ライフサイエンスコーパス: CHD

1 CHD case fatality was higher among black versus white me

2 CHD clinicians and scientists are interested not only in

3 CHD events, including myocardial infarction, resuscitate

4 greater number of comorbidities (P<0.0001), CHDs with univentricular outcome (P<0.0001), intrauterin

5 ow-up, there were 4,450 recurrent MIs, 6,250 CHD events, and 14,311 deaths.

6 se-control studies (14 286 CHD cases, 13 275 CHD-free controls).

7 icipants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls).

8 years of follow-up (44152 person-years), 405 CHD and 228 stroke events occurred.

9 se-control studies (18 817 CHD cases, 39 652 CHD-free controls).

10 cipants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls).

11 exome sequencing of a single cohort of 2,871 CHD probands, including 2,645 parent-offspring trios, im

12 Second-trimester fetuses diagnosed with a CHD between 2007 and 2013 were also compared with Group

13 outcome of fetuses, either diagnosed with a CHD in the first trimester (Group I, 127 fetuses) or onl

14 with Group III (532 fetuses diagnosed with a CHD in the second trimester from 1996 to 2001, the perio

15 me of fetuses and children born alive with a CHD.

16 patients at higher risk estimated by the ABC-CHD (Age, Biomarkers, Clinical-Coronary Heart Disease) r

17 This "ABC-CHD" model had high discriminatory ability for CV death

18 rticipants to visit a website to learn about CHD (odds ratio [OR], 4.88 [confidence interval (CI), 1.

19 Acute CHD events included myocardial infarctions (MIs; nonfata

20 d deaths </=28 days of an acute MI and acute CHD deaths.

21 arctions (MIs; nonfatal and fatal) and acute CHD deaths.

22 Management of acute CHD risk may be important for individuals surviving a se

23 Risk of acute CHD was higher for sepsis than nonsepsis controls after

24 information about how genetic factors affect CHD risk (OR, 2.11 [CI, 1.03-4.47]; P=0.04), access thei

25 ted to be TG lowering and protective against CHD.

26 d a hospital-based prevalence of 0.14% among CHD patients.

27 bdominal adiposity, with type 2 diabetes and CHD through the potential intermediates of blood lipids,

28 Estimates for type 2 diabetes and CHD were derived from summary statistics of 2 separate g

29 cardiometabolic traits, type 2 diabetes, and CHD was tested in a mendelian randomization analysis tha

30 ompared fatal and nonfatal CHD incidence and CHD case-fatality among blacks and whites in the Atheros

31 iations between plant-based diet indices and CHD incidence.

32 iological evidence linking HIV infection and CHD.

33 nd factors associated with HIV infection and CHD.

34 with an increased risk for recurrent MI and CHD events but not all-cause mortality.

35 sitively associated with total mortality and CHD mortality, whereas the association with cancer morta

36 the causal association between telomeres and CHD and metabolic risk factors.

37 nct leanness and reproduction traits between CHD and EUD.

38 The Chromodomain-Helicase-DNA binding (CHD) Type III proteins are a subfamily of SWI2/SNF2 prot

39 tern and, among healthy women, includes both CHD benefit and stroke risk.

40 strongest for fatal CVD, and applies to both CHD and stroke.

41 luation of patients and families affected by CHD.

42 pital admissions for delivery in California, CHD was associated with incident CHF, atrial arrhythmias

43 CPCs, induction of hypoxic responses caused CHD by repressing Isl1 and activating NK2 homeobox 5 (Nk

44 6 years is associated with incident clinical CHD, CVD, and all-cause mortality during 12.5 years of f

45 raphic scan are at elevated risk of clinical CHD, CVD, and death.

46 irst AT episode varied among the most common CHD.

47 Complex CHD was associated with greater adjusted odds of serious

48 tio [OR], 9.7; 95% CI, 4.7-20.0) and complex CHD (OR, 56.6; 95% CI, 17.6-182.5) were associated with

49 as, and fetal growth restriction and complex CHD was associated with ventricular arrhythmias and mate

50 (12%); moderate CHD, n=53 (37%); and complex CHD, n=73 (51%).

51 Noncomplex and complex CHD.

52 ] age, 28.6 [7.6] years) and 262 had complex CHD (mean [SD] age, 26.5 [6.8] years).

53 AT burden was highest in complex CHD, such as single ventricle (22.8%) and d-transpositio

54 wer than 10 women with noncomplex or complex CHD (<0.5% each).

55 d into 2 groups: group A (n=51) with complex CHD and group B (n=58) with simple CHD.

56 Patients with complex CHD have increased risk of procedural failure and atriov

57 We compared 30 newborns with complex CHD prior to surgery and 30 age-matched healthy controls

58 tcomes were rare, even in women with complex CHD.

59 CHD had poorer outcomes, those with critical CHD were significantly more likely to receive exceptiona

60 is associated with congenital heart defects (CHDs) as a group, but few studies have assessed risk for

61 on the spectrum of congenital heart defects (CHDs) later in pregnancy and on the outcome of fetuses a

62 Congenital heart disease (CHD) affects up to 1% of live births.

63 ) is associated with coronary heart disease (CHD) and cardiovascular disease (CVD); however, prognost

64 The association of coronary heart disease (CHD) and human immunodeficiency virus (HIV) infection ha

65 trial outcomes, and coronary heart disease (CHD) and overall CVD were additional designated outcomes

66 CVD events including coronary heart disease (CHD) and stroke.

67 ant tachycardia to congenital heart disease (CHD) and the outcome of catheter ablation in this popula

68 Patients with congenital heart disease (CHD) are assumed to be vulnerable to atrial fibrillation

69 ividuals born with congenital heart disease (CHD) are at risk of developing life-long neurological de

70 patients with stable coronary heart disease (CHD) are based on modest evidence.

71 Adults with congenital heart disease (CHD) are exposed to increasing amounts of low-dose ioniz

72 Congenital heart disease (CHD) constitutes the most prevalent and heterogeneous gr

73 es supplemented with coronary heart disease (CHD) data from CARDIoGRAMplusC4D (Coronary Artery Diseas

74 s of acute and fatal coronary heart disease (CHD) events after sepsis hospitalizations among communit

75 t increased risk for coronary heart disease (CHD) events and mortality.

76 or those born with congenital heart disease (CHD) have greatly improved over the past 3 decades.

77 Congenital heart disease (CHD) is the leading cause of mortality from birth defect

78 Women with congenital heart disease (CHD) may be at increased risk for adverse events during

79 Blacks have higher coronary heart disease (CHD) mortality compared with whites.

80 total mortality and coronary heart disease (CHD) mortality, but it is unclear to what extent the ass

81 adults living with congenital heart disease (CHD) than children.

82 ing genetic risk for coronary heart disease (CHD) to individuals influences information seeking and i

83 be a risk factor for coronary heart disease (CHD), and recently the association was suggested to be c

84 heart failure (HF), coronary heart disease (CHD), and stroke in participants with vs without CKD.

85 rtality and incident coronary heart disease (CHD), CVD, and cancer over a mean 8.9 (standard deviatio

86 e protective against coronary heart disease (CHD), independently of LDL cholesterol (LDL-C) levels.

87 iated with complex congenital heart disease (CHD), while the underlying biological mechanism remains

88 eduction in risk for coronary heart disease (CHD).

89 are associated with coronary heart disease (CHD).

90 type 2 diabetes and coronary heart disease (CHD).

91 metals and incident coronary heart disease (CHD).

92 ity in adults with congenital heart disease (CHD).

93 pid levels and hence coronary heart disease (CHD).

94 with 62240 cases of coronary heart disease (CHD).

95 t outcomes in stable coronary heart disease (CHD).

96 s in patients with congenital heart disease (CHD).

97 cular presentations (coronary heart disease [CHD], cerebrovascular disease, heart failure, and periph

98 CVD outcomes (i.e., coronary heart disease [CHD], stroke, or the combination of both).

99 The C-terminal homology domain (CHD) of Af4 was sufficient to confer this linkage.

100 ion between pregestational diabetes and each CHD phenotype with previous estimates.

101 tes (pregestational or gestational) and each CHD phenotype, adjusting for potential confounders.

102 betes was significantly associated with each CHD phenotype.

103 Fatal CHD included deaths </=28 days of an acute MI and acute

104 hospitalizations and future acute and fatal CHD events using Cox regression, Gray's model, and compe

105 ded nonfatal myocardial infarction and fatal CHD.

106 nce interval, 0.41-0.73) of developing fatal CHD compared with those least socially integrated (P for

107 ck men and women have similar risk for fatal CHD compared with white men and women, respectively.

108 nd 1.09 (0.62-1.93), respectively, for fatal CHD, and 0.64 (0.47-0.86) and 0.67 (0.48-0.95), respecti

109 nd 1.00 (0.54-1.85), respectively, for fatal CHD, and 0.70 (0.51-0.97) and 0.70 (0.46-1.06), respecti

110 nd 2.11 (1.32-3.38), respectively, for fatal CHD, and 0.82 (0.64-1.05) and 0.94 (0.69-1.28), respecti

111 nd 1.79 (1.06-3.03), respectively, for fatal CHD, and 1.47 (1.13-1.91) and 1.29 (0.91-1.83), respecti

112 Risk of fatal CHD was similarly higher for sepsis than nonsepsis indiv

113 ated with lower CHD risk, particularly fatal CHD.

114 smoking; however, the association with fatal CHD risk remained after accounting for these behaviors a

115 men (31 healthy volunteers and 17 with fetal CHD) that underwent fetal MRI during their second or thi

116 In pregnancies with fetal CHD, global placental perfusion significantly decreased

117 ecurrent MI, 1.51 (95% CI: 1.34 to 1.70) for CHD events, and 0.96 (95% CI: 0.87 to 1.06) for all-caus

118 775 events), 1.59 (95% CI: 1.38 to 1.83) for CHD (7,061 events), and 1.35 (95% CI: 1.23 to 1.48) for

119 lopment of precision medicine approaches for CHD and other diseases associated with genetic factors.

120 een TL and common metabolic risk factors for CHD is not well understood.

121 o examine whether metabolic risk factors for CHD mediate the causal pathway from short TL to increase

122 However, gene-lifestyle interactions for CHD have been difficult to identify.

123 BMI (1 SD approximately 4.6 kg/m(2); OR for CHD, 1.36; 95% CI, 1.22-1.52).

124 48% excess risk of CHD (odds ratio [OR] for CHD, 1.48; 95% confidence interval [CI], 1.28-1.71), sim

125 onal designated outcomes.Incidence rates for CHD and total CVD did not differ between the interventio

126 status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval,

127 ypothesized that disclosing genetic risk for CHD to individuals influences information seeking and sh

128 rol, lower triglycerides, and lower risk for CHD.

129 Disclosure of a genetic risk score for CHD increased information seeking and sharing.

130 fied children (<18 years of age) treated for CHD in Denmark from 1977 to 2015, their need for reinter

131 The discoveries from CHD genetic studies draw attention to biological pathway

132 culating TG levels and, hence, protects from CHD.

133 The majority, 86 of 109 (79%), had CHD resulting in right heart pressure or volume overload

134 risk differences of adjudicated incident HF, CHD, and stroke, comparing participants with vs without

135 According to a hierarchical CHD classification, patients with conotruncal defects ha

136 better discriminate between lower and higher CHD risk in older adults.

137 ted increase in T2D risk also confers higher CHD risk.

138 ing insulin level was associated with higher CHD risk (odds ratio, 1.86; 95% confidence interval, 1.0

139 ealthy plant foods is associated with higher CHD risk.

140 However, CHD HRs comparing these groups varied strongly with base

141 bolic syndrome (MetS) or diabetes identifies CHD and ASCVD prognostic indicators during a long follow

142 um and mutant cells lacking ChdC, a Type III CHD protein ortholog.

143 Type III CHDs are required for multicellular development of anima

144 me time pointing to remarkable complexity in CHD genetics.

145 ur understanding of neurological deficits in CHD.

146 Racial differences in CHD incidence were attenuated among older women.

147 en to the common goals of cardiac imaging in CHD, including assessment of structural and residual hea

148 ide an overview of cardiovascular imaging in CHD.

149 ith any CAC experienced a 5-fold increase in CHD events (hazard ratio [HR], 5.0; 95% CI, 2.8-8.7) and

150 of stem cell-based therapeutic strategies in CHD.

151 idely used noninvasive imaging techniques in CHD-echocardiography, cardiac magnetic resonance imaging

152 Incident CHD included fatal or nonfatal myocardial infarction, ac

153 followed up for 12.5 years, with 57 incident CHD events and 108 incident CVD events observed.

154 A total of 1,621 incident CHD cases and 1,621 controls free of major cardiovascula

155 s of follow-up, we documented 8,631 incident CHD cases.

156 rovided improved discrimination for incident CHD (C statistic, 0.735 vs 0.703; C statistics differenc

157 For incident CHD, net reclassification improvement with addition of C

158 ent in long-term prognostication of incident CHD and ASCVD using CAC scores among those with diabetes

159 ween social integration and risk of incident CHD in a large female prospective cohort.

160 usand three hundred and seventy-two incident CHD events occurred throughout follow-up.

161 age) had a greater association with incident CHD (C statistic, 0.733 vs 0.690; C statistics differenc

162 e was independently associated with incident CHD in multivariable analyses in those with diabetes (HR

163 Incident CVD included CHD, stroke, heart failure, and peripheral arterial dise

164 use it caused severe malformations including CHDs.

165 gical hypoxia during early pregnancy induces CHD, but the underlying reasons are unknown.

166 ases, including approximately 3% of isolated CHD patients and approximately 28% with both neurodevelo

167 foods is associated with substantially lower CHD risk, whereas a plant-based diet index that emphasiz

168 ated was significantly associated with lower CHD risk, particularly fatal CHD.

169 sk for recurrent myocardial infarction (MI), CHD events, and all-cause mortality in Medicare benefici

170 Recurrent MI, CHD events (recurrent MI or a coronary revascularization

171 Although the MLL-CHD fusion protein failed to immortalize HSPCs in myeloi

172 rlying CHD: simple CHD, n=18 (12%); moderate CHD, n=53 (37%); and complex CHD, n=73 (51%).

173 After multivariate adjustment, noncomplex CHD (odds ratio [OR], 9.7; 95% CI, 4.7-20.0) and complex

174 livery admissions, 3189 women had noncomplex CHD (mean [SD] age, 28.6 [7.6] years) and 262 had comple

175 children with both critical and noncritical CHD had poorer outcomes, those with critical CHD were si

176 ed with increased risk of fatal and nonfatal CHD during 12.5 years of follow-up.

177 We compared fatal and nonfatal CHD incidence and CHD case-fatality among blacks and whi

178 Fatal and nonfatal CHD incidence was assessed from baseline (ARIC=1987-1989

179 However, the risk for nonfatal CHD is consistently lower for black versus white men and

180 1.29 (0.91-1.83), respectively, for nonfatal CHD.

181 0.70 (0.46-1.06), respectively, for nonfatal CHD.

182 0.67 (0.48-0.95), respectively, for nonfatal CHD.

183 0.94 (0.69-1.28), respectively, for nonfatal CHD.

184 ver, a previous study suggests that nonfatal CHD risk may be lower for black versus white men.

185 s (95% confidence interval, 3-35; P=0.02) of CHD.

186 To determine the association of CHD with academic outcomes and compare outcomes accordin

187 The association of CHD with readmission was assessed to 7 years after deliv

188 few genes have been linked to some cases of CHD.

189 we are still unable to identify the cause of CHD for most patients, recent findings have provided us

190 c explanations for some nongenetic causes of CHD.

191 Complexity of CHD was associated with longer procedure duration.

192 patients was not influenced by complexity of CHD.

193 to identify all patients with a diagnosis of CHD who were born from 1970 to 1993.

194 f AT differed among the most common forms of CHD.

195 genetic causes of a significant fraction of CHD, while at the same time pointing to remarkable compl

196 o women in the Nurses' Health Study, free of CHD and stroke at baseline (1992), were followed until 2

197 I in 2 prospective studies of adults free of CHD.

198 evelopment, establish an in vivo function of CHD Type III chromatin remodeling proteins in this proce

199 g a new paradigm for the complex genetics of CHD.

200 =3381, women=4112), all without a history of CHD, were analyzed.

201 CAC score was also a prognostic indicator of CHD and ASCVD after controlling for diabetes duration of

202 Until recently, the cause of the majority of CHD was unknown.

203 Only a minority of CHD cases are attributed to genetic causes, suggesting a

204 The etiology of the increased prevalence of CHD in HIV-infected populations is the result of complex

205 about the effect of the rising prevalence of CHD on morbidity and mortality, as well its effect on he

206 n-years, respectively), a 43% higher rate of CHD events (62.5 vs. 43.8 per 1,000 person-years, respec

207 metabolic abnormalities had a higher risk of CHD (multivariate-adjusted hazard ratio [HR]: 1.49; 95%

208 0.08 U) associated with a 48% excess risk of CHD (odds ratio [OR] for CHD, 1.48; 95% confidence inter

209 poC-III was associated with a higher risk of CHD (pooled relative risk per standard deviation, 1.09;

210 2-72 years of age) were followed for risk of CHD from 2000 to 2002 through 2013.

211 d apoB was associated with a similar risk of CHD per unit change in apoB level (OR, 0.782 [95% CI, 0.

212 nce), but a significantly attenuated risk of CHD per unit change in LDL-C level (OR, 0.916 [95% CI, 0

213 l pathway from short TL to increased risk of CHD using a network Mendelian randomization design.

214 Risk of CHD, cerebrovascular disease, and heart failure in norma

215 f HDL that is associated with higher risk of CHD.

216 es were not related to age-adjusted risks of CHD, CVD, or cancer or to total or CVD mortality.

217 ompare outcomes according to the severity of CHD, we linked state educational records with a birth de

218 Interventional treatment of CHD has evolved from 1977 to 2015 and is now performed o

219 In Group III, significantly more cases of CHDs with univentricular outcome (P<0.0001), intrauterin

220 had a significant impact on the spectrum of CHDs and the outcomes of pregnancies with CHDs diagnosed

221 The spectrum of CHDs diagnosed in the first and second trimesters in the

222 The spectrum of CHDs, associated comorbidities, and outcome of fetuses,

223 infarction, resuscitated cardiac arrest, or CHD death.

224 l infarction, coronary revascularization, or CHD death.

225 without prior CVD had an intervention period CHD HR of 0.70 (95% CI: 0.56, 0.87) or 1.04 (95% CI: 0.9

226 rgent changes between Chinese domestic pigs (CHD) and European domestic pigs (EUD).

227 Compared with the background population, CHD was associated with lower survival in all 3 time per

228 funded animal research to evaluate sucrose's CHD risks.

229 plastic left heart syndrome (HLHS), a severe CHD, is multigenic and genetically heterogeneous.

230 F1 accounting for approximately 5% of severe CHD in Ashkenazim, recessive genotypes in MYH6 accountin

231 d matched cancer cases with controls on sex, CHD severity, birth year, and age.

232 ding to complexity of underlying CHD: simple CHD, n=18 (12%); moderate CHD, n=53 (37%); and complex C

233 h complex CHD and group B (n=58) with simple CHD.

234 blation is favorable in patients with simple CHD.

235 few studies have assessed risk for specific CHD phenotypes.

236 and improved counseling for risk of specific CHD phenotypes.

237 In patients with stable CHD, more physical activity was associated with lower mo

238 sed prediction model in patients with stable CHD.

239 ediction of CV death in patients with stable CHD.

240 reduced ADAMTS7 expression confers stronger CHD protection in never-smokers than in ever-smokers.

241 The CHD benefit among healthy normotensive women was partial

242 ould have (1) strengthened the case that the CHD risk of sucrose is greater than starch and (2) cause

243 2.11 [CI, 1.03-4.47]; P=0.04), access their CHD risk via a patient portal (OR, 2.99 [CI, 1.35-7.04];

244 [CI, 1.35-7.04]; P=0.01), and discuss their CHD risk with others (OR, 3.13 [CI, 1.41-7.47]; P=0.01),

245 These CHDs can mediate nucleosome translocation in vitro, but

246 with CKD should prioritize HF in addition to CHD prevention.

247 ely 440 genes were inferred to contribute to CHD.

248 This dependence also extends to CHD and SWI/SNF family remodellers, suggesting that the

249 risk of HF that was similar in magnitude to CHD and greater than stroke.

250 ascular imaging techniques as they relate to CHD is essential.

251 the causal pathway from shorter telomeres to CHD pathogenesis.

252 sk factors could explain pathways from TL to CHD warrants further attention.

253 n the evidence for genetic causes underlying CHD and discuss data supporting both monogenic and compl

254 ic and complex genetic mechanisms underlying CHD.

255 sified according to complexity of underlying CHD: simple CHD, n=18 (12%); moderate CHD, n=53 (37%); a

256 After 11.1 mean years of follow-up, CHD events occurred in 84 participants with diabetes (13

257 Primary outcomes were CHD, type 2 diabetes mellitus, and major stroke subtypes

258 ed with AF in children and young adults with CHD have not been compared with those in control subject

259 o the morbidity and mortality of adults with CHD.

260 rt may have on the well-being of adults with CHD.

261 dent cancer in the population of adults with CHD.

262 independent predictors of AT in adults with CHD.

263 types that have been shown to associate with CHD risk.

264 versely, uPDI was positively associated with CHD (HR: 1.32; 95% CI: 1.20 to 1.46; p trend <0.001).

265 that a p.G202V HAND2 variant associated with CHD and coronary artery diseases found in a large Lebane

266 d barium) were significantly associated with CHD based on trend tests from single-metal multivariable

267 odevelopmental abnormalities associated with CHD have been identified; however, the underlying causes

268 ial integration is inversely associated with CHD incidence in women, but is largely explained by life

269 Pcdha9, genes not previously associated with CHD, were validated by CRISPR-Cas9 genome editing in mic

270 Children with CHD had 1.24x the odds of not meeting standards in eithe

271 val, 1.12-1.37), with 44.6% of children with CHD not meeting standards in at least one of these areas

272 , and may be most relevant for children with CHD whose cardiac defects remain unrepaired for prolonge

273 cental dysfunction in fetuses diagnosed with CHD.

274 n age at entry 22.6 years, 50.6% males) with CHD (49% simple, 39% moderate, and 12% complex) prospect

275 Among 21 982 patients (51.6% men) with CHD and 219 816 matched control subjects, 654 and 328 de

276 reduce brain dysmaturation in newborns with CHD, and may be most relevant for children with CHD whos

277 Each patient with CHD was matched by birth year, sex, and county with 10 c

278 he study included 24 833 adult patients with CHD aged 18 to 64 years from 1995 to 2009.

279 most important complication in patients with CHD and AF, with a 10.7% (70 of 654) recorded diagnosis

280 AND One hundred and forty-four patients with CHD and atrial tachyarrhythmias undergoing radiofrequenc

281 d number of clinical trials on patients with CHD exist, and these primarily focus on hypoplastic left

282 o the age of 42 years, 1 of 12 patients with CHD had developed AF, and 1 of 10 patients with CHD with

283 ence interval, 19.26-25.12) in patients with CHD than control subjects.

284 ent on physicians who care for patients with CHD to be mindful of the effects that disease of organs

285 for radiation surveillance in patients with CHD where no regulation currently exists.

286 had developed AF, and 1 of 10 patients with CHD with AF had developed heart failure.

287 urvival has been documented in patients with CHD with renal dysfunction, restrictive lung disease, an

288 ablation in a large cohort of patients with CHD with special reference to complexity of underlying a

289 redictors of AT in a cohort of patients with CHD.

290 s and incident cancer in adult patients with CHD.

291 nt and affect clinical care of patients with CHD.

292 a can complicate the course of patients with CHD.

293 en genes with damaging DNMs in probands with CHD and autism was also found.

294 Of 5624 subjects with CHD and 10 832 with no structural birth defects, 2807 (5

295 and risk assessment for pregnant women with CHD at the time of delivery.

296 e hypothesized to be higher among women with CHD.

297 ntified compared with fetuses diagnosed with CHDs in the second trimester between 2007 and 2013.

298 of CHDs and the outcomes of pregnancies with CHDs diagnosed in the second trimester.

299 e of these areas compared with 37.5% without CHD.

300 etal outcomes between women with and without CHD by using multivariate logistic regression.