ライフサイエンスコーパス: cardiac disease

1 excluding patients with clinically manifest cardiac disease.

2 ents of advanced age and/or with preexisting cardiac disease.

3 mortality risk in drug-treated patients with cardiac disease.

4 rodent model of primary kidney and secondary cardiac disease.

5 injectable CGRP analogue may be effective in cardiac disease.

6 enabling broad application in patients with cardiac disease.

7 which have not been implicated previously in cardiac disease.

8 ) and repolarizing (Ito) currents altered in cardiac disease.

9 enetic causes or major risk contributors for cardiac disease.

10 tin on a genome-wide scale in the setting of cardiac disease.

11 ocardiography were used to evaluate possible cardiac disease.

12 of exercise and statins to treat age-related cardiac disease.

13 raphic (ECG) screening of young athletes for cardiac disease.

14 ale, 3 female), with no history of any overt cardiac disease.

15 ux and ameliorating morbidity in proteotoxic cardiac disease.

16 e in both healthy children and children with cardiac disease.

17 Two thousand sixteen survivors died of cardiac disease.

18 peutically, GM-CSF blockade markedly reduces cardiac disease.

19 e child had a history of difficult airway or cardiac disease.

20 ic DNA modification associated recently with cardiac disease.

21 ic risk is crucial for guiding management of cardiac disease.

22 well as its any potential therapeutic use in cardiac disease.

23 maller and they developed microphthalmia and cardiac disease.

24 play important roles in the pathogenesis of cardiac disease.

25 ibrillation occurs in patients without known cardiac disease.

26 role for Mbnl1 loss in the initiation of DM1 cardiac disease.

27 sion associated with PTWI were predictive of cardiac disease.

28 select patients with congenital or acquired cardiac disease.

29 ill patients, specifically in the setting of cardiac disease.

30 ac T1 mapping in 62 subjects with or without cardiac disease.

31 ergetic remodeling during the progression of cardiac disease.

32 ealing and smooth muscle cell dysfunction in cardiac disease.

33 ditions related to age, such as diabetes and cardiac disease.

34 donors, selected for their absence of overt cardiac disease.

35 of a road traffic accident and pre-existing cardiac disease.

36 potential novel therapeutic targets to treat cardiac disease.

37 y in these mice fully prevented the onset of cardiac disease.

38 relevant to novel redox-related therapies in cardiac disease.

39 ncluding neurological, ocular, skeletal, and cardiac disease.

40 d as therapeutic agents for the treatment of cardiac disease.

41 eal a clinical relevance of the SIV motif in cardiac disease.

42 agulants, antiplatelets and aspirin to treat cardiac disease.

43 considered unsuitable because of coexisting cardiac disease.

44 is important because it is often altered in cardiac disease.

45 an age, 54 years +/- 15) being evaluated for cardiac disease.

46 dormant in health, yet become functional in cardiac disease.

47 tic, diagnostic, and therapeutic proteins in cardiac disease.

48 dormant in health, yet become functional in cardiac disease.

49 eneration, and its potential contribution to cardiac disease.

50 ard toward clinical application as a cure of cardiac disease.

51 ovel isoform and how it contributes to human cardiac disease.

52 e heart, and their relative contributions in cardiac disease.

53 immunotherapeutic drugs for the treatment of cardiac disease.

54 lation, highlighting its importance in human cardiac disease.

55 multiple sclerosis, brain damage, nausea and cardiac disease.

56 successful management of pregnant women with cardiac disease.

57 nset of symptoms, arising from an underlying cardiac disease.

58 rrent chemotherapy, and 27% had pre-existing cardiac disease.

59 ell type- and stage-specific intervention in cardiac diseases.

60 ate, in relation to subclinical and clinical cardiac diseases.

61 -couplon-remodelling processes that underlie cardiac diseases.

62 l for screening variants involved in genetic cardiac diseases.

63 ardiac lincRNAs during heart development and cardiac diseases.

64 hould raise suspicion of other, superimposed cardiac diseases.

65 to be important biomarkers for diagnosis of cardiac diseases.

66 asingly popular for continuous monitoring of cardiac diseases.

67 excess deaths were accounted for by SPNs and cardiac diseases.

68 mendous benefit for the treatment of diverse cardiac diseases.

69 Myocardial fibrosis is a feature of many cardiac diseases.

70 HRV changes are associated with cardiac diseases.

71 ranslational regulatory mechanisms of JP2 in cardiac diseases.

72 proBNP increase in patients with preexistent cardiac diseases.

73 gly used for the diagnosis and management of cardiac diseases.

74 thus influences the evolution and outcome of cardiac diseases.

75 hereas it is common in patients with certain cardiac diseases.

76 wedish hospitals that provide care for acute cardiac diseases.

77 sfolded proteins are an emerging hallmark of cardiac diseases.

78 rtality and cardiovascular events in several cardiac diseases.

79 genesis of several chronic pressure overload cardiac diseases.

80 arrhythmogenesis and sudden death in several cardiac diseases.

81 d heart VGKC are related to neurological and cardiac diseases.

82 , can be a powerful tool for radiosurgery in cardiac diseases.

83 ossible window of action for cell therapy in cardiac diseases.

84 lthy relatives (25%) than in noninflammatory cardiac disease (1%), ischemic heart failure (1%), or he

85 iagnosis were attributable to SPNs (50%) and cardiac diseases (25%).

86 sthma (13 of 57 [23%] vs. 102 of 1297 [8%]), cardiac disease (26 of 55 [47%] vs. 115 of 1169 [10%]),

87 s (14.6%, P=0.00001) than in noninflammatory cardiac disease (3.75%), ischemic heart failure (2%), or

88 The cumulative incidence of cardiac disease 30 years from diagnosis was 4.8% (95% CI

89 were not candidates for CTA because of prior cardiac disease (41%) or imaging contraindications (16%)

90 Radiation-associated cardiac disease, a heterogeneous and complex disease, ma

91 o the prevalence and high mortality rates of cardiac diseases, a more detailed characterization of th

92 luripotent stem cell platform to model human cardiac disease according to a stage-specific cardiogeni

93 By monitoring human cardiac disease according to stage-specific cardiogenesi

94 1 [1.09-1.57] per 10-year increase), chronic cardiac disease (aHR 1.76 [1.08-2.86]), chronic pulmonar

95 n a prospective study of Dutch patients with cardiac disease (Alpha Omega Cohort), we examined the ri

96 Studies of cardiac disease among adult survivors of childhood cance

97 In almost all cardiac diseases, an increase in extracellular matrix (E

98 toring, further investigation for structural cardiac disease and a diagnostic workup for arterial hyp

99 sociation of blood biomarkers of subclinical cardiac disease and clinically manifest cardiac diseases

100 s study found that 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 cardial fat accumulation as a consequence of cardiac disease and epicardium to adipocyte differentiat

103 patients with severe chronic renal, lung, or cardiac disease and greater in older patients and in tho

104 actor in the progression of various forms of cardiac disease and heart failure(2).

105 y present as a promising option for treating cardiac disease and heart failure.

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 f a VA event onset among patients with known cardiac disease and indication for implanted cardioverte

109 milar clinical presentations, the underlying cardiac disease and precipitating factors may vary great

110 1 patients were less likely to have advanced cardiac disease and renal involvement.

111 y may reveal new insights into mechanisms of cardiac disease and serve as a test bed for drug screeni

112 ncentrations are associated with subclinical cardiac disease and with new heart failure and coronary

113 white noise; (e) HRV changes associated with cardiac diseases and aging can be interpreted as deterio

114 ing relative to the high prevalence of acute cardiac diseases and comorbidities.

115 ing performed to uncover the causes of human cardiac diseases and develop potential therapies.

116 es with the current literature when defining cardiac diseases and events across different studies and

117 Murine models of cardiac diseases and human heart biopsies were analyzed

118 that this protocol will improve modeling of cardiac diseases and testing of drugs.

119 d to identify molecular mechanisms for other cardiac diseases and traits.

120 tic variability associates with diagnoses of cardiac diseases and with modifiable risk factors which

121 ions, how these systems remodel/adapt during cardiac disease, and finally how such knowledge can be l

122 oth is normally very low but is increased by cardiac disease, and genetic gain- or loss-of-function s

123 e eventually die at about 270 d, likely from cardiac disease, and hyperoxia-treated mice die within d

124 onset AF is common, linked to age, diabetes, cardiac disease, and neoadjuvant therapy.

125 years of age, subsequent primary neoplasms, cardiac disease, and other circulatory conditions accoun

126 how mutations in these proteins may lead to cardiac disease, and outlines future challenges in the f

127 p of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle

128 eneration that could further inform acquired cardiac disease applications.

129 different microdomains and their changes in cardiac disease are not well understood.

130 alignancies, neurodegenerative diseases, and cardiac diseases) are, on a molecular level, associated

131 ed numerous de novo variants associated with cardiac disease as standing variation in ExAC, thus thes

132 hy (HCM) has been considered a heterogeneous cardiac disease ascribed solely to single sarcomere gene

133 metic peptide into a mouse model of diabetic cardiac disease associated with LTCC abnormalities resto

134 apeutic strategy for preventing and treating cardiac diseases associated with cardiac remodeling.

135 lation of Cav1 may reduce arrhythmic risk in cardiac diseases associated with renin-angiotensin syste

136 Conclusion In patients without underlying cardiac disease at baseline, the addition of trastuzumab

137 de novo variants previously associated with cardiac disease based on a large population-representati

138 al metabolism affecting multiple organs with cardiac disease being the leading cause of death.

139 LI1) looking at 1-year survival showed donor cardiac disease, black ethnicity, and steatosis to be ad

140 sociated with emergency surgery and advanced cardiac disease but not stent type or timing of surgery

141 ional recruitment of SK channels not only in cardiac disease, but also in normal physiology, contribu

142 The younger patient had no evidence of cardiac disease, but met possible ARVC diagnosis with on

143 should undergo clinical screening for occult cardiac disease, but the diagnostic yield from screening

144 Some cardiac disease-causing mutations, however, have been as

145 Cardiac disease (CD) is one of the major side effects of

146 icular cardiomyopathy (ARVC) is an inherited cardiac disease characterized by fibrofatty replacement

147 yopathy (DCM) is a genetically heterogeneous cardiac disease characterized by progressive ventricular

148 c gene network is conserved across different cardiac diseases characterized by fibrosis: human and mu

149 circRNAs already known to be associated with cardiac diseases (circDNAJC6) and/or being highly abunda

150 d, the standardized mortality ratios for all cardiac diseases combined was greatest for individuals d

151 Cardiac disease constitutes an increasing proportion of

152 Furthermore, cardiac diseases contribute to disease severity in patie

153 rcutaneous Administration of Gene Therapy In Cardiac Disease (CUPID 1) study was a phase 1/phase 2 fi

154 for a family history of sudden death receive cardiac disease diagnoses (14%), but clinical findings o

155 ]), idiopathic cardiomyopathy (0.4 [0.2-1]), cardiac disease duration greater than 2 years pre-extrac

156 n factors contributing to adenovirus-induced cardiac disease during acute and persistent infection.

157 Given the importance of ECM deposition in cardiac disease, ECM imaging could be a valuable clinica

158 ner and contribute to the pathophysiology of cardiac diseases, especially in cells lacking organized

159 In many cardiac disease etiologies, the T-system is perturbed, w

160 With aging and in cardiac disease, fibrosis caused by collagen deposition

161 supporting a role for cardiac lymphatics in cardiac disease, focusing on the current evidence linkin

162 c metabolism and abnormal redox state during cardiac diseases foment arrhythmogenic substrates throug

163 xt-generation sequencing assay for detecting cardiac disease gene mutations with improved accuracy, f

164 Eighty-nine cardiac disease genes were evaluated.

165 h lack mechanistic specificity, paradigms of cardiac disease have evolved to conceptualize myocardial

166 Subclinical and clinical cardiac diseases have been previously linked to magnetic

167 ase, are well-characterized proteinopathies, cardiac diseases have recently been associated with alte

168 s) prior to hospital admission, having known cardiac disease, having already participated in the tria

169 n multivariable analysis (MVA), pre-existing cardiac disease (hazard ratio [HR], 2.96; 95% CI, 1.07 t

170 Entire cohort participants free of cardiac disease, hypertrophy, hypertension, and diabetes

171 s SCA cases presented with known preexisting cardiac disease in 16% and >/=1 cardiovascular risk fact

172 Patients were diagnosed with heritable cardiac disease in 39 cases (9.3%).

173 Atrial fibrillation (AF) is a common cardiac disease in aging populations with high comorbidi

174 prescribed for secondary prevention of fetal cardiac disease in anti-SSA/Ro-exposed pregnancies.

175 Clinicians should not screen for cardiac disease in asymptomatic, low-risk adults with re

176 se (KD) is the most common cause of acquired cardiac disease in children in developed countries.

177 ese mechanisms provide new ways to attenuate cardiac disease in elders by preemptive treatment of age

178 eutic targets and mechanistic biomarkers for cardiac disease in females.

179 ld be considered as a potential biomarker of cardiac disease in FRDA and the evaluation of its expres

180 The management of cardiac disease in NMDs is made challenging by the broad

181 Each patient was assigned a Cardiac Disease in Pregnancy (CARPREG) II score based on

182 e an under-recognized component of inherited cardiac disease in some cases.

183 , and age at exposure on risk for late-onset cardiac disease in survivors of childhood cancer remain

184 The diagnosis of cardiac disease in the fetus is mostly made with ultraso

185 e link with metabolic syndrome, obesity, and cardiac disease in the general population require transl

186 sted as playing a role in the development of cardiac disease in the mdx mouse model of Duchenne muscu

187 olic processes underlying the development of cardiac disease in type II diabetes are not fully unders

188 The aim of the ALICE (Airflow Limitation in Cardiac Diseases in Europe) study was to investigate the

189 actors are disproportionately prone to these cardiac diseases in the setting of alcohol abuse.

190 The cardiac disease included cardiac conduction disease (CCD

191 Nav1.5 function is associated with multiple cardiac diseases including long-QT3 and Brugada syndrome

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 dysregulation is associated with a range of cardiac diseases, including dilated cardiomyopathy (DCM)

195 A link between excess dietary sugar and cardiac disease is clearly evident and has been largely

196 Mitral regurgitation in people without prior cardiac disease is considered a degenerative disease wit

197 their susceptibility to chemotherapy-induced cardiac disease is not well documented.

198 is beneficial for drug-treated patients with cardiac disease is not yet clear.

199 However, cardiac disease is reduced and survival of heterozygote

200 liver cirrhosis in the absence of underlying cardiac disease is termed cirrhotic cardiomyopathy.

201 ributable to the stent versus the underlying cardiac disease is uncertain, as prior studies lack a co

202 The hallmark of most cardiac diseases is the progressive loss of cardiomyocyt

203 stress, associated with a variety of common cardiac diseases, is well recognized to affect the funct

204 ultimately contribute to the progression of cardiac disease, leading to an increase in interstitial

205 suggest that lncRNAs may be associated with cardiac disease, little is known about lncRNAs in the se

206 cardiac arrhythmias and to be upregulated in cardiac disease, little is known about the fundamental p

207 ng assessment of their clinical potential as cardiac disease markers.

208 s attending a memory clinic, suggesting that cardiac disease may contribute to the development of CMI

209 ited by TF mutations is crucial to elucidate cardiac disease mechanisms.

210 Physiologic adaptation, structural cardiac disease, medication use, and degree of concurren

211 e, has gained attention as a risk factor for cardiac disease, metabolic syndrome, and cerebrovascular

212 rived cardiomyocytes are well established as cardiac disease model..

213 The cardiac disease models were administered with a locked n

214 enable development of personalized, in vitro cardiac disease models.

215 tudy examined how hemoglobin (Hgb) level and cardiac disease modify the relationship of RBC transfusi

216 storage is altered, for instance, diabetes, cardiac disease, muscular disorders, cancer, and glycoge

217 s of a reference healthy group without known cardiac disease (n = 28).

218 viduals and in controls with noninflammatory cardiac disease (n=160), ischemic heart failure (n=141),

219 5% bounds of a reference group without known cardiac disease (n=28).

220 = 24), cardiomyopathy, arrhythmia, and other cardiac diseases (n = 42), and diabetes and endocrine di

221 e of patients with paediatric and congenital cardiac disease, optimization of outcomes remains a cons

222 symptoms, medication, and family history of cardiac disease or sudden death were collected.

223 There is no association of EMAP with AMD cardiac diseases or cardiac risks, including cigarette s

224 No association was found with cardiac diseases or their risk factors.

225 hronic pulmonary disease, immune deficiency, cardiac disease, or previous episodes of wheezing or inh

226 Of them, 111 had a normal ECG, different cardiac diseases, or were lost to follow-up and exited t

227 male gender, Caucasian race, increased age, cardiac disease, organ failures, and disease severity.

228 me extent as do other chronic disorders (eg, cardiac diseases, osteoarthritis, lung disease, and poor

229 d a multicentre study to evaluate mortality, cardiac disease outcome, and risk factors for malignant

230 ionally ( P<0.001) and had worse measures of cardiac disease ( P<0.001) at the time of diagnosis, a g

231 nificant associations were also observed for cardiac disease (p = 0.010) and BMI >/=25 kg/m(2) (p = 0

232 x (P = .009), kidney dysfunction (P = .001), cardiac diseases (P = .005), diabetes mellitus (P = .03)

233 its dysregulation plays an important role in cardiac disease pathogenesis.

234 eliable pharmacological data and measures of cardiac disease phenotype in experimental cell, animal,

235 ing naproxen derivative, on the skeletal and cardiac disease phenotype in mdx mice.

236 (3) activation of autophagy ameliorated the cardiac disease phenotype in this mouse model.

237 Through genetic association studies with cardiac disease phenotypes and Mendelian randomization,

238 t may have clinical value in prognosticating cardiac disease progression in patients.

239 cial in the heart, it largely contributes to cardiac disease progression when dysregulated.

240 tein that enhances expression of a subset of cardiac disease-promoting genes.

241 a biochemical signature of early subclinical cardiac disease, providing an opportunity for targeted p

242 e been numerous stem cell studies focused on cardiac diseases, ranging from proof-of-concept to phase

243 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

244 models, we evaluated the association between cardiac disease rates and demographic and treatment char

245 t) were associated with an increased rate of cardiac disease (relative rate, 1.6; 95% CI, 1.1 to 2.3)

246 Cardiac disease remains the leading cause of morbidity a

247 lating PKA/PDE4D3 molecular signaling during cardiac diseases, remains unclear.

248 Proteinopathy causes cardiac disease, remodeling, and heart failure but the p

249 For many neuromuscular diseases (NMDs), cardiac disease represents a major cause of morbidity an

250 The Registry on Pregnancy and Cardiac Disease (ROPAC) is a global, prospective observa

251 mporary, worldwide Registry of Pregnancy and Cardiac disease (ROPAC), we describe the pregnancy outco

252 ath (SCD) and prevention and intervention of cardiac diseases, SCD remains a major cause of death.

253 long telomeres protect mice from the lethal cardiac disease seen in humans with the same genetic def

254 nding the effect of miRNA-based therapies in cardiac disease settings in males and females.

255 Clinical suspicion for cardiac disease should be high and threshold for cardiac

256 ndings with data on proteins responsible for cardiac disease should lead to the development of refine

257 Subjects with no signs of cardiac disease showed a decrease in CD127(+)CD132(+) ce

258 een systemic reductions in glycosylation and cardiac disease, showing that clinically relevant change

259 rimarily applied in the fields of cancer and cardiac disease so far, this metabolic imaging method ha

260 tic processes are increasingly identified in cardiac disease states.

261 was stronger in waitlisted patients without cardiac disease (subhazard ratio, 2.2; 95% CI, 1.6-3.1)

262 on of both modalities in assessment of other cardiac diseases such as inflammation and of other syste

263 s known to play a role in different types of cardiac disease, such as arrhythmogenic or hypertrophic

264 latory pathways are triggered in response to cardiac disease, such as those involving RNA-binding pro

265 actile dysfunction in inherited and acquired cardiac diseases, such as catecholaminergic polymorphic

266 beta-blockade therapy in cocaine users with cardiac disease suggest that beta-blockers are not unsaf

267 In cardiac disease, t-tubule loss occurs and affects the sy

268 myopathy describes the clinical phenotype of cardiac disease that accompanies CKD and is perhaps best

269 g-term adverse health risks, particularly of cardiac disease that is increased in other cancer popula

270 ed care must respond to the preponderance of cardiac disease that now occurs in combination with the

271 (MIF) is a histological hallmark of several cardiac diseases that alter myocardial architecture and

272 ide a framework to study the early stages of cardiac diseases that develop in utero.

273 infection by RBC threshold for patients with cardiac disease, the critically ill, those with acute up

274 curs in individuals without previously known cardiac disease, the identification of patients at risk

275 Among patients diagnosed with a heritable cardiac disease, the nearest affected relative was almos

276 ledge of strong associations between EAT and cardiac disease, these findings may suggest that EAT is

277 ect serum cardiac troponin I, a biomarker of cardiac disease to 100 pg/ml within 4 mins, which is fas

278 ly unexplained cardiac arrest and no evident cardiac disease to identify the pathogenesis of cardiac

279 rglabin, two anti-inflammatory agents new to cardiac diseases, to preserve cardiac function and atten

280 etes were diagnosed with potentially serious cardiac disease using all 3 criteria.

281 of C-reactive protein (CRP), a biomarker for cardiac disease, using a carbon nanofiber based biosenso

282 od to address patient-specific proclivity to cardiac disease utilizes induced pluripotent stem cell-d

283 and functional improvement in patients with cardiac disease warrants identification of a novel stem

284 Cardiac disease was defined as a history of atrial fibri

285 Nonheritable cardiac disease was diagnosed in another 5.5% of patient

286 Cardiac disease was established in 44.5% of athletes, wi

287 gia is a prevalent condition with or without cardiac disease we should contemplate issues surrounding

288 nal z-disc proteins that might contribute to cardiac disease, we employed an in silico screen for car

289 ify homozygous JPH2 variants associated with cardiac disease, we identified variants in JPH2 in a wor

290 anisms regulating gap junction remodeling in cardiac disease, we sought to identify the functional pr

291 History of difficult airway and cardiac disease were also associated with cardiac arrest

292 Patients with preexisting cardiac disease were excluded.

293 s demonstrated that older age and history of cardiac disease were the most consistent predictors of c

294 Cardiac diseases were also highly prevalent (22% coronar

295 ical cardiac disease and clinically manifest cardiac diseases were associated with CMIs on 3-T MRI in

296 Obese individuals without cardiac disease with (OB/MS+, n=124) and without (OB/MS-

297 iac-specific BEX1 transgenic mice show worse cardiac disease with stress stimulation, whereas Bex1 ge

298 ical cardiac disease and clinically manifest cardiac diseases with CMIs graded on 3-T MRI in a memory

299 dies and the outlook for future treatment of cardiac diseases with stem cell therapies.

300 Inflammation is a key component of cardiac disease, with macrophages and T lymphocytes medi