ライフサイエンスコーパス: CHD

1 CHD DNVs altered transcription levels in 5 of 31 enhance

2 CHD dried protein powder showed excellent powder charact

3 CHD is a fast and efficient filtering strategy for massi

4 CHD rates in women versus men were 6.3 versus 10.7 among

5 CHD severity and comorbidities varied across sites, with

6 CHD was defined as >=1 inpatient code or >=2 outpatient

7 CHDs were categorized as severe or not severe, excluding

8 val [CI]: 1.31 to 1.46; p for trend <0.001), CHD (HR: 1.46; 95% CI: 1.36 to 1.56; p for trend <0.001)

9 ) = 1.24, 95% CI, 1.03-1.50, P value = 0.02; CHD OR = 1.21, 95% CI, 1.01-1.45, P value = 0.04); howev

10 In univariate models, CP (P = 0.034), CHD (P < 0.001), and hs-CRP (P < 0.001) were significant

11 in its crystallographic unit cell to give 1.CHD as a room temperature stable product.

12 HLHS/TGA (n = 24), CHD-other (50), and CHD-related (34) groups each had gen

13 = 33), patients with periodontitis (n = 31), CHD (n = 29), and a combination of periodontitis + CHD (

14 % CAC >=100), 574 incident ASCVD events (333 CHD and 241 stroke) were observed over 12.3-year follow-

15 e at baseline, 56 years [SD, 8 years]), 4607 CHD and 3253 stroke events were recorded (median follow-

16 n with incident CHD in 944 participants (472 CHD cases) in the WHI-OS (Women's Health Initiative Obse

17 e at baseline, 63 years [SD, 9 years]), 5078 CHD and 3932 stroke events were recorded (median follow-

18 , 95% CI, 1.43, 2.37, P value = 2.0 x 10-6), CHD (OR = 1.64, 95% CI, 1.28-2.09, P value = 8.07 x 10-5

19 nnectome status and analyzed data from 3,684 CHD subjects and 1,789 controls for connectome gene muta

20 o CHD, we compared genome sequences from 749 CHD probands and their parents with those from 1,611 una

21 .76, 95% confidence interval; CI 0.73-0.79), CHD (aHR 0.66, 95% CI 0.62-0.69) and stroke (aHR 0.84, 9

22 median), 6378 participants had experienced a CHD event.

23 HRs with 95% CIs for a CHD event, in relation to intake of GI, GL, and carbohyd

24 CHD diagnoses; "CHD-related," healthy with a CHD family history; and "optimal control," healthy witho

25 mechanisms through which this locus affects CHD risk, we measured 35 intracellular metabolites invol

26 full-mouth periodontal exam (N = 6,300) and CHD outcomes through 2017 were obtained from the Atheros

27 HLHS/TGA (n = 24), CHD-other (50), and CHD-related (34) groups each had generally smaller brain

28 was independently associated with ASCVD and CHD risk in all groups and with stroke risk in the overa

29 resulted in greater improvement in ASCVD and CHD risk reclassification and discrimination indexes tha

30 sclerotic cardiovascular disease (ASCVD) and CHD among asymptomatic subjects.

31 liva in comparison with healthy controls and CHD.

32 gest that comorbidity between depression and CHD arises largely from shared environmental factors.

33 l information of intellectual disability and CHD by conducting systems biology analyses of genes prio

34 rios for five neuropsychiatric disorders and CHD.

35 chizophrenia, epileptic encephalopathies and CHD.

36 test whether cardiovascular risk factors and CHD are likely to be causally related to depression usin

37 art development, cardiomyocyte function, and CHD genetics-in discrete subpopulations of cardiomyocyte

38 ombined outcome of myocardial infarction and CHD death (hazard ratio, 1.03 [95% CI, 0.92-1.16]; I(2)=

39 e was composite of myocardial infarction and CHD death.

40 te suPAR as a biomarker of periodontitis and CHD.

41 mpact of gingival health, periodontitis, and CHD on suPAR levels in plasma and saliva and to evaluate

42 of the genetic relationship between T2D and CHD is beginning to provide the promise for improved pre

43 o the etiologic relationship between T2D and CHD.

44 ence for shared genetic loci between T2D and CHD; by examining the formal testing of this interaction

45 icates from 1999 to 2017 to calculate annual CHD mortality by age at death, race/ethnicity, and sex.

46 hy control fetuses and fetuses with SV or AO CHD (DeltaR2* per week, 0.1 sec(-1) +/- 0 [P < .01], 0.2

47 maternal hyperoxia in fetuses with SV or AO CHD (mean DeltaR2*, 0.7 sec(-1) +/- 0.2 [P = .01] and 0.

48 x- or race-based CAC interactions for ASCVD, CHD, and stroke events were observed.

49 ne the diagnostics of Framingham score-based CHD-prediction.

50 ple mathematical equations, outline the best CHD prevention strategy using lifestyle control only.

51 ovo non-synonymous variants in chromodomain (CHD) genes was observed among individuals with CM1 (comb

52 ts were followed for ASCVD events comprising CHD, cerebrovascular disease, and PAD events until Decem

53 Patients with CHD and CP + CHD presented higher levels of salivary and serum ADMA c

54 atients with CHD, 35 patients with both CP + CHD, and 35 healthy subjects.

55 ontitis (CP), CHD, or of both diseases (CP + CHD) on salivary and serum ADMA levels.

56 ) mumol/g protein, P < 0.01] and in the CP + CHD [serum: 1.8 (1.4 to 2.0) mumol/L; salivary 1.5 (1.2

57 pact of gingival health, periodontitis (CP), CHD, or of both diseases (CP + CHD) on salivary and seru

58 ensity when the molecule 1,3-cyclohexadiene (CHD) is optically excited.

59 stallizes with a molecule of cyclohexadiene (CHD) in its crystallographic unit cell to give 1.CHD as

60 d with CICU mortality included age <30 days, CHD, vasoactive infusions, ventricular tachycardia, mech

61 egnancy related to congenital heart defects (CHD) in Shaanxi province, Northwestern China.

62 ound In women with congenital heart defects (CHD), changes in blood volume, heart rate, respiration,

63 rt tube results in congenital heart defects (CHD).

64 Studies on congenital heart defects (CHDs) were excluded because of a recent systematic revie

65 The etiology of congenital heart defects (CHDs), which are among the most common human birth defec

66 h lowest fetal cerebral substrate delivery; "CHD-other," with other CHD diagnoses; "CHD-related," hea

67 Further, we found that the DeltaTMAO-CHD relationship was strengthened by unhealthy dietary p

68 ically predicted PCOS with risk of diabetes, CHD, or stroke.

69 ery; "CHD-other," with other CHD diagnoses; "CHD-related," healthy with a CHD family history; and "op

70 Congenital heart disease (CHD) accounts for ~40% of deaths in US children with bir

71 comorbidity between coronary heart disease (CHD) and depression is evident, it is unclear whether th

72 sucrose with risk of coronary heart disease (CHD) and its risk factors (i.e., type 2 diabetes, adipos

73 events, inclusive of coronary heart disease (CHD) and stroke, and is a decision-making aid for primar

74 ites associated with coronary heart disease (CHD) and type 2 diabetes.

75 sk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) coho

76 ily history (FHx) of coronary heart disease (CHD) are individually associated with cardiovascular ris

77 y in children with congenital heart disease (CHD) are lacking, thus warranting the need to summarize

78 ses, including 9,794 coronary heart disease (CHD) cases and 6,174 strokes.

79 Patients with congenital heart disease (CHD) comprised 57% of the cohort.

80 Rates for recurrent coronary heart disease (CHD) events have declined in the United States.

81 ciated with incident coronary heart disease (CHD) events.

82 been associated with coronary heart disease (CHD) in type 2 diabetes.

83 changes in TMAO with coronary heart disease (CHD) incidence.

84 Congenital heart disease (CHD) is associated with abnormal brain development in ut

85 nt in fetuses with congenital heart disease (CHD) may result from inadequate cerebral oxygen supply i

86 AD versus those with coronary heart disease (CHD) or cerebrovascular disease.

87 olled trial in 1,002 coronary heart disease (CHD) patients, whose primary objective is to compare the

88 infarction (MI) and coronary heart disease (CHD) risks (MI odds ratio (OR) = 1.24, 95% CI, 1.03-1.50

89 for population-wide coronary heart disease (CHD) screening.

90 Congenital heart disease (CHD) survivors are at risk for neurodevelopmental disabi

91 ic rates of incident coronary heart disease (CHD) than men.

92 tric disorders and congenital heart disease (CHD) which use de novo mutations (DNMs) from parent-offs

93 ith type 2 diabetes, coronary heart disease (CHD), and stroke.

94 ose with established coronary heart disease (CHD), are lacking.

95 e has been linked to coronary heart disease (CHD), but studies have been inconclusive.

96 variants, including coronary heart disease (CHD), CKD, PAD and neuropathy.

97 in increased risk of coronary heart disease (CHD), whereas oral conjugated equine estrogens (CEE) did

98 d of patients with congenital heart disease (CHD), with 8% of cases attributable to coding de novo va

99 defects including congenital heart disease (CHD).

100 may increase risk of coronary heart disease (CHD).

101 ajor risk factor for coronary heart disease (CHD).

102 es in infants with congenital heart disease (CHD).

103 protein lipids cause coronary heart disease (CHD).

104 ators causes human congenital heart disease (CHD); however, the underlying CHD gene regulatory networ

105 festyle in abetting Coronary Heart Diseases (CHD) have mostly focused on deterrent health factors, li

106 Congenital heart diseases (CHDs), including hypoplastic left heart syndrome (HLHS),

107 wo drying methods (conductive hydro-drying - CHD and freeze-drying - FD) on the physical and function

108 nsortium involving patients with established CHD at baseline.

109 rombotic events in patients with established CHD.

110 ncluded myocardial infarction (MI) and fatal CHD.

111 Prediction of 10-year first CHD events (including myocardial infarctions, fatal coro

112 CES-D score, 19 vs 1) were 36.3 vs 29.0 for CHD events, 28.0 vs 24.7 for stroke events, and 62.8 vs

113 es of 4 or higher vs 0 were 20.9 vs 14.2 for CHD events, 15.3 vs 10.2 for stroke events, and 36.2 vs

114 ighest RR of 1.79 (95% CI: 1.08 to 2.96) for CHD as compared with those with consistently low TMAO le

115 The predictive value of CAC categories for CHD and stroke separately and across sex and race groups

116 studies assessing whether T2D is causal for CHD); and then turn to the implications of this genetic

117 y improved the rate of genetic diagnosis for CHD but the cause in the majority of cases remains uncer

118 t the potential clinical utility of PRSs for CHD as well as the need to assemble diverse cohorts to g

119 risk discrimination and reclassification for CHD but not for stroke events.

120 clear whether women remain at lower risk for CHD events versus men following a myocardial infarction

121 The HR per 1-SD higher depression score for CHD was 1.07 (95% CI, 1.03-1.11); stroke, 1.05 (95% CI,

122 The HR per 1-SD higher depression score for CHD was 1.11 (95% CI, 1.08-1.14); stroke, 1.10 (95% CI,

123 this genetic relationship for therapies for CHD, for therapies for T2D, and for therapies that affec

124 4% across all ages, mortality resulting from CHD declined 39.4% overall.

125 Mortality resulting from CHD significantly declined among all races/ethnicities s

126 ohorts, 4 randomized trials) from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) cons

127 The GL-CHD association did not differ between men [HR: 1.19 (95

128 High GL was associated with greater CHD risk [HR 1.16 (95% CI: 1.02, 1.31) highest vs. lowes

129 igh sugar intake was associated with greater CHD risk [HR: 1.09 (95% CI: 1.02, 1.17) per 50 g/d].

130 ble carbohydrate was associated with greater CHD risk [HR: 1.11 (95% CI: 1.03, 1.18) per 50 g/d].

131 glucose response is associated with greater CHD risk.

132 ence (p = 2.6 x 10(-9)), with many harboring CHD rare variants having macrocephaly.

133 ic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0-3%; p

134 ncreases in TMAO were associated with higher CHD risk, and repeated assessment of TMAO over 10 years

135 ocytes and predicts candidate GRNs for human CHDs, with implications for quantitative transcriptional

136 ral health, it may be effective at impacting CHD incidence in only certain groups of people.

137 In CHD subjects, the top 12 NDD genes with damaging DNVs th

138 to 2006 demonstrated an overall decrease in CHD mortality.

139 ens may partially mediate the differences in CHD risk between the 2 WHI-HT trials.

140 iants in Notch pathway genes are enriched in CHD patients.

141 a better balance of vascular homeostasis in CHD patients, even in those with severe endothelial dysf

142 We hypothesized that NDD in CHD may be attributable to genes altering both neural co

143 These data suggest that NDD in CHD patients may be attributable to genes that alter bot

144 with both disorders, suggesting that NDD in CHD survivors may be of genetic origin.

145 Here, we show that two genes implicated in CHDs, Megf8 and Mgrn1, interact genetically and biochemi

146 Incident CHD events occurred in 696 participants (14.4%) and 227

147 Incident CHD was moderately significantly associated with a speci

148 ink between periodontal disease and incident CHD.

149 th the number of SDH for both fatal incident CHD (0 SDH, 1.30; 1 SDH, 1.44; 2 SDH, 2.05; >=3 SDH, 2.8

150 ly adjusted hazard ratios for fatal incident CHD among those with >=3 SDH were 3.00 (95% CI, 2.17 to

151 comes were expert adjudicated fatal incident CHD and nonfatal MI.

152 independent associations for fatal incident CHD.

153 ed with nonfatal MI than with fatal incident CHD.

154 .23-1.90), and 1.27 (1.13-1.43) for incident CHD in EA, HE, and AA individuals, respectively.

155 to determine hazard ratios (HR) for incident CHD, congestive heart failure (CHF), and other causes of

156 d with a graded increase in risk of incident CHD, with greater magnitude and independent associations

157 levels, age, body mass index, race, incident CHD, prevalent hypertension, and diabetes.

158 Associations of CAC with incident CHD and stroke events were evaluated using multivariable

159 were evaluated for association with incident CHD in 944 participants (472 CHD cases) in the WHI-OS (W

160 by HT type and were associated with incident CHD in the WHI-OS; a metabolite score estimated in a Lea

161 s not significantly associated with incident CHD.

162 emic load (GL) are associated with increased CHD risk.

163 pomorphic DLL4 allele as a cause of isolated CHD.

164 es were followed until December 2017 for MI, CHD (i.e., MI or coronary revascularization), and in Med

165 The lower risk for MI, CHD, and all-cause mortality in women versus men is cons

166 impact of a healthy lifestyle in mitigating CHD risk.

167 <5 years with RSV-ALRI with underlying or no CHD.

168 derlying CHD as compared to those without no CHD.

169 ough higher for patients with CHD versus non-CHD (19% versus 11%; P<0.001).

170 s established to functionally evaluate novel CHD gene candidates, based on whole-genome and iPSC RNA

171 able expressivity and penetrance of observed CHD in families carrying Notch pathway variants.

172 l influences, play roles in the aetiology of CHD.

173 mpare their causal roles in the aetiology of CHD.

174 Incident cases of CHD (n = 380) were identified after the second blood col

175 e regulatory noncoding DNVs in a fraction of CHD at least as high as that observed for damaging codin

176 Of 22 152 participants free of CHD at baseline, 58.8% were women and 42.0% were Black;

177 th and the other without a family history of CHD, to explore the contribution of shared genes and/or

178 nces in a control group without a history of CHD.

179 tabolites were associated with lower odds of CHD.

180 rovide new insights into the pathogenesis of CHD.

181 d CAC was consistently a better predictor of CHD than stroke.

182 is [n = 4,845], Down syndrome by presence of CHD [n = 22,317], and trisomy 18 [n = 2,174]) were inclu

183 icantly associated with an increased risk of CHD (relative risk [RR] in the top tertile: 1.58 [95% co

184 : 0.77-0.89; P < 0.001) to lower the risk of CHD, but these effect estimates attenuated substantially

185 entification of people with a higher risk of CHD.

186 ationship of lipoprotein lipids with risk of CHD.

187 care to identify individuals at high risk of CHD.

188 t estimates consistent with a higher risk of CHD.

189 Causal effects of PCOS on risks of CHD and stroke were evaluated in European cohorts.

190 ssociations between the presence/severity of CHD and stillbirth, preterm birth, and adverse condition

191 , 9 and 10; at certain pH, the solubility of CHD protein was higher than that of the FD counterparts.

192 ematic review of population-based studies of CHD survival.

193 ly favored CEE alone over CEE+MPA in term of CHD risk.

194 tuses with CHD were more similar to those of CHD-related than optimal controls, suggesting genetic or

195 ibited an incompletely penetrant syndrome of CHDs with heterotaxy.

196 ward deciphering oligogenic underpinnings of CHDs, including hypoplastic left hearts.

197 , e.g. fruits/vegetables, cereals can offset CHD risk factors over a period of time.

198 Given a small effect on CHD cannot be excluded, further investigation with stron

199 of sucrose on dental caries but no effect on CHD.

200 ablishes gender independence of lifestyle on CHD, refuting long held assumptions and unqualified beli

201 ranks the impact of the negative outliers on CHD and then quantifies the impact of the positive healt

202 CVD event rate among patients with PAD only, CHD only, and cerebrovascular disease only was 34.7 (95%

203 with cerebrovascular disease only (43.0%) or CHD only (51.7%).

204 substrate delivery; "CHD-other," with other CHD diagnoses; "CHD-related," healthy with a CHD family

205 ined as >=1 inpatient code or >=2 outpatient CHD diagnosis codes >30 days apart documented outside of

206 ory of 1, 2, and 3 conditions including PAD, CHD, and cerebrovascular disease was 40.8 (95% confidenc

207 e health insurance who had a history of PAD, CHD, or cerebrovascular disease on December 31, 2014.

208 ients with periodontitis and periodontitis + CHD presented higher suPAR levels in both plasma and sal

209 = 29), and a combination of periodontitis + CHD (n = 29) were enrolled in the present study.

210 odontitis (P <.001) and with periodontitis + CHD (P <.001) presented higher median plasma and salivar

211 , suggesting that such treatment may prevent CHD in 1q25 risk allele carriers.

212 000 and 2010 were identified from the Quebec CHD database.

213 dried in 210 min; with higher drying rates, CHD samples showed no significant changes in powder char

214 Recurrent CHD event rates decreased from 166.3 to 133.3 in women a

215 t MI, 0.80 (95% CI, 0.78-0.82) for recurrent CHD events, 0.99 (95% CI, 0.96-1.01) for heart failure h

216 were followed up for recurrent MI, recurrent CHD events (ie, recurrent MI or coronary revascularizati

217 y high, and rates of recurrent MI, recurrent CHD events, and death continue to be higher among men th

218 d sex differences in recurrent MI, recurrent CHD events, and mortality among patients with MI and com

219 Rates of recurrent MI, recurrent CHD events, heart failure hospitalization, and mortality

220 ites, with up to 20% of adults having severe CHD and >50% having >=1 additional cardiovascular comorb

221 More women with severe CHD, compared with nonsevere, experienced adverse condit

222 When removing three known syndromic CHD genes, the findings remained significant (OR = 3.69,

223 Results confirmed that CHD, a variant of the refractance window drying (RWD) of

224 We show that CHD risk can be lowered with incremental changes in life

225 The CHD associations of a subset of 4 metabolites including

226 The CHD samples were dried in 210 min; with higher drying ra

227 ), which is thus largely responsible for the CHD association in the general population.

228 An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CH

229 serum ADMA were significantly higher in the CHD group [serum: 1.5 (1.2 to 1.8) mumol/L; salivary 1.3

230 All twelve metabolites were altered in the CHD protective direction by CEE treatment.

231 ergone whole-exome sequencing as part of the CHD GENES study (Congenital Heart Disease Genetic Networ

232 tional consequences of reduced dosage of the CHD transcription factor, TBX5, in individual cells duri

233 deaths with 1 in 814 deaths attributable to CHD (n=58 599).

234 lthough overall US mortality attributable to CHD has decreased over the past 19 years, disparities in

235 Males had higher mortality attributable to CHD than females throughout the study, although both sex

236 assess the contribution of noncoding DNVs to CHD, we compared genome sequences from 749 CHD probands

237 ting directly attributable to and related to CHD by age, race/ethnicity, and sex.

238 ss current trends in US mortality related to CHD from infancy to adulthood over the past 19 years and

239 sk participants with established and treated CHD.

240 healthy control fetuses and fetuses with TV CHD but increased during maternal hyperoxia in fetuses w

241 ially hemodynamically significant underlying CHD, as compared those without CHD, supporting a need fo

242 heart disease (CHD); however, the underlying CHD gene regulatory network (GRN) imbalances are unknown

243 RI was higher among children with underlying CHD as compared to those without no CHD.

244 ed <5 years, comparing those with underlying CHD to those without CHD.

245 among children aged <5 years with underlying CHD, especially hemodynamically significant underlying C

246 s also higher among children with underlying CHD.

247 beta-sheet levels in both pulses dried using CHD.

248 diac network stability, including vulnerable CHD-linked nodes, is sensitive to TBX5 dosage.

249 Estimated proportions of adults with CHD-coded health care encounters varied greatly by locat

250 the first surveillance effort of adults with CHD-coded inpatient and outpatient health care encounter

251 lood sucrose was not clearly associated with CHD (OR 1.01, 95% CI 0.997-1.02, P = 0.14), nor with its

252 lifestyles during pregnancy associated with CHD differed in various areas of the province.

253 ing frequency was positively associated with CHD for 43.3% of participants (P < 0.05), with the highe

254 the best performing PRS, was associated with CHD in all three cohorts; hazard ratios (95% CI) per 1 S

255 AO levels were significantly associated with CHD incidence.

256 available carbohydrates are associated with CHD risk in both sexes.

257 GI was associated with CHD risk only in the continuous model [HR: 1.04 (95% CI:

258 risk score that is strongly associated with CHD risk was not associated with depression.

259 tion Operator regression was associated with CHD risk with an odds ratio of 1.47 per SD increase (95%

260 wide PRSs were more strongly associated with CHD than restricted PRSs were.

261 Associations with CHD, stroke, and CVD were log linear.

262 asma and salivary suPAR levels compared with CHD and healthy controls.

263 Compared with CHD-related, the HLHS/TGA group had smaller subplate (-1

264 >= 1/week was significantly correlated with CHD among about 24.7% of participants (P < 0.05), with O

265 ay modify the associations of DeltaTMAO with CHD risk.

266 ealthy fetuses and 30 fetuses diagnosed with CHD) between 22 and 39 weeks gestational age (GA) from M

267 .01], respectively), but not in fetuses with CHD and TV or non-AO.

268 The brains of fetuses with CHD were more similar to those of CHD-related than optim

269 Fetuses with CHD, especially those with lowest cerebral substrate del

270 ntified a burden of DNVs in individuals with CHD (n = 2,238 DNVs) compared to controls (n = 4,177; P

271 tea were more likely to have an infant with CHD (P < 0.05), with the highest OR values observed in N

272 livery (CDO(2)) was measured in infants with CHD (n = 49) using phase contrast MR imaging and the rel

273 al brain development in newborn infants with CHD compared to healthy controls using tensor-based morp

274 ompared brain development in 64 infants with CHD to 192 age- and sex-matched healthy controls.

275 significant volume reduction in infants with CHD were demonstrated bilaterally within the basal gangl

276 significant volume expansion in infants with CHD were identified in cerebrospinal fluid spaces (p < 0

277 s abnormal brain development in infants with CHD, identifying areas of particular vulnerability.

278 Patients with CHD and CP + CHD presented higher levels of salivary and

279 ty was 15% although higher for patients with CHD versus non-CHD (19% versus 11%; P<0.001).

280 d from 35 patients with CP, 33 patients with CHD, 35 patients with both CP + CHD, and 35 healthy subj

281 ns of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in the U.S.

282 odds ratios for the association of PRSs with CHD were similar in EA and HE cohorts but lower in AA co

283 kely to be taking a statin versus those with CHD or cerebrovascular disease.

284 We identified 2056 women with CHD (2334 pregnancies) and 1 374 982 women without (1 52

285 recommends providers of pregnant women with CHD assess cardiac health and discuss risks and benefits

286 iod to 90 days postpartum, 56% of women with CHD had comprehensive echocardiograms and, during pregna

287 Conclusions Women with CHD have elevated prevalence of adverse cardiac and obst

288 Women with CHD, compared with those without, experienced more adver

289 care use of adults ages 20 to 64 years with CHDs.

290 trospective cohort of women with and without CHD aged 15 to 44 years with private insurance covering

291 ars were 4.5 in women and 5.7 in men without CHD (hazard ratio [HR]: 0.64; 95% confidence interval [C

292 ear to 687,588 women and 671,972 men without CHD.

293 men were 6.3 versus 10.7 among those without CHD (HR: 0.53; 95% CI: 0.51 to 0.54) and 84.5 versus 99.

294 en were 63.7 versus 59.0 among those without CHD (HR: 0.72; 95% CI: 0.71 to 0.73) and 311.6 versus 28

295 nt underlying CHD, as compared those without CHD, supporting a need for improved RSV prophylactics an

296 g those with underlying CHD to those without CHD.

297 re was significantly associated with 10-year CHD incidence in ARIC with hazard ratios per SD incremen

298 cohorts of asymptomatic individuals, 10-year CHD-to-stroke incidence ratio was higher with increasing

299 Ten-year CHD-to-stroke incidence ratio increased significantly ac

300 Ten-year CHD-to-stroke incidence ratios across CAC score categori