents for the treatment of cardiac disease.
25 eal a clinical relevance of the SIV motif in cardiac disease.
26 agulants, antiplatelets and aspirin to treat cardiac disease.
27  considered unsuitable because of coexisting cardiac disease.
28 rrent chemotherapy, and 27% had pre-existing cardiac disease.
29  is important because it is often altered in cardiac disease.
30 and may accentuate structural and functional cardiac disease.
31  are at high risk of complications including cardiac disease.
32 se in a community-based cohort without overt cardiac disease.
33  in the pathogenesis of CHD as well as adult cardiac disease.
34 rs following exposure in patients with known cardiac disease.
35  approximately 2-fold in individuals without cardiac disease.
36  ERbeta agonists as HDAC modulators to treat cardiac disease.
37 lopment and/or progression of HIV-associated cardiac disease.
38 ation of their expression has been linked to cardiac disease.
39 n status varies in different mouse models of cardiac disease.
40 ty, including safety in patients with stable cardiac disease.
41 pite being potential therapeutic targets for cardiac disease.
42 nd may provide a novel therapeutic target in cardiac disease.
43  adult survivors previously undiagnosed with cardiac disease.
44 therapeutic strategy to limit the effects of cardiac disease.
45 impaired relaxation with 15 controls without cardiac disease.
46 anges to Na(v)1.5 in congenital and acquired cardiac disease.
47 ion has important diagnostic implications in cardiac disease.
48 mortality risk in drug-treated patients with cardiac disease.
49 rodent model of primary kidney and secondary cardiac disease.
50 injectable CGRP analogue may be effective in cardiac disease.
51  enabling broad application in patients with cardiac disease.
52 which have not been implicated previously in cardiac disease.
53 ) and repolarizing (Ito) currents altered in cardiac disease.
54 enetic causes or major risk contributors for cardiac disease.
55 tin on a genome-wide scale in the setting of cardiac disease.
56 ocardiography were used to evaluate possible cardiac disease.
57 of exercise and statins to treat age-related cardiac disease.
58 raphic (ECG) screening of young athletes for cardiac disease.
59 ale, 3 female), with no history of any overt cardiac disease.
60 ux and ameliorating morbidity in proteotoxic cardiac disease.
61 e in both healthy children and children with cardiac disease.
62       Two thousand sixteen survivors died of cardiac disease.
63 ranslational regulatory mechanisms of JP2 in cardiac diseases.
64 l for screening variants involved in genetic cardiac diseases.
65 gly used for the diagnosis and management of cardiac diseases.
66 thus influences the evolution and outcome of cardiac diseases.
67 hereas it is common in patients with certain cardiac diseases.
68 wedish hospitals that provide care for acute cardiac diseases.
69 sfolded proteins are an emerging hallmark of cardiac diseases.
70 rtality and cardiovascular events in several cardiac diseases.
71 he genetic and molecular basis of hereditary cardiac diseases.
72 pared with secondary prevention in inherited cardiac diseases.
73 g the benefit of PKG stimulation in treating cardiac diseases.
74 ded and without history of diabetes or other cardiac diseases.
75  those derived from patients with hereditary cardiac diseases.
76 ial thickness (LVMT) is a feature of several cardiac diseases.
77 al data with regard to the use of PDE5Is for cardiac diseases.
78 ardiac lincRNAs during heart development and cardiac diseases.
79 hould raise suspicion of other, superimposed cardiac diseases.
80  to be important biomarkers for diagnosis of cardiac diseases.
81 ate, in relation to subclinical and clinical cardiac diseases.
82 excess deaths were accounted for by SPNs and cardiac diseases.
83     Myocardial fibrosis is a feature of many cardiac diseases.
84 -couplon-remodelling processes that underlie cardiac diseases.
85 ages in 300 consecutive participants free of cardiac disease (169 women; 65.6 +/- 8.5 years) of the M
86  hemorrhage (18.8%), cardiomyopathy or other cardiac disease (18.3%), genitourinary infection (11.5%)
87 iagnosis were attributable to SPNs (50%) and cardiac diseases (25%).
88 were not candidates for CTA because of prior cardiac disease (41%) or imaging contraindications (16%)
89 rbidities (including varicose veins, IBD, or cardiac disease), a body mass index (BMI) of 30 kg/m(2)
90 luripotent stem cell platform to model human cardiac disease according to a stage-specific cardiogeni
91                          By monitoring human cardiac disease according to stage-specific cardiogenesi
92 ry endpoint was hospitalization/death due to cardiac disease after 2 years.
93 n a prospective study of Dutch patients with cardiac disease (Alpha Omega Cohort), we examined the ri
94       We investigated the characteristics of cardiac disease among adolescents with HIV infection dia
95                                   Studies of cardiac disease among adult survivors of childhood cance
96                                In almost all cardiac diseases, an increase in extracellular matrix (E
97     Obese patients are at increased risk for cardiac disease and are more likely to need invasive car
98  and other drugs are in development to treat cardiac disease and cancer and to improve cognitive func
99 s study found that biomarkers of subclinical cardiac disease and clinically manifest cardiac diseases
100 sociation of blood biomarkers of subclinical cardiac disease and clinically manifest cardiac diseases
101 onin I, which have important implications in cardiac disease and could also have potential as a model
102 strategies to decrease the risk of premature cardiac disease and death in children with CKD.
103                       The disentanglement of cardiac disease and device-related concerns is difficult
104 cardial fat accumulation as a consequence of cardiac disease and epicardium to adipocyte differentiat
105 patients with severe chronic renal, lung, or cardiac disease and greater in older patients and in tho
106                                 Pre-existing cardiac disease and higher mean heart dose were signific
107 f Cavbeta2 both in a mouse model of diabetic cardiac disease and in 6 diabetic and 7 nondiabetic card
108 ephrine has been used safely in mothers with cardiac disease and in pregnancies with suspected fetal
109 atients should include consideration of both cardiac disease and noncardiac conditions.
110 1 patients were less likely to have advanced cardiac disease and renal involvement.
111                 Prevention and management of cardiac disease and vascular risk factors may reduce the
112 ncentrations are associated with subclinical cardiac disease and with new heart failure and coronary
113 ing relative to the high prevalence of acute cardiac diseases and comorbidities.
114 ing performed to uncover the causes of human cardiac diseases and develop potential therapies.
115                             Murine models of cardiac diseases and human heart biopsies were analyzed
116 ions, how these systems remodel/adapt during cardiac disease, and finally how such knowledge can be l
117 oth is normally very low but is increased by cardiac disease, and genetic gain- or loss-of-function s
118 e eventually die at about 270 d, likely from cardiac disease, and hyperoxia-treated mice die within d
119 onset AF is common, linked to age, diabetes, cardiac disease, and neoadjuvant therapy.
120  years of age, subsequent primary neoplasms, cardiac disease, and other circulatory conditions accoun
121  how mutations in these proteins may lead to cardiac disease, and outlines future challenges in the f
122 p of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle
123 splantation comorbidities were pulmonary and cardiac diseases, and respiratory failure was the primar
124 eneration that could further inform acquired cardiac disease applications.
125      Depression and anxiety in patients with cardiac disease are common and independently associated
126  different microdomains and their changes in cardiac disease are not well understood.
127 n threshold level, which might be reduced in cardiac disease as a consequence of sensitization of rya
128 ion and anxiety disorders in inpatients with cardiac disease as part of a care management trial, an i
129  modulating QRS duration in subjects without cardiac disease as predictors of subsequent arrhythmias.
130 ed numerous de novo variants associated with cardiac disease as standing variation in ExAC, thus thes
131 metic peptide into a mouse model of diabetic cardiac disease associated with LTCC abnormalities resto
132    This includes the detection of underlying cardiac disease associated with sudden cardiac death and
133 lation of Cav1 may reduce arrhythmic risk in cardiac diseases associated with renin-angiotensin syste
134                                              Cardiac disease at baseline was assessed from the partic
135    Conclusion In patients without underlying cardiac disease at baseline, the addition of trastuzumab
136  de novo variants previously associated with cardiac disease based on a large population-representati
137 al metabolism affecting multiple organs with cardiac disease being the leading cause of death.
138 LI1) looking at 1-year survival showed donor cardiac disease, black ethnicity, and steatosis to be ad
139 sociated with emergency surgery and advanced cardiac disease but not stent type or timing of surgery
140 s) offer a new paradigm for modeling genetic cardiac diseases, but it is unclear whether mouse and hu
141  17-91 years; 143-200 cm; 32-240 kg) without cardiac disease by standard transthoracic echocardiograp
142                                         Some cardiac disease-causing mutations, however, have been as
143                                              Cardiac disease (CD) is one of the major side effects of
144 a population without preexisting symptomatic cardiac disease, children with CKD potentially receive s
145 ients were more likely to have advanced age, cardiac disease, chronic obstructive pulmonary disease,
146 d, the standardized mortality ratios for all cardiac diseases combined was greatest for individuals d
147                                              Cardiac disease constitutes an increasing proportion of
148                                 Furthermore, cardiac diseases contribute to disease severity in patie
149 rcutaneous Administration of Gene Therapy In Cardiac Disease (CUPID 1) study was a phase 1/phase 2 fi
150                            Patients with any cardiac disease, drug-positive urine test, electrolyte a
151 ]), idiopathic cardiomyopathy (0.4 [0.2-1]), cardiac disease duration greater than 2 years pre-extrac
152 n factors contributing to adenovirus-induced cardiac disease during acute and persistent infection.
153    Given the importance of ECM deposition in cardiac disease, ECM imaging could be a valuable clinica
154 ol for cause determination of arrhythmogenic cardiac diseases, efficient screening of family members,
155        Depression is common in patients with cardiac disease, especially in patients with heart failu
156 nsitivity is commonly observed with multiple cardiac diseases, especially familial cardiomyopathies.
157 ner and contribute to the pathophysiology of cardiac diseases, especially in cells lacking organized
158                            With aging and in cardiac disease, fibrosis caused by collagen deposition
159 c metabolism and abnormal redox state during cardiac diseases foment arrhythmogenic substrates throug
160 raphy in 439 participants free of stroke and cardiac disease from the Cardiovascular Abnormalities an
161 xt-generation sequencing assay for detecting cardiac disease gene mutations with improved accuracy, f
162                                  Eighty-nine cardiac disease genes were evaluated.
163          However, a role for this pathway in cardiac disease has not been evaluated.
164 rt failure, but clinical use of CPX in other cardiac diseases has been limited, in part because of a
165 rebral embolic events related to carotid and cardiac disease have been known for decades.
166 h lack mechanistic specificity, paradigms of cardiac disease have evolved to conceptualize myocardial
167                                         Many cardiac diseases have been associated with increased fib
168                     Subclinical and clinical cardiac diseases have been previously linked to magnetic
169 ase, are well-characterized proteinopathies, cardiac diseases have recently been associated with alte
170 s) prior to hospital admission, having known cardiac disease, having already participated in the tria
171 n multivariable analysis (MVA), pre-existing cardiac disease (hazard ratio [HR], 2.96; 95% CI, 1.07 t
172 ions regarding microRNA-mRNA interactions in cardiac disease, how disease alters mRNA targeting by sp
173 eserves cardiac function in animal models of cardiac disease; however, the mechanisms underlying thes
174           Entire cohort participants free of cardiac disease, hypertrophy, hypertension, and diabetes
175 s SCA cases presented with known preexisting cardiac disease in 16% and >/=1 cardiovascular risk fact
176 cules for personalized medicine and modeling cardiac disease in a dish, it is important to standardiz
177         Atrial fibrillation (AF) is a common cardiac disease in aging populations with high comorbidi
178             Clinicians should not screen for cardiac disease in asymptomatic, low-risk adults with re
179 ese mechanisms provide new ways to attenuate cardiac disease in elders by preemptive treatment of age
180 eutic targets and mechanistic biomarkers for cardiac disease in females.
181                            The management of cardiac disease in NMDs is made challenging by the broad
182 e an under-recognized component of inherited cardiac disease in some cases.
183                             The diagnosis of cardiac disease in the fetus is mostly made with ultraso
184 e link with metabolic syndrome, obesity, and cardiac disease in the general population require transl
185 olic processes underlying the development of cardiac disease in type II diabetes are not fully unders
186 ommon cause of acute vasculitis and acquired cardiac disease in US children.
187  The aim of the ALICE (Airflow Limitation in Cardiac Diseases in Europe) study was to investigate the
188 actors are disproportionately prone to these cardiac diseases in the setting of alcohol abuse.
189                                          The cardiac disease included cardiac conduction disease (CCD
190  Nav1.5 function is associated with multiple cardiac diseases including long-QT3 and Brugada syndrome
191 resent a novel approach for the treatment of cardiac disease, including atrial arrhythmias.
192 O3 genomic region and miRNAs associated with cardiac disease, including miR-208a, miR-208b, and miR-4
193 ns of intracellular ADP in specific types of cardiac disease, including those where myocardial energy
194     GJA1 mutations have been associated with cardiac diseases, including atrial fibrillation.
195 ncluded patients with a variety of high-risk cardiac diseases, including congestive heart failure (n=
196  dysregulation is associated with a range of cardiac diseases, including dilated cardiomyopathy (DCM)
197                        Similarly, many adult cardiac diseases involve transcriptional changes and som
198                        Stem cell therapy for cardiac disease is an exciting but highly controversial
199                                              Cardiac disease is an independent risk factor for naMCI;
200            The spectrum of radiation-induced cardiac disease is broad, potentially involving any comp
201      A link between excess dietary sugar and cardiac disease is clearly evident and has been largely
202 Mitral regurgitation in people without prior cardiac disease is considered a degenerative disease wit
203 their susceptibility to chemotherapy-induced cardiac disease is not well documented.
204 is beneficial for drug-treated patients with cardiac disease is not yet clear.
205 ributable to the stent versus the underlying cardiac disease is uncertain, as prior studies lack a co
206  is produced at elevated levels during human cardiac disease, is a pathogenic fragment that is suffic
207  stress, associated with a variety of common cardiac diseases, is well recognized to affect the funct
208 ted to exert cytoprotective effects in acute cardiac diseases, its effects on chronic heart failure a
209  ultimately contribute to the progression of cardiac disease, leading to an increase in interstitial
210  suggest that lncRNAs may be associated with cardiac disease, little is known about lncRNAs in the se
211 ng assessment of their clinical potential as cardiac disease markers.
212 s attending a memory clinic, suggesting that cardiac disease may contribute to the development of CMI
213           Physiologic adaptation, structural cardiac disease, medication use, and degree of concurren
214 rived cardiomyocytes are well established as cardiac disease model..
215                                          The cardiac disease models were administered with a locked n
216 enable development of personalized, in vitro cardiac disease models.
217 tudy examined how hemoglobin (Hgb) level and cardiac disease modify the relationship of RBC transfusi
218 f patients with no diagnoses consistent with cardiac disease (N = 74,785).
219 e of patients with paediatric and congenital cardiac disease, optimization of outcomes remains a cons
220                  Of 323 participants without cardiac disease or hypertension and with all regions eva
221  symptoms, medication, and family history of cardiac disease or sudden death were collected.
222     There is no association of EMAP with AMD cardiac diseases or cardiac risks, including cigarette s
223                No association was found with cardiac diseases or their risk factors.
224 y contribute to the pathogenesis of multiple cardiac diseases or traits.
225 hronic pulmonary disease, immune deficiency, cardiac disease, or previous episodes of wheezing or inh
226  male gender, Caucasian race, increased age, cardiac disease, organ failures, and disease severity.
227 me extent as do other chronic disorders (eg, cardiac diseases, osteoarthritis, lung disease, and poor
228 d a multicentre study to evaluate mortality, cardiac disease outcome, and risk factors for malignant
229 nificant associations were also observed for cardiac disease (p = 0.010) and BMI >/=25 kg/m(2) (p = 0
230 its dysregulation plays an important role in cardiac disease pathogenesis.
231 eliable pharmacological data and measures of cardiac disease phenotype in experimental cell, animal,
232 ing naproxen derivative, on the skeletal and cardiac disease phenotype in mdx mice.
233  (3) activation of autophagy ameliorated the cardiac disease phenotype in this mouse model.
234           Although LVT is altered in various cardiac diseases, physiological factors that affect LVT
235 t may have clinical value in prognosticating cardiac disease progression in patients.
236 cial in the heart, it largely contributes to cardiac disease progression when dysregulated.
237 tein that enhances expression of a subset of cardiac disease-promoting genes.
238 a biochemical signature of early subclinical cardiac disease, providing an opportunity for targeted p
239 e been numerous stem cell studies focused on cardiac diseases, ranging from proof-of-concept to phase
240    In the absence of metabolic or structural cardiac disease, rapid ventricular tachycardia (>200 bpm
241 se (rate ratio, 20.1; 95% CI, 17.2 to 23.4), cardiac disease (rate ratio, 3.7; 95% CI, 3.2 to 4.2), i
242 lating PKA/PDE4D3 molecular signaling during cardiac diseases, remains unclear.
243                         Proteinopathy causes cardiac disease, remodeling, and heart failure but the p
244      For many neuromuscular diseases (NMDs), cardiac disease represents a major cause of morbidity an
245                The Registry on Pregnancy and Cardiac Disease (ROPAC) is a global, prospective observa
246 mporary, worldwide Registry of Pregnancy and Cardiac disease (ROPAC), we describe the pregnancy outco
247  long telomeres protect mice from the lethal cardiac disease seen in humans with the same genetic def
248  of QRS duration in 5272 individuals without cardiac disease selected from electronic medical record
249 nding the effect of miRNA-based therapies in cardiac disease settings in males and females.
250                       Clinical suspicion for cardiac disease should be high and threshold for cardiac
251                    Subjects with no signs of cardiac disease showed a decrease in CD127(+)CD132(+) ce
252 tion of these pathways could be important in cardiac disease states affecting muscle compliance.
253 tic processes are increasingly identified in cardiac disease states.
254 tor (ICD) therapy in patients with inherited cardiac diseases stem from observational studies and are
255 ng claims before bevacizumab for thrombosis, cardiac disease, stroke, hemorrhage, hemoptysis, or GI p
256  was stronger in waitlisted patients without cardiac disease (subhazard ratio, 2.2; 95% CI, 1.6-3.1)
257 on of both modalities in assessment of other cardiac diseases such as inflammation and of other syste
258 s known to play a role in different types of cardiac disease, such as arrhythmogenic or hypertrophic
259 latory pathways are triggered in response to cardiac disease, such as those involving RNA-binding pro
260 actile dysfunction in inherited and acquired cardiac diseases, such as catecholaminergic polymorphic
261                                           In cardiac disease, t-tubule loss occurs and affects the sy
262 g-term adverse health risks, particularly of cardiac disease that is increased in other cancer popula
263 ed care must respond to the preponderance of cardiac disease that now occurs in combination with the
264 ide a framework to study the early stages of cardiac diseases that develop in utero.
265        Acute and chronic hypoxias are common cardiac diseases that lead often to arrhythmia and impai
266 infection by RBC threshold for patients with cardiac disease, the critically ill, those with acute up
267 curs in individuals without previously known cardiac disease, the identification of patients at risk
268  macrophage-associated biomarkers of CNS and cardiac disease, the role of antiretroviral therapy on t
269 ect serum cardiac troponin I, a biomarker of cardiac disease to 100 pg/ml within 4 mins, which is fas
270 ly unexplained cardiac arrest and no evident cardiac disease to identify the pathogenesis of cardiac
271 amines the epidemiology of radiation-induced cardiac disease together with its pathophysiology and ex
272 ty-seven participants with HIV without known cardiac disease underwent cardiac 18F-FDG-PET for assess
273 etes were diagnosed with potentially serious cardiac disease using all 3 criteria.
274 of C-reactive protein (CRP), a biomarker for cardiac disease, using a carbon nanofiber based biosenso
275 te analysis were age, APACHE II score, AIDS, cardiac disease, vascular disease, diabetes, SCCmec type
276  and functional improvement in patients with cardiac disease warrants identification of a novel stem
277                                              Cardiac disease was associated with an increased risk of
278                                              Cardiac disease was associated with an increased risk of
279                                              Cardiac disease was defined as a history of atrial fibri
280                                              Cardiac disease was established in 44.5% of athletes, wi
281                                              Cardiac disease was not associated with any type of MCI
282                      A significant burden of cardiac disease was seen among adolescents with vertical
283 nal z-disc proteins that might contribute to cardiac disease, we employed an in silico screen for car
284 years; range, 3 months-18 years) mostly with cardiac disease, we evaluated by multivariate analysis t
285   Because miR-378 significantly decreases in cardiac disease, we sought to compensate for its loss th
286 anisms regulating gap junction remodeling in cardiac disease, we sought to identify the functional pr
287              History of difficult airway and cardiac disease were also associated with cardiac arrest
288                    Patients with preexisting cardiac disease were excluded.
289  elevated NT-proBNP (>125 pg/ml) but free of cardiac disease were randomized.
290 s demonstrated that older age and history of cardiac disease were the most consistent predictors of c
291                                              Cardiac diseases were also highly prevalent (22% coronar
292 ical cardiac disease and clinically manifest cardiac diseases were associated with CMIs on 3-T MRI in
293 d April 1, 2011, 354 patients with inherited cardiac diseases were treated with ICDs.
294 cted involving patients without a history of cardiac disease who underwent elective cardiac catheteri
295                    Obese individuals without cardiac disease with (OB/MS+, n=124) and without (OB/MS-
296           Dengue viruses were shown to cause cardiac disease with clinical manifestations ranging fro
297  3-step approach to identify inpatients with cardiac disease with depression, generalized anxiety dis
298 iac-specific BEX1 transgenic mice show worse cardiac disease with stress stimulation, whereas Bex1 ge
299 ical cardiac disease and clinically manifest cardiac diseases with CMIs graded on 3-T MRI in a memory
300 dies and the outlook for future treatment of cardiac diseases with stem cell therapies.

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