ライフサイエンスコーパス: heart

1 l subpopulations in the developing zebrafish heart.

2 0 subclusters of cell types within the human heart.

3 terious metabolic adaptations of the failing heart.

4 e that rejuvenates the infarcted area of the heart.

5 henotypes in the brain, skeletal muscle, and heart.

6 ble to sustained VF as the untreated failing heart.

7 easures of contractile function in the mouse heart.

8 n and improves cardiac function in infarcted hearts.

9 ventricle of RyR2 wild type or mutant mouse hearts.

10 ricular assist device treatment) adult human hearts.

11 omography-computed tomography scans in human hearts.

12 Embryonic hearts (19 out of 21 days of incubation) mounted on a La

13 r organs saw similar decreases: lung (-70%), heart (-43%), and liver (-37%).

14 gnificant increase in AlexaFFA uptake in the heart (58 +/- 12%) and BAT (278 +/- 19%) compared to war

15 ave discovered that mature frataxin in mouse heart (77%), brain (86%), and liver (47%) is predominant

16 e-associated protein newly identified in the heart, acts as a significant mediator of cardiac protect

17 smooth muscle of terminal arterioles in the heart, adipose tissue and skeletal muscle.

18 In October 2018, the U.S. heart allocation system expanded the number of priority

19 ransplantation Network (OPTN) modified adult heart allocation to better stratify candidates and provi

20 ular mechanisms that govern both early human heart and brain development remain elusive.

21 ne bodies as the metabolic substrate for the heart and kidneys, reduced oxidative stress, lowered ser

22 ntification of blood flow in the human fetal heart and major vessels.

23 lity, and a mostly female group with smaller hearts and proinflammatory signaling.

24 tified 110 kidney, 67 liver, 85 pancreas, 68 heart, and 43 lung TRRs.

25 (SAN) is the primary pacemaker of the human heart, and abnormalities in its structure or function ca

26 structures, including the pharyngeal arches, heart, and anterior somites.

27 is more prone to sustain VF than the normal heart, and is at least as susceptible to sustained VF as

28 unique characteristics of blood vessels, the heart, and the kidney of giraffes and how these function

29 delays cardiomyocyte maturation in postnatal hearts, and markedly enhances cardiomyocyte proliferatio

30 ir production and recruitment to the injured heart are unclear.

31 on of prepregnancy adherence to the American Heart Association (AHA) diet recommendations and the Die

32 the American College of Cardiology/American Heart Association 2013 pooled cohort risk equation.

33 itiative, a partnership between the American Heart Association and the Robert J.

34 ensor is approved for patients with New York Heart Association Class III heart failure (HF) and a pri

35 nters within the United States with New York Heart Association class III HF and a prior HFH within 12

36 th clinical HF characterized by 65% New York Heart Association Class III or IV, nearly all on a loop

37 tudy the relationship between LVEF, New York Heart Association class on presentation, and the end poi

38 Left ventricular function and New York Heart Association class were assessed at baseline (after

39 ely to experience an improvement in New York Heart Association functional class and were 20% to 40% l

40 s likely to experience worsening of New York Heart Association functional class, with statistically s

41 fractory heart failure to disabling New York Heart Association functional classes III/IV (5.2%/year);

42 2019 American College of Cardiology/American Heart Association guideline on the primary prevention of

43 2019 American College of Cardiology/American Heart Association guideline recommendations together wit

44 The American Heart Association has previously published statements ad

45 The American Heart Association must look internally to correct its ow

46 this scientific statement from the American Heart Association, we provide rationale for the widespre

47 The 2018 American Heart Association/American College of Cardiology Multi-S

48 b protein is undetectable in the adult mouse heart at baseline, but mRNA and protein are induced afte

49 ion dynamics in the mouse blood and ischemic heart at the single-cell level, and reveal a process of

50 ce analysis of pn-csERRalpha/gamma knockdown hearts at 5 weeks of age combined with chromatin immunop

51 ate the Effects of ACT-246475 in Adults With Heart Attack; NCT03487445, 2018-000765-36 [EudraCT]).

52 After two heart attacks in three years, an associate professor dis

53 The developing heart begins as a seemingly straight tube, but it soon u

54 epends on the morphological structure of the heart, but also on its subcellular (ultrastructural) arc

55 re greater in Taz(KD) than in wild-type (WT) hearts, but there were no differences in oxidative phosp

56 and decrease to levels typical of the native heart by 90 d.

57 essed with invasive procedures such as right heart catheterization and histopathology.

58 nvasive hemodynamic evaluation through right heart catheterization plays an essential role in the dia

59 Efficient communication between heart cells is vital to ensure the anisotropic propagati

60 investigated the interaction of neonatal rat heart cells with engineered spider silk protein (eADF4(C

61 specification of neutrophils in the ischemic heart characterized by the acquisition of a SiglecF(hi)

62 re of this septation, phenocopying the human heart defect persistent truncus arteriosus (PTA), which

63 style during pregnancy related to congenital heart defects (CHD) in Shaanxi province, Northwestern Ch

64 y and increased offspring risk of congenital heart defects.

65 Maturation is the last phase of heart development that prepares the organ for strong, ef

66 incident CVD cases, including 9,794 coronary heart disease (CHD) cases and 6,174 strokes.

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

68 iple congenital defects including congenital heart disease (CHD).

69 nal brain volumes in infants with congenital heart disease (CHD).

70 scular diseases (CVDs), principally ischemic heart disease (IHD) and stroke, are the leading cause of

71 sm (OR 1.22, 95% CI 1.12-1.34) and ischaemic heart disease (OR 1.30, 95% CI 1.15-1.47).

72 aki disease is the leading cause of acquired heart disease among children in the USA.

73 iated with a lower risk of incident coronary heart disease among participants with the Hp2-2 phenotyp

74 associated with polygenic risk for coronary heart disease and type 2 diabetes.

75 eart syndrome (HLHS) is a complex congenital heart disease characterized by abnormalities in the left

76 standard of care for patients with valvular heart disease for many decades, but transcatheter heart

77 ny recommendations from the earlier valvular heart disease guidelines have been updated with new evid

78 ell (iPSC) disease model of a common form of heart disease involving the aortic valve (AV).

79 ing RV hypertrophy and failure in congenital heart disease is unknown.

80 to show a significant reduction in coronary heart disease or total mortality to the design of the tr

81 Ischemic heart disease remains the foremost cause of death global

82 ter menopause and typically develop coronary heart disease several years later than men.

83 In patients with congenital heart disease undergoing open-heart surgery, de novo var

84 cation improvements for early-onset coronary heart disease, atrial fibrillation and prostate cancer.

85 terval, 8.38 to 15.50), followed by coronary heart disease, atrial fibrillation, and stroke.

86 spid regurgitation in adults with congenital heart disease, but the prevalence and prognostic implica

87 used to determine hazard ratios for coronary heart disease, CVD, and all-cause mortality according to

88 cohorts (with high income, cancer, and with heart disease, respectively).

89 inical outcomes in patients with nonischemic heart disease.

90 nsient ischemic attack and no known coronary heart disease.

91 ions for diagnosis and treatment of valvular heart disease.

92 ay a key role in the development of Coronary Heart Disease.

93 gery; 15.6 (95% CI 9.57-25.4) for congenital heart disease; 1.74 (95% CI 1.33-2.29) for diabetes mell

94 e of a modern lifestyle in abetting Coronary Heart Diseases (CHD) have mostly focused on deterrent he

95 ucing viral replication in the blood, brain, heart (ducklings), and ovaries.

96 may be a therapeutic strategy for preventing heart dysfunction and arrhythmias in DMD patients.

97 fraction after MI (7% versus 12%), previous heart failure (10% versus 19%), atrial fibrillation (6%

98 Acute decompensated heart failure (ADHF) is a highly morbid condition among

99 atients hospitalized for acute decompensated heart failure (ADHF) was well-tolerated and led to impro

100 ased risk of ESKD, with the highest risk for heart failure (hazard ratio, 11.40; 95% confidence inter

101 , 95% CI, 1.28-2.09, P value = 8.07 x 10-5), heart failure (HF) (OR = 1.61, 95% CI, 1.32-1.95, P valu

102 ts with New York Heart Association Class III heart failure (HF) and a prior HF hospitalization (HFH)

103 compensated hypertrophy (CH) until signs of heart failure (HF) are apparent using a trans-aortic pre

104 Heart failure (HF) is a major source of morbidity and mo

105 As a leading cause of death and morbidity, heart failure (HF) is responsible for a large portion of

106 nctional Mitral Regurgitation), treatment of heart failure (HF) patients with moderate-severe or seve

107 a major determinant of clinical outcomes in heart failure (HF) patients.

108 h has been implicated in the pathogenesis of heart failure (HF) with preserved ejection fraction (HFp

109 Heart failure (HF), the leading cause of death in develo

110 Ten trials were of heart failure (n = 4068 patients), 11 of mixed disease (

111 ntation, and the end points of mortality and heart failure admissions in the CASTLE-AF study (Cathete

112 and typical cardiovascular diagnoses such as heart failure and acute myocardial infarction, need freq

113 pulmonary vasculature that results in right heart failure and death, are usually assessed with invas

114 ning the molecular mechanisms of age-related heart failure and highlight exercise as a valuable exper

115 management of volume status in patients with heart failure and may represent a mechanism contributing

116 on and cardiovascular death in patients with heart failure and reduced ejection fraction (HFrEF).

117 of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure

118 elephone follow-up after hospitalization for heart failure can increase 7-day follow-up and reduce in

119 a 57% increased risk of developing incident heart failure compared to a subject at the 10th percenti

120 pro BNP in Patients Stabilized From an Acute Heart Failure Episode), the in-hospital initiation of sa

121 uctural remodeling ( EF >5% and ESV 10%) and heart failure event/cardiovascular death.

122 t of SGLT2 inhibition on fatal and non-fatal heart failure events and renal outcomes in all randomly

123 invasive Remote Monitoring for Prediction of Heart Failure Exacerbation) examined the performance of

124 prognosis remains poor as many patients with heart failure experience symptoms that negatively impact

125 01), with a significant increase in reported heart failure from 1.64% (95% CI 0.82-2.65) to 11.72% (3

126 re enrolled during hospitalisation for acute heart failure from 358 centres in 44 countries on six co

127 bundance of Proteobacteria in the congestive heart failure group (p = 0.014), particularly due to an

128 Heart failure has previously been linked to sleep disord

129 217 total heart failure hospitalisations occurred in the ferric ca

130 otransporter 2 inhibitors reduce the risk of heart failure hospitalization and cardiovascular death i

131 cotransporter-2 (SGLT-2) inhibitors reduced heart failure hospitalization and end-stage renal diseas

132 herapies and presented an increased risk for heart failure hospitalization that warrants further stud

133 recurrent MI or coronary revascularization), heart failure hospitalization, and all-cause mortality (

134 strain for a combined end point (events) of heart failure hospitalizations and cardiovascular death.

135 Empagliflozin reduced the total number of heart failure hospitalizations that required intensive c

136 ffective in both prevention and treatment of heart failure in 2 preclinical animal models.

137 ardiomyopathies, which are a common cause of heart failure in young people, have increased during the

138 tions between brain structure and markers of heart failure including ejection fraction and NT-proBNP.

139 tions, during sympathetic activation, and in heart failure is a major determinant of cardiac physiolo

140 Heart failure is a major public health problem affecting

141 Heart failure is a prominent complication of type 2 diab

142 ns in the OptiLink HF trial (Optimization of Heart Failure Management Using OptiVol(TM) Fluid Status

143 ion-, and myocardial infarction (MI)-induced heart failure mouse models.

144 combined risk of death, hospitalization for heart failure or an emergent/urgent heart failure visit

145 were older, presented with acute congestive heart failure or non-ST-segment-elevation myocardial inf

146 anism contributing to the superior long-term heart failure outcomes observed with these agents.

147 e number of patients with MI develop chronic heart failure over time.

148 nt of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitat

149 nt of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitat

150 During the pandemic, the heart failure program at New York-Presbyterian Hospital

151 The diabetic, hypertensive heart failure rat (mRen27/tetO-shIR) were treated with e

152 of developing the outcomes of mortality and heart failure remained similar across years, although th

153 munodeficiency virus (HIV) imparts increased heart failure risk to women.

154 ed for Meta-Analysis Global Group in Chronic Heart Failure score, genotype, level of BB exposure, and

155 he Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart

156 Failure Society of America and the Japanese Heart Failure Society.

157 site of (1) death; (2) rehospitalization for heart failure symptoms and valve prosthesis complication

158 ve higher rates of hospitalization for acute heart failure than other race/ethnic groups.

159 induces pathological cardiac hypertrophy and heart failure through persistent activation of mTOR.

160 61 other patients (52%) developed refractory heart failure to disabling New York Heart Association fu

161 tion for heart failure or an emergent/urgent heart failure visit requiring intravenous treatment (415

162 rdiovascular death or hospital admission for heart failure was 0.38 (95% CI 0.30-0.47).

163 cardial infarction, or rehospitalization for heart failure was not different between the 2 groups (od

164 ight be able to identify those patients with heart failure who have a cardio-inflammatory phenotype a

165 duces cardiac inflammation in a rat model of heart failure with preserved ejection fraction (HFpEF).

166 age are at high risk for the development of heart failure with preserved ejection fraction (HFpEF).

167 es correlated with NAFLD among patients with heart failure with preserved ejection fraction (HFpEF).

168 Patients with heart failure with reduced ejection fraction (HFrEF; hea

169 use a cohort of Medicare beneficiaries with heart failure with reduced ejection fraction and existin

170 ending to patients without diabetes who have heart failure with reduced ejection fraction.

171 ilure with reduced ejection fraction (HFrEF; heart failure with reduced left ventricular ejection fra

172 theter Ablation for Atrial Fibrillation With Heart Failure) population.

173 e BeAT-HF (Baroreflex Activation Therapy for Heart Failure) trial was a multicenter, prospective, ran

174 cular Remodeling During Entresto Therapy for Heart Failure).

175 al fibrillation, 1.75 (95% CI 1.56-1.97) for heart failure, 1.76 (95% CI 1.51-2.05) for acute myocard

176 w RGS2 protein levels, such as hypertension, heart failure, and anxiety.

177 Cardiac arrhythmias, heart failure, and nonfatal coronary syndromes are also

178 cardiovascular death, rehospitalization for heart failure, and pacemaker implantation after a TAVR p

179 licly available data sets of human and mouse heart failure, demonstrated that EPRS acted as an integr

180 alve surgery can mitigate the progression to heart failure, disability, and death.

181 lity care to a large cohort of patients with heart failure, heart transplantation, and left ventricul

182 apies to target macrophage metabolism during heart failure, including antidiabetic therapies, anti-in

183 Heart failure, induced via myocardial infarction, causes

184 For heart failure, the pooled proportion, based on 38 studie

185 SAVR, TAVR, and disease symptoms (congestive heart failure, unstable angina, non-ST-elevation myocard

186 enal outcomes, including hospitalization for heart failure, with this benefit extending to patients w

187 o become a therapeutic target for preventing heart failure-associated ventricular arrhythmia.

188 inical trials for cardiovascular disease and heart failure.

189 d functional changes in the heart leading to heart failure.

190 fects of SDOH in an underserved patient with heart failure.

191 namely arrhythmogenesis and progression into heart failure.

192 ated pulmonary vascular resistance and right heart failure.

193 r, this has never been investigated in human heart failure.

194 bally, with survivors at risk for subsequent heart failure.

195 pressure regulation and reducing the risk of heart failure.

196 adian pattern of occurrence in patients with heart failure.

197 improve self-care behaviour in patients with heart failure.

198 ociated with acute myocardial infarction and heart failure.

199 iated with excess morbidity and mortality in heart failure.

200 -dose intravascular cocaine results in acute heart failure.

201 ment of KEs as a treatment for patients with heart failure.

202 lar and renal outcomes with empagliflozin in heart failure.

203 ach to ameliorate metabolic dysregulation in heart failure.

204 r than expected was observed in the lung and heart for up to 24 h.

205 ual Ca(2+)/voltage optical mapping in intact hearts from alcohol-exposed or aged mice (where JNK2 is

206 compared the structure and morphology of 16 hearts from chimpanzees (Pan troglodytes) which were eit

207 me relationships fundamental to the study of heart function and remodeling with health and disease.

208 ac biomechanics intricately affect long-term heart function, but whether regenerated cardiac muscle i

209 experimental studies to treat and understand heart function, respectively, in-silico models play an i

210 without impairment of hemodynamics or right heart function.

211 se testing, demonstrates that that the right heart has enormous contractile reserve, with a three- or

212 ment; percutaneous coronary intervention; or heart/heart-lung transplant).

213 and interconnected metabolic pathways of the heart; however, normalization of metabolite abundance to

214 dial trabeculae in the function of the adult heart, identify conserved pathways that regulate structu

215 e feasibility of computer simulations of the heart in understanding the arrhythmic behavior in novel

216 Interestingly, hearts in animal species with substantial cardiac regene

217 ng by serial expert committees, the National Heart Institute opted against an explanatory diet trial

218 d protein expression levels in blood, brain, heart, intestine, kidney, liver, lung, muscle and spleen

219 The failing heart is characterized by changes in gene expression.

220 In this study, we show that the T2D heart is metabolically inflexible and almost exclusively

221 Further, we found that the treated failing heart is more prone to sustain VF than the normal heart,

222 Myocardial infarction, following heart ischemia and reperfusion, is associated with profo

223 ses structural and functional changes in the heart leading to heart failure.

224 notoxicity of different organs including the heart, liver, kidney, lungs, immune system, gastro-intes

225 National Institutes of Health, National Heart, Lung, and Blood Institute.

226 pediatric solid-organ transplant recipients (heart, lung, liver, kidney, multiorgan) at The Hospital

227 TC and ETC activities in both populations of heart mitochondria in T2DM rats were unchanged.

228 one toxin, ATXII) Na(+) channel GOF isolated heart model and modulate extracellular spaces via osmoti

229 HCV+ nonviremic (HCV-NV) and viremic (HCV-V) hearts nationally and by UNOS region.

230 Molecular motors are at the heart of cellular machinery, and they are involved in co

231 itor cells in the dental follicle lie at the heart of the coupling of these 2 processes, providing a

232 At the heart of these endeavors is institutional accountability

233 apeutics and vaccine design should be at the heart of this enterprise.

234 iomaterials efforts and the Total Artificial Heart program at the time, while providing the foundatio

235 alculated HBP flux at ~2.3 and 2.5 nmol/g of heart protein/min, respectively.

236 .4 versus 22.7+/-4.0 mL/kg/min; P<0.001) and heart rate (122+/-20 versus 155+/-14 bpm; P<0.001) were

237 P < 0.001) compared to Amb, without changing heart rate (P = 0.6) or vascular-sympathetic baroreflex

238 tein Gs by beta(1)-ARs, leading to increased heart rate and contractility.

239 ted in a dose-dependent higher HRV and lower heart rate at 5 days post-fertilization.

240 The PQ interval also responded to the heart rate changes with a delay which was highly sex dep

241 increased sensitivity of the QT interval to heart rate changes.

242 l, these findings support the acquisition of heart rate deceleration concurrently with fMRI to provid

243 and mediate increases in blood pressure and heart rate induced by falls in brain perfusion.

244 and the averaged baseline measures of HRV to heart rate recovery (HRR) following maximal exercise.

245 here were no significant differences in peak heart rate response during static handgrip between group

246 the relationship of a single day measure of heart rate variability (HRV), and the averaged baseline

247 Heart rate variability (time and frequency domain) and a

248 ress event (sham clipping) and compared with heart rate variability and salivary cortisol.

249 at 26 of them (81%) had alterations in their heart rate, number of daily steps or time asleep.

250 uivalency to existing clinical standards for heart rate, respiration rate, temperature and blood oxyg

251 subjects led to increased blood pressure and heart rate, similar to traditional cigarettes.

252 external measurements (e.g., motion capture, heart rate, skin conductance, respiration, eye tracking,

253 EMW outperformed heart rate-corrected QT interval as a predictor of sympt

254 n important role in the autonomic control of heart rate.

255 ta3 AR agonists did not significantly change heart rates or blood pressures.

256 dial survival and proliferation, and overall heart regeneration, accompanied by decreased fibrosis.

257 egulated at the injury site during zebrafish heart regeneration, and that absence of runx1 results in

258 r cardiomyocyte proliferation and subsequent heart regeneration.

259 shortened APD(80) in DBH-Sap but not control hearts, resulting in a significant increase in APD(80) d

260 6971 genetic polymorphism in human brain and heart samples.

261 n glucose and lipid metabolism in the liver, heart, skeletal muscle, and adipose tissue.

262 d non-viral-mediated gene transfer to liver, heart, skeletal muscle, and the central nervous system,

263 hin restoration in approximately half of the heart still allows for marked vulnerability to injury.

264 American Indian participants from the Strong Heart Study (1989-1991) and evaluated these associations

265 d 0.954 for the ADNI study, AIBL, Framingham Heart Study and NACC datasets, respectively.

266 f at least 1 parent did so in the Framingham Heart Study cohorts, and estimated the incidence rates a

267 years of age who participated in the Strong Heart Study in 1989-1991.

268 plasma proteins measured in FHS (Framingham Heart Study) participants.

269 ith congenital heart disease undergoing open-heart surgery, de novo variants were associated with wor

270 Hypoplastic left heart syndrome (HLHS) is a complex congenital heart dise

271 ps: "HLHS/TGA" fetuses with hypoplastic left heart syndrome (HLHS) or transposition of the great arte

272 s for synchronized activation in the healthy heart, the dysregulated excess in this pathway underscor

273 In Langendorff-perfused hearts, there were no differences in mean action potenti

274 me expression, rendering knockout-engineered heart tissue sensitive to metabolic stress such as serum

275 n of metabolite abundance to sample input in heart tissues remains a technical challenge.

276 nal specializations in cardiomyocytes as the heart transits from fetal to adult states.

277 e use of hemodynamic assessment in pediatric heart transplant (HT) patients, expected intracardiac pr

278 dded cardiogenic shock requirements for some heart transplant candidates listed with specific types o

279 ty panel reactive antibody [CDC PRA+], C1q+) heart transplant candidates were treated with the combin

280 ation in VSMCs isolated from 151 multiethnic heart transplant donors.

281 Act (ACA) has been associated with increased heart transplant listings among blacks, who are dispropo

282 ey sent electronically to 1643 United States heart transplant providers between June and August 2019.

283 recipients, 1 liver transplant recipient, 1 heart transplant recipient, and 1 lung transplant recipi

284 /year); 67% have survived, including 31 with heart transplant.

285 mortality, LV assist device implantation, or heart transplantation was assessed.

286 large cohort of patients with heart failure, heart transplantation, and left ventricular assist devic

287 we compared trends in the utilization rates (hearts transplanted/donors recovered) of HCV-uninfected

288 patient with Tetralogy of Fallot, a serious heart valve defect, affects the substrate selectivity of

289 owth factor (HB-EGF), a crucial regulator of heart valve development in mice.

290 d family members presenting with progressive heart valve disease early in life.

291 italization; coronary artery bypass surgery; heart valve repair/replacement; percutaneous coronary in

292 Timely heart valve surgery can mitigate the progression to hear

293 disease for many decades, but transcatheter heart valve therapy has revolutionized the field in the

294 Polymeric heart valves seem to be an attractive alternative to mec

295 trophysiological properties in failing human heart ventricles have not been examined for a circadian

296 ercellular communication networks within the heart, we identified key intercellular trophic relations

297 n pattern in the ventricles of failing human hearts, which may underlie a circadian pattern of ventri

298 (at 30 nmol/L, n=7/12 and 100 nmol/L n=8/12 hearts without EADs and PVTs).

299 Consistent survival of life-supporting pig heart xenograft recipients beyond 90 days was recently r

300 In anticipation of the "first-in-human" heart xenotransplantation trial, we propose a set of pat