ライフサイエンスコーパス: cardiac

1 34 LB/B variants, mostly in cancer (40%) and cardiac (27%) risk genes.

2 zations during the repolarization phase of a cardiac action potential that can trigger fatal ventricu

3 scular disease (CVD) were recruited from the Cardiac Ageing Study.

4 Klotho deficiency causes cardiac aging via impairing the Nrf2-GR pathway.

5 between cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on p

6 ho have exhibited early onset or accelerated cardiac allograft vasculopathy.

7 promising approach for extending survival of cardiac allografts from CMV-infected donors.

8 of RyR2 an important therapeutic target for cardiac alternans.

9 Cardiac amyloidosis may be an additional risk factor for

10 formed our ability to diagnose transthyretin cardiac amyloidosis noninvasively and unmasked a hithert

11 vel approaches for the diagnostic imaging of cardiac amyloidosis.

12 ished conditioned fear in rodents and lacked cardiac and behavioral side effects, suggesting its pote

13 rst to summarize the emerging picture of the cardiac and musculoskeletal deficits in human AD.

14 pposite roles by ARID1A to govern both early cardiac and neural development from pluripotent stem cel

15 of TRPC6 inhibition in treating pathological cardiac and renal conditions, mechanistic understanding

16 Chronic conditions, including cardiac and respiratory diseases and mental health condi

17 rous essential cellular functions, including cardiac and skeletal muscle contraction.

18 arcomere order is paramount in evaluation of cardiac and skeletal myocytes.

19 rsus 78.7%), acute noncardiac organ failure, cardiac arrest (34.3% versus 35.7%), and received less-f

20 Among patients with out-of-hospital cardiac arrest (OHCA) and ventricular fibrillation, more

21 transport to hospital during out-of-hospital cardiac arrest (OHCA) resuscitative efforts.

22 er was arrhythmic death (AD) or resuscitated cardiac arrest (RCA).

23 l benefit in select patients with refractory cardiac arrest but there is insufficient data on the fre

24 prove overall survival after out-of-hospital cardiac arrest from shock-refractory ventricular fibrill

25 ardized survival rate (RSSR) for in-hospital cardiac arrest has emerged as an important metric to ben

26 assessed at 3 months and beyond 1 year after cardiac arrest if resources are available.

27 6, we identified patients who had refractory cardiac arrest in the ED.

28 68 piglets were randomized to cardiac arrest or sham procedure with continuous monitor

29 t not neurologic outcomes in out-of-hospital cardiac arrest patients compared with placebo.

30 Initial interdisciplinary training in cardiac arrest prevention followed by clinical practice

31 Mean monthly cardiac arrest rate was 17.2 per 1,000 patient days befo

32 Neurologic damage following cardiac arrest remains a major burden for modern resusci

33 rdinal severity score (worst to best: death, cardiac arrest, mechanical ventilation with mechanical c

34 in the chain of survival for out-of-hospital cardiac arrest.

35 ent in comatose survivors of out-of-hospital cardiac arrest.

36 parents/caregivers of children who survived cardiac arrest.

37 R delivery and survival from out-of-hospital cardiac arrest.

38 D implantation, ventricular arrhythmias, and cardiac arrest: 0.96% (95% CI: 0.77% to 1.18%) for sarco

39 brillation (AF) is the most common sustained cardiac arrhythmia in clinical practice and is known to

40 The main inherited cardiac arrhythmias are long QT syndrome, short QT syndr

41 Cardiac arrhythmias, heart failure, and nonfatal coronar

42 outcome of 30-day SAEs, including death and cardiac (arrhythmic and nonarrhythmic) and noncardiac ev

43 Furthermore, AV-Shunt(Gap27) showed less cardiac arrhythmogenesis and cardiac hypertrophy index c

44 a seizure) and interictal (between seizure) cardiac arrhythmogenesis following SE using continuous e

45 We investigated the integrity of cardiac beta-receptor responsiveness, an important mecha

46 esis, patients with HFpEF displayed impaired cardiac beta-receptor sensitivity compared with senior c

47 onary artery calcification, exercise-induced cardiac biomarker release, myocardial fibrosis, and atri

48 nts with LVH (LV septum >11 mm) and elevated cardiac biomarkers (N-terminal pro-B-type natriuretic pe

49 of endurance athletes have raised levels of cardiac biomarkers (troponins and B-type natriuretic pep

50 ensitive quantitative detection of multiplex cardiac biomarkers in human serum to expedite medical de

51 t ventricular hypertrophy (LVH) and elevated cardiac biomarkers in middle age are at high risk for th

52 Cardiac biomechanics intricately affect long-term heart

53 rspectives regarding the potential causes of cardiac birth defects.

54 Changing activity of cardiac Ca(V)1.2 channels under basal conditions, during

55 using (99m)Tc-tetrofosmin and a solid-state cardiac camera.

56 pharmaco-invasive strategy, and the risk of cardiac catheterization laboratory provider infection re

57 6 died or were euthanized due to a possible cardiac cause.

58 The functional benefit of cardiac cell therapy is thus due to an acute inflammator

59 ate the regulation and function of PDE10A in cardiac cells and in the progression of cardiac remodeli

60 However, due to their high energy demands, cardiac cells are disproportionately targeted by mitocho

61 ucidate the complex role played by CYP2J2 in cardiac cells, we performed targeted silencing of CYP2J2

62 n experiments on both atrial and ventricular cardiac cells.

63 in an in vitro model of MI/IRI in mammalian cardiac cells.

64 fic antibody, posttransplant diabetes (PTD), cardiac complications, estimated glomerular filtration r

65 Cardiac computed tomography showed a hypodense area in t

66 tly attenuated, after considering antecedent cardiac conditions (ie, heart failure/cardiomyopathy, hy

67 nderstand the molecular mechanisms of AF and cardiac conduction phenotypes.

68 proximate 8-fold change in expression of the cardiac contractile regulatory gene cmlc2 was also seen

69 Increased cardiac contractility during the fight-or-flight respons

70 ultrastructural) architecture, which enables cardiac contraction.

71 Chick cardiac crest ablation results in failure of this septat

72 k crest with the ability to rescue PTA after cardiac crest ablation.

73 that define one subtype of neural crest, the cardiac crest, and demonstrate their ability to reprogra

74 strate their ability to reprogram trunk into cardiac crest.

75 c imaging tools such as echocardiography and cardiac CT or CT angiography are the first-line modaliti

76 ce-area product (RAP) were obtained for each cardiac cycle and their dynamic response to a step chang

77 ith a peak and trough that correlates with a cardiac cycle as revealed by a reference pulse oximeter

78 extremes of the pressure waveform during the cardiac cycle.

79 Thus, cardiac D1R has the potential to become a therapeutic ta

80 inistration of atorvastatin during MI limits cardiac damage, improves cardiac function, and mitigates

81 ce mortality (RR, 0.98 [95% CI, 0.87-1.11]), cardiac death (RR, 0.89 [95% CI, 0.71-1.12]; P=0.33), or

82 emerging factors to be considered in sudden cardiac death risk stratification.

83 Ventricular tachyarrhythmias and sudden cardiac death show a circadian pattern of occurrence in

84 a low- or intermediate 5-year risk of sudden cardiac death underwent cardiac magnetic resonance imagi

85 attern of ventricular tachyarrhythmia/sudden cardiac death.

86 is an uncommon but important cause of sudden cardiac death.

87 rdiac-specific overexpression of YAP rescues cardiac defects in Xinbeta knock-out mice-indicating a f

88 NPs (natriuretic peptides) are cardiac-derived hormones that promote natriuresis, diure

89 light a lymphoangiocrine role of LECs during cardiac development and injury response, and identify RE

90 regulate digit number, body patterning, and cardiac development.

91 disease, prosthetic valve, previous IE, and cardiac device.

92 Cardiac devices included pacemakers (46%), ICDs (30%), c

93 ion of Hoxb1 in embryonic stem cells arrests cardiac differentiation, whereas Hoxb1-deficient mouse e

94 b1-deficient mouse embryos display premature cardiac differentiation.

95 early lethality, defects in neurogenesis and cardiac dilation.

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

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

98 eneration, and its potential contribution to cardiac disease.

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

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

101 ing antiviral, antibacterial, anticancer and cardiac drugs(6,7).

102 ins where Ca(V) channels reside, such as the cardiac dyad.

103 C4KO mice developed modest cardiac dysfunction and dilation in response to exercise

104 s its contribution to systolic and diastolic cardiac dysfunction and impaired clinical outcomes in pa

105 roponins and B-type natriuretic peptide) and cardiac dysfunction for 24-48 h after events, but what i

106 Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in patients with end-stage liver dis

107 suggesting a potential synergistic effect of cardiac dysfunction on fibrosis risk in NAFLD.

108 the important role of ECC remodeling in the cardiac dysfunction secondary to chronic sympathetic act

109 or necrosis factor-alpha levels and improved cardiac dysfunction, myocardial inflammation, and oxidat

110 on by deletion of ACC2 prevented HFD-induced cardiac dysfunction, pathological remodeling, and mitoch

111 o prevent its phosphorylation by PKB display cardiac dysfunction.

112 g been appreciated that these changes in the cardiac ECM result in altered mechanical properties of i

113 We conclude that cardiac electrical activity provides important informati

114 She was born at term and experienced no cardiac events until 4 years of age, at which point she

115 We assess the cardiac failure risk in patients receiving osimertinib b

116 variations in collagen organization regulate cardiac fibroblast phenotype through mechanical activati

117 Aligned mimetics caused cardiac fibroblasts to elongate while randomly organized

118 Eprs(flox/+); Postn(MCM/+)) strongly reduces cardiac fibrosis (~50% reduction) in isoproterenol-, tra

119 g candidates for therapeutic applications in cardiac fibrosis and diastolic dysfunction.

120 h an angiotensin II-mediated murine model of cardiac fibrosis in both preventive and therapeutic sett

121 nd flow, on the basis of sex, by quantifying cardiac flow characteristics and relating them to cardia

122 injury in DM mice, as evidenced by improved cardiac function (increased LVEF and +/-Dp/dt), decrease

123 uced cardiac rupture incidence, and improved cardiac function after MI.

124 further understand the relationship between cardiac function and flow, on the basis of sex, by quant

125 with the aim of inducing cardiomyopathy, and cardiac function and remodeling was assessed by echocard

126 t year (Y) 7 (Y7) and Y15 examinations, with cardiac function assessed at Y30 after adjustment for ke

127 o attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothel

128 ces cardiomyocyte proliferation and improves cardiac function in infarcted hearts.

129 dentify an endocrine role for BAT to enhance cardiac function that is mediated by regulation of calci

130 rvous system is essential for maintenance of cardiac function via activation of post-junctional adren

131 that transplantation of BAT (+BAT) improves cardiac function via the release of the lipokine 12,13-d

132 5% CI 0.82-2.65) to 11.72% (3.00-24.53) when cardiac function was evaluated post-chemotherapy (p=0.01

133 in during MI limits cardiac damage, improves cardiac function, and mitigates remodeling to a larger e

134 ower BA levels were associated with improved cardiac function, reduced myocardial damage, shock, lung

135 r aortic pathologies and diminished baseline cardiac function.

136 n and ICAM-1 with subclinical alterations in cardiac function.

137 mitochondrial toxins resulting in a loss of cardiac function.

138 yocardial infarction, in each case improving cardiac function.

139 way by recruiting NF2 to the ICD to modulate cardiac function.

140 the myocardium and corresponding decline in cardiac function.

141 ut administration of contrast media, and non-cardiac-gated multidetector CT with and without contrast

142 Cardiac glucose uptake and oxidation are reduced in diab

143 I-A(d)) or third-party (C3H, H2K(k), I-A(k)) cardiac grafts.

144 er glucose availability or workload regulate cardiac HBP flux.

145 DO could play a key role to locally regulate cardiac homeostasis after MI.

146 nder hemodynamic stress induces pathological cardiac hypertrophy and heart failure through persistent

147 ermline deletion of Grb14 in mice results in cardiac hypertrophy and impaired systolic function, whic

148 ation, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by imp

149 ging cell type crosstalk during pathological cardiac hypertrophy but also shed light on strategies fo

150 ll population that can be regulated to treat cardiac hypertrophy by improving neovascularization and

151 27) showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-Shunt(Scr).

152 ainst pressure overload-induced pathological cardiac hypertrophy.

153 ment suppressed CKD-induced hypertension and cardiac hypertrophy.

154 a context-specific model of beta-adrenergic cardiac hypertrophy.

155 al delay, intellectual disability as well as cardiac hypertrophy.

156 in medical/surgical ICUs, 59 (20.2%) were in cardiac ICUs.

157 native valve IE than prosthetic valve IE and cardiac implantable electronic devices IE.

158 t tailoring the rate-response programming of cardiac implantable electronic devices in patients with

159 and 55 Gy caused slowing and interruption of cardiac impulse propagation at the atrioventricular junc

160 ctive of our study is to describe changes in cardiac index, mean arterial pressure, and their relatio

161 Cardiac index-responsiveness and mean arterial pressure-

162 ur studies suggest that Mcub is a protective cardiac inducible gene that reduces mitochondrial Ca(2+)

163 ation was recorded regarding severity, type (cardiac, infectious, etc), etiology (surgical/medical),

164 Cardiac inflammation before implantation was negatively

165 of vagus nerve at the tragus (LLTS) reduces cardiac inflammation in a rat model of heart failure wit

166 AZM use resulted in a remarkable decrease in cardiac inflammatory neutrophils and the infiltration of

167 lammation, cytokine storm, and elevations of cardiac injury biomarkers.

168 ted in communication defects associated with cardiac injury, namely arrhythmogenesis and progression

169 Background Cardiac involvement is the leading cause of mortality in

170 s been associated with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.

171 challenging because of its similarity to the cardiac isoform.

172 on unresponsive to initial standard advanced cardiac life support (ACLS) treatment.

173 Advance in determining cardiac lineage diversification has often been limited b

174 cells before differentiating into nonmyocyte cardiac lineages, such as vascular smooth muscle cells,

175 We aimed to test the efficacy of ablating cardiac magnetic resonance (CMR)-detected atrial fibrosi

176 f 2276 participants with available FGF23 and cardiac magnetic resonance at 10-year follow-up, partici

177 electrogram locations were coregistered with cardiac magnetic resonance images.

178 -year risk of sudden cardiac death underwent cardiac magnetic resonance imaging.

179 tensities are both associated with potential cardiac maladaptations, including accelerated coronary a

180 f diverse adverse functional and morphologic cardiac manifestations in PEX, involving signs of abnorm

181 c-deprived hypertensive phenotype, including cardiac manifestations.

182 is and function, serve a role in the broader cardiac maturation program.

183 The associations between eGFR, cardiac mechanics, and cardiovascular events were partly

184 an impaired ability to differentiate towards cardiac mesoderm.

185 previously implicated in regulation of adult cardiac metabolism.

186 sought to evaluate the impact of implantable cardiac monitoring (ICM) in the prevention of stroke rec

187 n-Hodgkin lymphoma and stresses the need for cardiac monitoring during and after chemotherapy.

188 pplied to human adult Ultrasound data from a Cardiac Motion Analysis Challenge (CMAC), the proposed m

189 age registration is thus a viable option for cardiac motion estimation that can still have good accur

190 , abdominal studies in which respiratory and cardiac motion is visible, and a whole-body survey.

191 enation alterations with current noninvasive cardiac MRI blood oxygen level-dependent (BOLD) techniqu

192 This case series examines cardiac MRI findings in four children and adolescents ad

193 dvances, blood oxygen level-dependent (BOLD) cardiac MRI for myocardial perfusion is limited by inade

194 Cardiac MRI LGE showed myocardial scar in three of 17 ca

195 untreated showed no change in any FDG PET or cardiac MRI parameter.

196 rwent electrocardiography, echocardiography, cardiac MRI with and without administration of contrast

197 At follow-up cardiac MRI, patients who improved to or were maintained

198 d the increase in diffuse reflectance of the cardiac muscle beneath the endocardial layer.

199 tailed mechanisms of drug-induced effects on cardiac muscle contractility.

200 Cardiac muscle hypercontractility is a key pathophysiolo

201 (P6), representing a barrier to building new cardiac muscle in adults.

202 term heart function, but whether regenerated cardiac muscle is biomechanically similar to native myoc

203 ac flow characteristics and relating them to cardiac muscle performance in young adults.

204 orm to investigate extracellular signals for cardiac muscle survival, substantiating human cardioprot

205 mental, and regulatory roles in skeletal and cardiac muscle.

206 in several splicing defects in skeletal and cardiac muscles.

207 We followed changes in cardiac myocyte Ca(2+) and Na(+) regulation from the for

208 ce with established cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and fla

209 A with selective inhibitor TP-10, attenuated cardiac myocyte pathological hypertrophy induced by Angi

210 hrine, and isoproterenol, but did not affect cardiac myocyte physiological hypertrophy induced by IGF

211 human induced pluripotent stem cell-derived cardiac myocytes (hiPSC-CM) demonstrated that ERRgamma a

212 lial cells and vascular smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/m

213 electron microscopy we identified, in adult cardiac myocytes, a Na(V)1.5 subpopulation in close prox

214 In cardiac myocytes, clusters of type-2 ryanodine receptors

215 onary arteries during development and during cardiac neovascularization after injury are poorly under

216 ulation therapy of stimulation of epicardial cardiac nerves passing along the posterior surface of th

217 quenced the transcriptomes of 287 269 single cardiac nuclei, revealing 9 major cell types and 20 subc

218 They also had a higher European System for Cardiac Operative Risk Evaluation and more often underwe

219 The findings suggest a key role of cardiac Orai1 channels and the potential for Orai1 chann

220 Damaging GATA6 variants cause cardiac outflow tract defects, sometimes with pancreatic

221 g CPT, there was a moderate relation between cardiac output and BP responses after placebo administra

222 resistance, which constrains stroke volume, cardiac output and O(2) delivery, thereby impairing VO2

223 In contrast, at isotime, minute ventilation, cardiac output and systemic oxygen delivery did not diff

224 f increase in pulmonary pressure relative to cardiac output with exercise >3 mm Hg/l/min.

225 tion in the mouse sinoatrial node (SAN), the cardiac pacemaker.

226 an integrated node among the ARSs in various cardiac pathogenic processes.

227 d in heart failure is a major determinant of cardiac physiology and pathophysiology.

228 elf, which is challenging due to the altered cardiac physiology in these patients and current guideli

229 However, the contribution of ZO-1 to cardiac physiology remains poorly defined.

230 In terms of cardiac physiology, acute exposure to e-cigarette aeroso

231 pathways that drive atrial remodeling during cardiac pressure overload are poorly defined.

232 ETV1 is downregulated in the LA during cardiac pressure overload, contributing to both electric

233 so develop following aortic valve disease or cardiac procedures.

234 the heart, acts as a significant mediator of cardiac protection against pressure overload-induced pat

235 provide a novel therapeutic target to treat cardiac proteinopathies.

236 Cardiac pumping depends on the morphological structure o

237 integrin (CD51) as an essential regulator of cardiac PW1(+) cells fibrogenic behavior.

238 cally relevant therapeutic target to improve cardiac recovery and reduce heart failure post-MI in hum

239 turbed caudal fin regeneration and abrogated cardiac regeneration altogether.

240 We dissected a cardiac regeneration enhancer in zebrafish to elucidate

241 This analysis also revealed that cardiac regeneration enhancers are not only activated by

242 y, hearts in animal species with substantial cardiac regenerative capacity dominantly comprise diploi

243 Cardiac rehabilitation (CR) is recommended in clinical p

244 Following hospitalization, he completes cardiac rehabilitation.

245 filled potentially teratogenic or fetotoxic cardiac-related prescriptions.

246 Adverse cardiac remodeling after myocardial infarction (MI) caus

247 A in cardiac cells and in the progression of cardiac remodeling and dysfunction.

248 ibition of PP2A signaling prevents eccentric cardiac remodeling induced by myocardial infarction, in

249 bition of RSK3 signaling prevents concentric cardiac remodeling induced by pressure overload, while i

250 e metabolic dysfunction, particularly during cardiac remodeling, are not fully understood.

251 the injured myocardium and are essential for cardiac repair as they can adopt both pro-inflammatory o

252 Cardiac resynchronization therapy (CRT) is an establishe

253 vices included pacemakers (46%), ICDs (30%), cardiac resynchronization therapy (CRT) pacemakers (4%),

254 ices included 38 dual-chamber pacemakers, 17 cardiac resynchronization therapy defibrillators, and 2

255 , implantable cardioverter defibrillator and cardiac resynchronization therapy implantation, LVEF imp

256 ynchronization therapy defibrillators, and 2 cardiac resynchronization therapy pacing systems.

257 undle branch block may respond positively to cardiac resynchronization therapy.

258 e coronary sinus is the mainstay approach of cardiac resynchronization therapy.

259 ce restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function

260 ng FR-beta, which were also present in human cardiac sarcoid lesions.

261 The myocardium of patients with cardiac sarcoidosis showed many FR-beta-positive macroph

262 fect "heart regeneration", replacing injured cardiac scar tissue with concomitant electrical integrat

263 -18 years; 27 of 48 [56%] male) referred for cardiac screening 1.5-T MRI between 2014 and 2017.

264 on in cardiomyocytes did not affect baseline cardiac size or function in young adult mice.

265 cted within the right fibrous trigone of the cardiac skeleton.

266 Cardiac sodium channel expression, I(Na) and atrial acti

267 K, the effect of SF-PreCon was determined in cardiac-specific AMPKalpha2 dominant negative expressing

268 Cardiac-specific overexpression of YAP rescues cardiac d

269 This study used a cardiac-specific VCP transgenic mouse model to understan

270 The pulmonary and cardiac standard uptake value and volume 1-M post-exposu

271 in men and displayed moderate correlation to cardiac strain metrics.

272 iptomic alterations induced by VCP under the cardiac stress caused by pressure overload.

273 mal homeostasis of cardiomyocytes and during cardiac stress, which could make it an interesting targe

274 Cardiac structural abnormalities, left ventricular hyper

275 rides are associated with adverse changes in cardiac structure and function, in particular in relatio

276 th postoperative AF (5-year incidence 32% in cardiac surgery and 39% in noncardiothoracic surgery).

277 ew Oral Anticoagulants vs. Warfarin for post Cardiac Surgery Atrial Fibrillation: The NEW-AF Trial.

278 The cardiac surgery literature consists mostly of small, sin

279 tients undergoing cardiac surgery, and 1% of cardiac surgery patients will require mechanical circula

280 shock occurs in 2-6% of patients undergoing cardiac surgery, and 1% of cardiac surgery patients will

281 nagement of patients with CAD undergoing non-cardiac surgery, including those treated with stents.

282 ociated with hemodynamic compromise, sepsis, cardiac surgery, or exposure to nephrotoxins.

283 the most severe and feared complications of cardiac surgery.

284 (Synergy Between PCI With TAXUS and Cardiac Surgery: SYNTAX Extended Survival [SYNTAXES], NC

285 reservation were randomized at 7 specialized cardiac surgical centers.

286 hich could make it an interesting target for cardiac therapy.

287 ariants located in exons highly expressed in cardiac tissue (TTN(LOF)).

288 scular disease due to its ability to remodel cardiac tissue and generate angiotensin II.

289 we found that CYP2J2 expression is lower in cardiac tissue from patients with cardiomyopathy compare

290 for the survival of existing and regenerated cardiac tissue.

291 The presence of methanogens in vascular and cardiac tissues was assessed by indirect immunofluoresce

292 ncoding LMP2 and LMP7 by immunization with a cardiac TnI peptide.

293 ly reduced triptolide-associated hepatic and cardiac toxicities.

294 TA binding protein 4), a lineage-determining cardiac transcription factor not previously implicated i

295 ng pathways during IRI, we treated syngeneic cardiac transplant recipients at 1-hour posttransplant w

296 vely inherited null variants in TRDN-encoded cardiac triadin.

297 The structured use of serial cardiac troponin has the potential to facilitate risk st

298 croarray analysis of serum biomarkers (e.g., cardiac troponin I) afforded up to 130-fold enhancement

299 nges in coronary artery, thoracic aorta, and cardiac valve calcium scores and pulse wave velocity wer

300 Reducing cardiac workload in beating and nonbeating Langendorff p