ライフサイエンスコーパス: cardiac

1 on without affecting noncardiac tissues; the cardiac abnormalities could be noninvasively captured by

2 NTS: Severe aortic valve diseases are common cardiac abnormalities that are associated with poor long

3 Morphant embryos displayed cardiac abnormalities, including pericardial edema and h

4 diac arrest is defined as the termination of cardiac activity associated with loss of consciousness,

5 incidence of death, sudden death, and other cardiac adverse events.

6 lerated, even among the 72% of patients with cardiac AL involvement.

7 as defined as the occurrence of respiratory, cardiac, allergic, or neurological complications requiri

8 o shed light on the underlying mechanisms of cardiac alternans especially when the relative strength

9 meters has been suggested for distinguishing cardiac amyloidosis (CA) from other causes of myocardial

10 tors included demographics, anthropometrics, cardiac and blood measures, diet and exercise, physical

11 Major adverse cardiac and cardiovascular event rate at 30 days was low

12 In-hospital major adverse cardiac and cerebral events occurred in 2.0% in fTRA and

13 Investigated cardiac and inflammatory markers included high-sensitivi

14 using a new method that incorporates various cardiac and mediastinal segmentation schemes in which up

15 the potential to differentiate into multiple cardiac and mesenchymal lineages, with preferential diff

16 Treatment with serelaxin prevented cardiac and renal dysfunction in DOCA-salt rats.

17 y was restored, concomitant with ameliorated cardiac and renal hypertrophy.

18 ed data from which we reconstruct volumetric cardiac and respiratory motion phases, contrast-agent dy

19 t failure specialists, cardiac surgeons, and cardiac anesthesiologists may help pair the right patien

20 ted cardiac overexpression of Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorub

21 FRD significantly augmented cardiac apoptosis in WT vs. CD-WT mice, which was preven

22 Out-of-hospital cardiac arrest (OHCA) commonly presents with nonshockabl

23 roportion of black patients with in-hospital cardiac arrest achieved larger survival gains over time.

24 To describe death and cardiac arrest among triathlon participants.

25 idal-thalamo-cortical mesocircuit induced by cardiac arrest and pave the way for the use of combined

26 ienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014.

27 Exclusion of selected cardiac arrest cases from public reporting was not assoc

28 a from the Toronto Regional RescuNET Epistry cardiac arrest database.

29 The occurrence of sudden cardiac arrest due to structural heart disease was uncom

30 er an AED to the scene of an out-of-hospital cardiac arrest for bystander use.

31 Cardiac arrest in this study was defined by intra-aortic

32 Cardiac arrest is defined as the termination of cardiac

33 All 939 patients with out-of-hospital cardiac arrest of presumed cardiac cause that had been i

34 Patients with cardiogenic shock or cardiac arrest on presentation were excluded.

35 aluate the role of CMR in determining sudden cardiac arrest pathogenesis and prognosis in survivors.

36 With the use of INTCAR (International Cardiac Arrest Registry), an 87-question data set repres

37 a total of 112139 patients with in-hospital cardiac arrest who were hospitalized in intensive care u

38 risk and improve the triage of survivors of cardiac arrest without ST-segment-elevation myocardial i

39 zation, cardiovascular mortality, or aborted cardiac arrest), its components, and all-cause mortality

40 Patients with cardiac arrest, thrombolytic therapy, prior revasculariz

41 where their loss culminates in fibrillatory cardiac arrest.

42 ins staff in the recognition and response to cardiac arrest.

43 Tracheal intubation during cardiac arrest.

44 Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with a 5-fold incre

45 ttack, peripheral arterial complication, and cardiac arrhythmia), as well.

46 s on the ECG and increased susceptibility to cardiac arrhythmias and sudden death.

47 death through day 30 or use of a mechanical cardiac assist device through day 5.

48 rction through day 5, or use of a mechanical cardiac assist device through day 5; and a two-component

49 sion of Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved card

50 R, potentially reflecting down-regulation of cardiac beta-adrenergic receptor function in chronic hyp

51 osensor platform capable of high performance cardiac-bioassays for point-of-care applications.

52 ce during or after treatment, measurement of cardiac biomarkers and other surrogate endpoints, and in

53 We used the dystrophic cardiac calcification phenotype of Abcc6(-/-) mice as an

54 investigated the potential role of NDPK-C in cardiac cAMP formation and contractility.

55 studied echocardiographically (n=23) and by cardiac catheterization (n=5) after primary repair (n=4)

56 hs to 25 years of age presenting for routine cardiac catheterization during 2015 to 2016.

57 nd quality improvement activity performed in cardiac catheterization laboratories, but best practices

58 tients with LGSAS and preserved EF underwent cardiac catheterization with comparison of hemodynamic m

59 h out-of-hospital cardiac arrest of presumed cardiac cause that had been included in the TTM-trial.

60 LVEF drop, or death of definite or probable cardiac causes.

61 nic CD4(+) T cells (and, to a lesser extent, cardiac CD3(+) T cells) from donor mice with HF induced

62 SNRK also decreases cardiac cell death in a UCP3-dependent manner.

63 ork and transcriptional resource of multiple cardiac cell populations during cardiac development, rep

64 e primary safety end point was major adverse cardiac, cerebrovascular, and renal events at 1 month.

65 to fine-tune gene expression levels in each cardiac chamber.

66 We further detected novel cardiac chemical signatures related to the severity and

67 The total cardiac clearance of amitriptyline was calculated as 0.3

68 tablished in African Americans persons whose cardiac comorbidities and structural abnormalities diffe

69 artery anomalies may cause life-threatening cardiac complications; however, developmental mechanisms

70 ntrast BVES and CAP2 murine knockouts caused cardiac conduction defects.

71 henotypes, including dilated cardiomyopathy, cardiac conduction disturbance, atrial fibrillation, and

72 a subset of macrophages residing within the cardiac conduction system, which orchestrates cardiac rh

73 Slowed cardiac conduction was associated with significant atria

74 normalized adrenergic response and preserved cardiac contractile reserve in HFD-fed mice.

75 ifferences were noted in the rates of 1-year cardiac death (44 [4.0%] for the bivalirudin group vs 48

76 ereas for patients >70 years old, the sudden cardiac death rate was 1.6 (95% CI, 0.8-3.2) and nonsudd

77 For patients </=70 years old, the sudden cardiac death rate was 1.8 (95% CI, 1.3-2.5) and nonsudd

78 ac event (MACE) assessed as the composite of cardiac death, myocardial infarction, and target vessel

79 eart muscle disorder, predisposing to sudden cardiac death, particularly in young patients and athlet

80 at the greatest risk of sudden and nonsudden cardiac death.

81 , which in turn predisposes to VA and sudden cardiac death.

82 Brugada syndrome patients having implantable cardiac defibrillator were enrolled: 63 (group 1) having

83 proteins play important roles in regulating cardiac development via paracrine signaling.

84 of multiple cardiac cell populations during cardiac development, repair, and regeneration.

85 Then, important genes related to cardiac differentiation and function were analyzed by re

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

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

88 We investigated the impact of genome-wide cardiac DNA methylation on global gene expression in myo

89 RT plans and cardiac doses were reviewed.

90 ces likely contributes to the development of cardiac dysfunction in this setting.

91 , systemic blockade of HCN channels produces cardiac effects that limit this approach.

92 an increase in leptin levels has protective cardiac effects with respect to rescuing the cellular he

93 A primary cardiac end point was defined as symptomatic congestive

94 Instead, cardiac endothelial cells were likely to proliferate and

95 for which heart rate is a key determinant of cardiac energy demand, AMPK functions in an organ-specif

96 ions in an organ-specific manner to maintain cardiac energy homeostasis and determines cardiac physio

97 y recorded the occurrence of a major adverse cardiac event (MACE) assessed as the composite of cardia

98 icant differences in composite major adverse cardiac event scores at each time point up to 48 months.

99 ns (25.7%), anastomotic leakage (15.9%), and cardiac events (13.5%).

100 rtality or hospitalization for major adverse cardiac events (aHR: 0.30; 95% CI: 0.12 to 0.78) were lo

101 gy with respect to the rate of major adverse cardiac events at 12 months.

102 nts were followed-up for medically certified cardiac events from January 1994 to December 2014.

103 Major adverse cardiac events occurred in 1.1% and 4.2% of everolimus-t

104 ts included clinical outcomes (major adverse cardiac events), use of healthcare resources, and impact

105 o reduce the risk for mortality, stroke, and cardiac events.

106 re significantly associated with grade >/= 3 cardiac events.

107 Symposium Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias

108 Of 7,106 patients undergoing cardiac extracorporeal life support, the majority of pat

109 rred through week 24 were anaemia (10 [5%]), cardiac failure (5 [2%]), pyrexia (4 [2%]), and pneumoni

110 known about whether T cells directly impact cardiac fibroblasts (CFBs) to promote cardiac fibrosis (

111 asts using Tcf21 (MerCreMer) or in activated cardiac fibroblasts using periostin (Postn) (MerCreMer)

112 ce beta-catenin loss of function in resident cardiac fibroblasts using Tcf21 (MerCreMer) or in activa

113 impact cardiac fibroblasts (CFBs) to promote cardiac fibrosis (CF) in nonischemic heart failure (HF).

114 This was accompanied by cardiac fibrosis and up-regulation of NFAT-c2, reflectin

115 PAI-1 is an essential repressor of cardiac fibrosis in mammals.

116 n to its suppressive role during spontaneous cardiac fibrosis in multiple species, we hypothesized th

117 d suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus a

118 ce, and eventual lethality in the absence of cardiac fibrosis.

119 th systolic dysfunction and comparable intra-cardiac fibrosis.

120 deficient (PAI-1(-/-)) mice developed severe cardiac fibrosis.

121 ive reference standard for the evaluation of cardiac function and viability.

122 Recovery of cardiac function in response to mechanical unloading was

123 However, the in vivo cardiac function of IF1 and the potential therapeutic ap

124 strated that Cas9 expression does not affect cardiac function or gene expression.

125 ypertrophic response and decreases sustained cardiac function, but the cardiomyocyte-specific effects

126 TCM, or nCPC-derived exosomes in recovering cardiac function, stimulating neovascularization, and pr

127 irst review the key role of Ca(2+) in normal cardiac function-in particular, excitation-contraction c

128 transverse aortic constriction and improved cardiac function.

129 atrophy induced by doxorubicin and improved cardiac function.

130 lex, which associate with ZNF281, stimulates cardiac gene expression.

131 roduction, such as physiologic or pathologic cardiac growth, remain elusive.

132 Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(l

133 ngs identify PABPC1 as a direct regulator of cardiac hypertrophy and define a new paradigm of gene re

134 e that Honokiol exerts beneficial effects on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity

135 of DLST in wild-type mice protected against cardiac hypertrophy and dysfunction in vivo.

136 associated with numerous diseases, including cardiac hypertrophy and heart failure.

137 re, VDR 4-1 therapy significantly suppressed cardiac hypertrophy and progression to heart failure in

138 Cpt2M(-/-) mice developed cardiac hypertrophy and systolic dysfunction, evidenced

139 In vivo, MR-409 mitigated cardiac hypertrophy in mice subjected to transverse aort

140 ic regulator, is critical for stress-induced cardiac hypertrophy.

141 fed a ketogenic diet, yet it did not improve cardiac hypertrophy.

142 evated atrial natriuretic peptide message of cardiac hypertrophy.

143 onsideration is given to the common goals of cardiac imaging in CHD, including assessment of structur

144 Considerations for cardiac imaging in pregnancy are also discussed.

145 nnular calcium (MAC), commonly identified by cardiac imaging, is associated with cardiovascular event

146 tional and international cardio-oncology and cardiac-imaging organisations recommend increased cardia

147 The use of cardiac implantable electronic devices (CIED) is increas

148 coxsackieviruses are responsible for chronic cardiac infections.

149 hown by a reduced cardiac inflammation (less cardiac infiltrates and suppression of proinflammatory c

150 ce (starting 4 weeks after ligation) reduced cardiac infiltration of CD4(+) T cells and prevented pro

151 CVB3-mediated effects as shown by a reduced cardiac inflammation (less cardiac infiltrates and suppr

152 ed that PAI-1 also regulates fibrosis during cardiac injury.

153 e and other baseline characteristics and (1) cardiac involvement at baseline and (2) the incidence of

154 Cardiac involvement was also detected in D2-mdx myocardi

155 LV1-44 patients were more likely to have cardiac involvement.

156 For example, the cardiac LIM protein, cysteine- and glycine-rich protein

157 Living with Heart Failure Questionnaire) and cardiac limitation on exercise testing (reduced peak oxy

158 es via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane pot

159 Cardiac magnetic resonance has unparalleled tissue chara

160 Cardiac magnetic resonance imaging (cMRI) has become the

161 We examined the right ventricle with cardiac magnetic resonance imaging in the same cohorts.

162 Cardiac magnetic resonance imaging was repeated at 3 mon

163 iterature to support the prognostic value of cardiac magnetic resonance imaging with late gadolinium

164 nitroglycerin (7.2 mg over 2 days) on early cardiac magnetic resonance imaging-assessed infarct size

165 We used cardiac magnetic resonance measurements of extracellular

166 METHODS AND We performed cardiac magnetic resonance myocardial feature tracking i

167 after recanalization of the culprit artery, cardiac magnetic resonance performed during index hospit

168 Secondary end points included cardiac magnetic resonance-determined myocardial salvage

169 ated a predictive computational model of the cardiac mechano-signaling network in order to elucidate

170 lycine-rich protein 3, is thought to mediate cardiac mechanotransduction and stress responses, wherea

171 for fabricating a new class of instrumented cardiac microphysiological devices via multimaterial thr

172 ought to validate in vivo DT-CMR measures of cardiac microstructure against histology, characterize m

173 tment, and the increased release of ROS from cardiac mitochondria and other sources likely contribute

174 Using isolated cardiac mitochondria, we demonstrate a novel mechanism b

175 nal, and clinical markers, three-dimensional cardiac motion improved survival prediction (area under

176 c and diastolic function were evaluated with cardiac MRI and normalized to body surface area.

177 design may potentially improve tolerance of cardiac MRI and therefore allow to examine an even broad

178 expression of CD47 (don't eat me signal) on cardiac MSCs after both TLR4 stimulation in vitro and tr

179 Although transplantation of cardiac MSCs and subcutaneous MSCs from LVD and sham hea

180 did not improve LV remodeling and function, cardiac MSCs from LVD exacerbated anterior wall thinning

181 LVD switched cardiac MSCs toward an inflammatory phenotype, with incr

182 with heart failure, a condition with reduced cardiac muscle cBIN1, both of which support cBIN1 releas

183 dystrophin protein expression in dystrophic cardiac muscles to a level approaching 40%.

184 sitive potassium channels (KATP channels) in cardiac myocytes adjust contractile function to compensa

185 parts of the calcium signalling apparatus in cardiac myocytes is unknown.

186 2+) spark initiation after Ca(2+) release in cardiac myocytes should inhibit further Ca(2+) release d

187 METHODS AND Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxy

188 In cardiac myocytes, there are several Ca(2+) -sensitive po

189 ugs with novel mechanisms of action, such as cardiac myosin activators, are under investigation for p

190 e same exercise was repeated for human alpha-cardiac myosin S1 and rabbit fast skeletal muscle S1.

191 ct and substituted it for the VELC of bovine cardiac myosin subfragment 1.

192 MYBPC3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequentl

193 Here, using human beta-cardiac myosin-S1, we combine published data from transi

194 The cardiac natriuretic peptides (NPs), atrial NP and B-type

195 VCs affect critical populations of intrinsic cardiac nervous system neurons and alter cardiac repolar

196 ratory workup, and imaging were negative for cardiac or neurologic etiology.

197 bute to TOF in 22q11.2DS and may function in cardiac outflow tract development.

198 athy, a condition characterized by increased cardiac output and a reduced ventricular response to str

199 x is strongly associated with a reduction in cardiac output and may not be related to other pathophys

200 cutaneous vasodilatation and the increase in cardiac output during passive heating.

201 and resuscitation in large pigs, noninvasive cardiac output monitoring has acceptable agreement with

202 Over the wide range of cardiac output produced by hemorrhage and resuscitation

203 has acceptable agreement with thermodilution cardiac output.

204 (adeno-associated virus serotype 9)-mediated cardiac overexpression of Qki5 prevented cardiac apoptos

205 Cardiac pacing is an effective treatment for patients wi

206 Cardiac patches were created from spheroids (CM:FB:EC =

207 s biomaterial scaffolds to create functional cardiac patches.

208 heses implicating telomere length in various cardiac pathologies.

209 are mostly related to the implant procedure: cardiac perforation, device dislocation, and femoral vas

210 s segmentation need only be performed at one cardiac phase, while wall position in the other cardiac

211 diac phase, while wall position in the other cardiac phases is found by image registration.

212 hermore, Sesn2-knockout hearts demonstrate a cardiac phenotype and response to ischemic stress that i

213 e of this protein in chromatin structure and cardiac phenotype.

214 monstrated the use of Drosophila to evaluate cardiac phenotypes resulting from specific, patient-deri

215 lamin A and C, typically cause age-dependent cardiac phenotypes, including dilated cardiomyopathy, ca

216 in cardiac energy homeostasis and determines cardiac physiological adaptation to exercise by modulati

217 rt guide RNAs targeting 3 genes critical for cardiac physiology, Myh6, Sav1, and Tbx20, using a cardi

218 The effect of these common gene variants on cardiac PITX2 mRNA is currently under study.

219 In a third phase, cardiac precursor differentiation resumes and contribute

220 3.3%, P=0.98) and also underwent concomitant cardiac procedures (AVR+ARE: 68% versus AVR: 67%, P=0.31

221 harmacological/genetic modification of human cardiac progenitor cells (hCPCs) are necessary intervent

222 ogous stem cell therapy using human c-Kit(+) cardiac progenitor cells (hCPCs) is a promising therapeu

223 generate expandable and multipotent induced cardiac progenitor cells (iCPCs) from mouse adult fibrob

224 differentiation of mouse and human PSCs into cardiac progenitor cells, followed by intramyocardial de

225 d signaling-directed (CASD) reprogramming to cardiac progenitors.

226 The authors characterized cardiac PW1-expressing cells and their cell fate potenti

227 ivities of natural stem cells in therapeutic cardiac regeneration.

228 sits after discharge and who participated in cardiac rehabilitation were more likely to take high-int

229 iplatelet agent prescriptions, and attending cardiac rehabilitation within 30 days following discharg

230 Favorable cardiac remodeling at 6 months included decreases in end

231 fate potentials in normal hearts and during cardiac remodeling following myocardial infarction (MI).

232 Post-MI cardiac remodeling is a multifaceted process that includ

233 tential to counteract the effects of adverse cardiac remodeling, thereby improving survival and quali

234 indicating a role for T cells in profibrotic cardiac repair and healing after ischemia, little is kno

235 n vivo with extremely low or high changes in cardiac repolarization in response to a pharmacological

236 sic cardiac nervous system neurons and alter cardiac repolarization.

237 bitory influence of inflammatory pathways on cardiac reprogramming, blockade of these pathways with a

238 Isolated cardiac resident PW1(+) cells form colonies and have the

239 se model of dilated cardiomyopathy driven by cardiac restricted overexpression of TNF (tumor necrosis

240 to concentrate therapeutics within a unique, cardiac-restricted compartment to allow sustained drug p

241 s with congestive heart failure eligible for cardiac resynchronization therapy (CRT) either do not re

242 onses such as neuronal bursting activity and cardiac rhythm.

243 ardiac conduction system, which orchestrates cardiac rhythm.

244 iven by the prevalence of elevated predicted cardiac risk and diabetes mellitus.

245 hannel model is consistent with the RyR1 and cardiac RyR (RyR2) open-channel structures reported whil

246 ength measurements in relatively small human cardiac samples and offers an attractive technique to te

247 Mice with cardiac-specific deletion of CTCF (a ubiquitous chromati

248 ering the fundamental mechanisms controlling cardiac specification is critical for our understanding

249 e-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosph

250 ught to determine the role of gamma2-AMPK in cardiac stress response using bioengineered cell lines a

251 current pharmacologic vasodilators used for cardiac stress testing.

252 ci identified in this large meta-analysis of cardiac structure and function provide insights into the

253 e effects on cardiovascular hemodynamics and cardiac structure and function, and increases the preval

254 into the underlying genetic architecture of cardiac structure and warrant follow-up in future functi

255 al cardiologists, heart failure specialists, cardiac surgeons, and cardiac anesthesiologists may help

256 All patients undergoing cardiac surgery and congenital interventions in the Unit

257 Cardiac surgery ICUs in Pennsylvania.

258 We randomized 156 adult subjects undergoing cardiac surgery with evidence of early AKI to receive in

259 ality are lower in obese patients undergoing cardiac surgery, although the nature of this association

260 In MRSA-colonized patients undergoing cardiac surgery, SSI occurred in 8/346 (2.3%) patients w

261 of brain injury is increased during neonatal cardiac surgery, where pre-existing hemodynamic instabil

262 th native valve MR who were at high risk for cardiac surgery.

263 reducing the time to recovery from AKI after cardiac surgery.

264 of developing dementia within 5 years after cardiac surgery.

265 ny patients at extreme risk for conventional cardiac surgery.

266 cations, duration of mechanical ventilation, cardiac surgical ICU readmissions, and surgical postpone

267 ac-imaging organisations recommend increased cardiac surveillance during or after treatment, measurem

268 Cardiac sympathetic denervation (CSD) has been shown to

269 fibrillators alone in 25 (4%) patients, left cardiac sympathetic denervation alone in 18 (3%) patient

270 an electrocardiogram and an troponin if any cardiac symptoms are present in a patient with acute Zik

271 remained stable over time, whereas rates of cardiac tamponade and pacemaker implantation significant

272 Major hemorrhage or cardiac tamponade leading to reoperation occurred in 1.4

273 remodelling was prevented in AC3I mice, with cardiac-targeted CaMKII inhibition.

274 e register who underwent initial noninvasive cardiac testing with either coronary computed tomography

275 Results from cardiac testing, laboratory workup, and imaging were neg

276 framework for the enhanced activation of the cardiac TF over the skeletal TF by Ca(2+) and lead to a

277 mechanistic model for the regulation of the cardiac TF.

278 AI-1 is a molecular switch that controls the cardiac TGF-beta axis and its early transcriptional effe

279 exciting avenues for selective and prolonged cardiac therapeutics.

280 rials potentially applicable as scaffolds in cardiac tissue engineering (TE).

281 In cardiac tissue engineering cells are seeded within porou

282 was also revealed in simulations of fibrotic cardiac tissue, where hMSC PS protected from potential p

283 ted to lead to more physiologically relevant cardiac tissue-like in vitro models for mechanistic biol

284 a disulfide-bonded variant of the I91 human cardiac titin polyprotein.

285 lar system was incorporated into 58 extended cardiac-torso (XCAT) patient phantoms.

286 ing the role of epigenetic regulation of key cardiac transcription regulators.

287 Previous cardiac transcriptional profiling of LmnaH222P/H222P mou

288 lymphatic flow index following heterotrophic cardiac transplantation in a murine model of chronic rej

289 ents have died and 3 LQT3 patients underwent cardiac transplantation.

290 , ventricular assist device implantation, or cardiac transplantation.

291 s explored risk factors for interim death or cardiac transplantation.

292 myocardial infarction using high-sensitivity cardiac troponin (hs-cTn) concentrations irrespective of

293 thway with a pathway that incorporates lower cardiac troponin concentrations to risk stratify patient

294 ospective studies measuring high-sensitivity cardiac troponin I concentrations in patients with suspe

295 high sensitivity assay for the detection of cardiac troponin I using electrical double layer gated h

296 199 (equivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated

297 or heart failure, and valve disease) and non-cardiac variables (body-mass index, chronic kidney disea

298 Independent predictors of mortality included cardiac variables (New York Heart Association Functional

299 method, we compared well and poorly healing cardiac ventricles using a transgenic fish model that ex

300 We sought the genetic cause of cardiac, vertebral, and renal defects, among others, in