ライフサイエンスコーパス: myocardial

1 These results imply that low myocardial (18)F-FDG uptake before the initiation of dox

2 Myocardial active relaxation and restoring forces are kn

3 We observed an initial decrease in myocardial and endocardial cavity volumes at day 3, foll

4 he impact of aPC on inflammasome activity in myocardial and renal IRIs.

5 phosphorylated AKT levels and an increase in myocardial apoptosis.

6 way networks of ischemia-affected and remote myocardial areas after repetitive ischemia/reperfusion (

7 Myocardial blood flow (MBF) and myocardial flow reserve

8 r a novel mechanism through which endodermal-myocardial communication can guide the cell movements th

9 elemental analysis was used to measure total myocardial concentrations of Ca, Na, and other elements.

10 Although myocardial conduction of excitation has been widely desc

11 was associated with increased expression of myocardial connexin 43.

12 uld be exploited to quantify the severity of myocardial damage due to complement activation.

13 In addition, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and a

14 or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of

15 Assessment of regional longitudinal myocardial deformation in the inferior region provided i

16 RATIONALE: Myocardial delivery of human mesenchymal stem cells (hMS

17 cardium, studies have mainly utilized direct myocardial delivery.

18 ardiac disease have evolved to conceptualize myocardial disease and patient vulnerability based on th

19 iles for further study in different types of myocardial disease.

20 Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complemen

21 g-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosc

22 t (or myocarditis) is the proximate cause of myocardial dysfunction, causing injury that can range fr

23 e that therapeutic effects accrue from local myocardial effects of engrafted MSCs.

24 etermined disease stage-dependent changes in myocardial efficiency and effects of myectomy surgery.

25 myocardial oxygen consumption, and improved myocardial efficiency defined as stroke work/myocardial

26 d Na(+) (NaV) channels are key regulators of myocardial excitability, and Ca(2+)/calmodulin-dependent

27 METHODS AND Myocardial external efficiency (MEE) was determined in 2

28 Quantifying myocardial fibrosis (MF) with myocardial extracellular volume measures acquired during

29 AND We performed cardiac magnetic resonance myocardial feature tracking in 22 patients with HFpEF an

30 nd extramyocellular lipid signals, the angle myocardial fibres in the spectroscopy voxel take with th

31 To investigate whether myocardial fibrosis (MF) is similarly prevalent both in

32 Quantifying myocardial fibrosis (MF) with myocardial extracellular v

33 nd determine the association between diffuse myocardial fibrosis and diastolic dysfunction.

34 ction (ECV) to discover and quantify diffuse myocardial fibrosis in 25 individuals with SCA (mean age

35 Myocardial fibrosis is linked with adverse clinical outc

36 Myocardial fibrosis quantified by extracellular volume (

37 Myocardial fibrosis was detected to a significantly lowe

38 s early transcriptional effects that lead to myocardial fibrosis.

39 Myocardial blood flow (MBF) and myocardial flow reserve (MFR) measured with PET have cli

40 Global myocardial function (ejection fraction [EF] and left ven

41 nd post-contrast T1 values and compared with myocardial function measured by echocardiography using P

42 has become the gold standard for evaluating myocardial function, volumes, and scarring.

43 In patients with dilated cardiomyopathy, myocardial Gal-3 expression correlated with cardiac fibr

44 In patients with iCMP, myocardial Gal-3 expression significantly correlated wit

45 or the resolving and nonresolving pathway in myocardial healing.

46 regulated in a number of diseases, including myocardial hypertrophy.

47 cular analyses revealed that the age-related myocardial impairment occurs in parallel with shifts in

48 (18)F-FDG PET/MR scans of a canine model of myocardial infarct and was demonstrated in a human subje

49 ere sustained decreases in PAC use for acute myocardial infarction (20.0 PACs placed per 1000 admissi

50 , they were more likely to have a history of myocardial infarction (28% versus 22%), higher body mass

51 onal criteria required for spontaneous acute myocardial infarction (280/397, 71%) versus those with a

52 te advances in treatment, mortality in acute myocardial infarction (AMI) complicated by cardiogenic s

53 ency department patients with possible acute myocardial infarction (AMI) has been shown to effectivel

54 dialysis revealed that mortality from acute myocardial infarction (AMI) has decreased, whereas the p

55 For acute myocardial infarction (AMI) without heart failure (HF),

56 creasing attention to young women with acute myocardial infarction (AMI), who represent an extreme ph

57 atory drugs (NSAIDs) use could trigger acute myocardial infarction (AMI).

58 1.38; 95% CI: 1.35 to 1.42; p < 0.0001) and myocardial infarction (HR: 1.03; 95% CI: 1.00 to 1.05; p

59 rt disease (HR: 1.45; 95% CI: 1.21 to 1.74), myocardial infarction (HR: 1.47; 95% CI: 1.23 to 1.78),

60 R: 1.72; 95% CI: 1.34 to 2.21), and nonfatal myocardial infarction (HR: 1.58; 95% CI: 1.42 to 1.76).

61 Negative control outcomes of myocardial infarction (MI) and herpes zoster were also s

62 igher risk of coronary artery disease (CAD), myocardial infarction (MI) and their risk factors.

63 statin use following hospital discharge for myocardial infarction (MI) between 2011 and 2014.

64 e, those at higher risk for future stroke or myocardial infarction (MI) derive more benefit from the

65 Myocardial infarction (MI) elicits inflammation, but the

66 reatment and outcomes of patients with acute myocardial infarction (MI) have been described, but litt

67 Ischemic heart disease resulting from myocardial infarction (MI) is the most prevalent form of

68 S hospitals within 1 year of the index acute myocardial infarction (MI) of 12365 patients enrolled in

69 In the DAPT Study, combined myocardial infarction (MI) or stent thrombosis and moder

70 s such as metoprolol (Meto) may improve post-myocardial infarction (MI) structural and functional out

71 a/reperfusion (r-I/R) injury without ensuing myocardial infarction (MI) to elaborate a spatial- and c

72 A total of 1,230 patients with acute myocardial infarction (MI) treated with primary percutan

73 Sex differences in early mortality after myocardial infarction (MI) vary by age.

74 ), which has been identified for early onset myocardial infarction (MI), modified the association of

75 ite outcome of periprocedural death, stroke, myocardial infarction (MI), or nonperiprocedural ipsilat

76 tality, major adverse cardiovascular events, myocardial infarction (MI), or target vessel revasculari

77 In chronic myocardial infarction (MI), segments with a transmural e

78 pathophysiological effects, but its role in myocardial infarction (MI)-induced cardiac remodeling re

79 chestrate cardiac recovery process following myocardial infarction (MI).

80 arts and during cardiac remodeling following myocardial infarction (MI).

81 e also elevated in patients with spontaneous myocardial infarction (n=63; P<6.17E-04).

82 cularly among patients with non-ST elevation myocardial infarction (NSTEMI).

83 so associated with a lower risk of death and myocardial infarction (odds ratio, 0.76; 95% confidence

84 we found moderate evidence of a reduction of myocardial infarction (OR, 0.62; 95% credible intervals,

85 ed in human failing myocardium and in a post-myocardial infarction (PMI) HF model evaluated in wild-t

86 6 to 1.72) and a 40% increased risk of acute myocardial infarction (RR 1.40; 95% CI, 1.23 to 1.59).

87 lar mortality (RR, 0.84; 95% CI, 0.59-1.18), myocardial infarction (RR, 0.47; 95% CI, 0.20-1.11), and

88 hanical reperfusion for ST-segment elevation myocardial infarction (STEMI) in settings where health-c

89 intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) may not be uniform over ti

90 In patients with ST-segment elevation myocardial infarction (STEMI), the use of percutaneous c

91 patients after an acute ST-segment-elevation myocardial infarction (STEMI).

92 spiratory failure (one [<1%] vs three [2%]), myocardial infarction (three [1%] vs none), lung infecti

93 e event in the active surveillance group was myocardial infarction (three patients).

94 predictors of out-of-hospital Thrombosis in Myocardial Infarction (TIMI) major or minor bleeding str

95 o on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial, which randomized 21,162

96 cute Treatment of Patients With ST-elevation Myocardial Infarction [DANAMI-3]; NCT01435408).

97 CE, a composite of all-cause death, nonfatal myocardial infarction [MI], heart failure, stroke, trans

98 lesion failure (cardiac death, target vessel myocardial infarction [TVMI], or ischemia-driven target

99 Of 199 162 myocardial infarction admissions, 9466 consecutive uniqu

100 he risk for a composite outcome of stroke or myocardial infarction among nondiabetic patients with in

101 eripheral artery disease had higher rates of myocardial infarction and acute limb ischemia, with simi

102 Patients with suspected myocardial infarction and an oxygen saturation of 90% or

103 Subsequent type 1 myocardial infarction and cardiac death were reported at

104 risk stratification in patients with type 2 myocardial infarction and myocardial injury.

105 re larger, treating more patients with acute myocardial infarction and performing more PCIs than nono

106 improvements driven mainly by differences in myocardial infarction and repeat revascularization.

107 nd in patients with non-ST-segment-elevation myocardial infarction and stable angina pectoris , simil

108 e of concern regarding an increased risk for myocardial infarction and stroke.

109 cardiac arrest without ST-segment-elevation myocardial infarction at the point of care.

110 pital outcomes of patients treated for acute myocardial infarction before and after a hospital had be

111 ients presenting with symptoms suggestive of myocardial infarction by 2 independent cardiologists by

112 piration during PCI for ST-segment-elevation myocardial infarction did not improve clinical outcomes.

113 ident respiratory diseases, hypertension and myocardial infarction from the life-course perspective,

114 anial hemorrhage, extracranial bleeding, and myocardial infarction identified from hospital claims am

115 disparities in evidence-based treatment for myocardial infarction in China have largely been elimina

116 Rates of myocardial infarction in firefighters are increased duri

117 between fire suppression activity and acute myocardial infarction in firefighters.

118 PCTP expression is associated with death/myocardial infarction in patients with cardiovascular di

119 e comparable to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous

120 th coronary artery disease had to have had a myocardial infarction in the past 20 years, multi-vessel

121 ndex type 1 myocardial infarction, or type 1 myocardial infarction or cardiac death at 30 days.

122 adverse cardiovascular events (eg, nonfatal myocardial infarction or cardiovascular death) and nonca

123 heart disease, defined as the first incident myocardial infarction or death owing to coronary heart d

124 oncardiovascular death, patients with type 2 myocardial infarction or myocardial injury have a simila

125 jority of excess deaths in those with type 2 myocardial infarction or myocardial injury were because

126 ardial strain imaging in patients with acute myocardial infarction or stable ischemic heart disease.

127 patients (13.2%) had PAD (1505 with no prior myocardial infarction or stroke).

128 aracteristics of patients suffering an acute myocardial infarction or undergoing cardiovascular surge

129 METHODS AND Consecutive ST-segment-elevation myocardial infarction patients from a defined health reg

130 ostic stratification of ST-segment-elevation myocardial infarction patients treated with primary perc

131 e study, 88 consecutive ST-segment-elevation myocardial infarction patients were enrolled within 12 h

132 nvestigating Underlying Disparities in Acute Myocardial Infarction Patients' Health Status) is an obs

133 linical risk factors in ST-segment-elevation myocardial infarction patients.

134 ral killer cell depletion 24 hours pre-acute myocardial infarction significantly improved infarct siz

135 rction, participants with CHIP had a risk of myocardial infarction that was 4.0 times as great as in

136 cement therapy through day 30, perioperative myocardial infarction through day 5, or use of a mechani

137 mortality among patients admitted for acute myocardial infarction to 2615 for mortality among patien

138 h-sensitivity cardiac troponin assays enable myocardial infarction to be ruled out earlier, but the o

139 ocate 10 061 men and women with a history of myocardial infarction to placebo or one of three doses o

140 t size in patients with ST-segment-elevation myocardial infarction undergoing percutaneous coronary i

141 rosclerosis, or MESA, who were free of prior myocardial infarction underwent both ECG and cardiac mag

142 -out and rule-in of non-ST-segment elevation myocardial infarction using high-sensitivity cardiac tro

143 f the association between dabigatran use and myocardial infarction varied in sensitivity analyses and

144 Acute myocardial infarction was diagnosed in the first physici

145 ary syndrome, including ST-segment-elevation myocardial infarction were enrolled.

146 rence in mortality and combined death/stroke/myocardial infarction were observed.

147 hat included cases (individuals with CAD and myocardial infarction) and noncases, with baseline data

148 confidence interval, 1.92-2.81 versus type 1 myocardial infarction).

149 ed ACS (excluding acute ST-segment-elevation myocardial infarction).

150 9.2%) with atrial fibrillation, 89 (8%) with myocardial infarction, 11 (0.9%) with ischemic stroke, a

151 als (4.1%) had 502 ischemic events (306 with myocardial infarction, 113 with stent thrombosis, and 83

152 Incident CHD included fatal or nonfatal myocardial infarction, acute coronary syndrome without m

153 sures were evaluated: (i) CVD events/deaths (myocardial infarction, acute coronary syndrome, stroke,

154 tes cardiac regeneration in adult mice after myocardial infarction, although the degree of cardiomyoc

155 risk prediction for cardiovascular disease, myocardial infarction, and heart failure over use of est

156 31 hospitalizations for heart failure, acute myocardial infarction, and pneumonia, respectively.

157 nts with psoriasis have an increased risk of myocardial infarction, and psoriasis is now recognized a

158 lar composite rates of cardiovascular death, myocardial infarction, and stroke when compared with pat

159 assessed as the composite of cardiac death, myocardial infarction, and target vessel revascularizati

160 ns are associated with hypertension, stroke, myocardial infarction, and vascular diseases.

161 aking a statin or fibrate, had no history of myocardial infarction, and were not being treated for an

162 s self-reported incident CVD, defined as new myocardial infarction, angina pectoris, or stroke, which

163 Myocardial infarction, cardiovascular death, and repeat

164 inistered off-the-shelf early after an acute myocardial infarction, comply with stringent criteria fo

165 nsplant death or major cardiovascular event (myocardial infarction, coronary angioplasty, coronary ar

166 Adverse events comprised CVD death, myocardial infarction, coronary insufficiency, index adm

167 cted adverse cardiovascular outcomes (death, myocardial infarction, coronary revascularization, or ce

168 infarction, acute coronary syndrome without myocardial infarction, coronary revascularization, or CH

169 of mortality or other medical complications (myocardial infarction, deep vein thrombosis, pulmonary e

170 rom cardiovascular causes, fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, hospita

171 cidence of cardiovascular disease (including myocardial infarction, heart failure, and stroke) and al

172 who were admitted to the hospital for acute myocardial infarction, heart failure, or pneumonia.

173 old, and a 18-fold higher risk of dying from myocardial infarction, heart failure, or stroke, respect

174 446 744 admissions with a diagnosis of acute myocardial infarction, in the second or later physician

175 nt was the composite of all-cause mortality, myocardial infarction, ischemia-driven revascularization

176 to assess CVEs, including fatal and nonfatal myocardial infarction, ischemic stroke, and cardiovascul

177 as all-cause mortality, hospitalization for myocardial infarction, ischemic stroke, and heart failur

178 In healing myocardial infarction, myofibroblast- and cardiomyocyte-

179 Study endpoints included myocardial infarction, new or worsening heart failure, a

180 f other glucose-lowering drugs for non-fatal myocardial infarction, non-fatal stroke, or atrial fibri

181 or cardiovascular events, including nonfatal myocardial infarction, nonfatal stroke, and CVD mortalit

182 wer risks of the primary end point (nonfatal myocardial infarction, nonfatal stroke, or death from ca

183 with higher post-discharge hazard of death, myocardial infarction, or bleeding (AKIN 1: hazard ratio

184 Primary efficacy outcomes were death, myocardial infarction, or cerebrovascular accident.

185 mposite of adjudicated cardiovascular death, myocardial infarction, or ischemic stroke.

186 te of the composite of death from any cause, myocardial infarction, or major bleeding was not lower a

187 y endpoint was a composite of cardiac death, myocardial infarction, or stent thrombosis.

188 e defined as the composite of cardiac death, myocardial infarction, or stent thrombosis.

189 ported for a primary outcome of index type 1 myocardial infarction, or type 1 myocardial infarction o

190 The primary end point was death, myocardial infarction, or unstable angina hospitalizatio

191 ol cohorts for the evaluation of early-onset myocardial infarction, participants with CHIP had a risk

192 However, for myocardial infarction, results for CEE+MPA were in the d

193 The primary outcome was all-cause mortality; myocardial infarction, revascularization, and stroke wer

194 were no significant differences in recurrent myocardial infarction, stent thrombosis, heart failure,

195 The primary endpoint was a composite of myocardial infarction, stroke, and death from cardiovasc

196 Cardiovascular outcomes were myocardial infarction, stroke, congestive heart failure,

197 been demonstrated to reduce the composite of myocardial infarction, stroke, or cardiovascular death i

198 etween 1) lipid species and the risk of CVD (myocardial infarction, stroke, or cardiovascular death);

199 No harm or benefit was observed for myocardial infarction, stroke, or hospital admission for

200 rization and a composite of all-cause death, myocardial infarction, stroke, or repeat revascularizati

201 Among patients undergoing PCI for myocardial infarction, the rate of the composite of deat

202 enic shock complicating ST-segment-elevation myocardial infarction, there may be no significant benef

203 a allowed enrollment of patients with recent myocardial infarction, total occlusions, bifurcations le

204 es of incident cardiovascular disease (CVD) (myocardial infarction, unstable angina, arterial revascu

205 ng on respiratory diseases, hypertension and myocardial infarction, with a particular focus from a li

206 red pattern of HSPC mobilisation 8 days post-myocardial infarction, with increased circulating neutro

207 ted according to the universal definition of myocardial infarction.

208 ntricular remodeling in ST-segment-elevation myocardial infarction.

209 -HDL cholesterol, and extended to stroke and myocardial infarction.

210 early atherosclerosis and its progression to myocardial infarction.

211 to percutaneous coronary occlusion to induce myocardial infarction.

212 ease, respectively, in the risk of death and myocardial infarction.

213 re at highest risk after discharge for acute myocardial infarction.

214 hypertension, but also in the case of healed myocardial infarction.

215 risk, but with lower specificity for type 1 myocardial infarction.

216 -day risk-standardized mortality after acute myocardial infarction.

217 d by the secretome of CPCs in the setting of myocardial infarction.

218 thetic axis were monitored for 3 weeks after myocardial infarction.

219 e cardiovascular events as those with type 1 myocardial infarction.

220 igh-intensity statin use and adherence after myocardial infarction.

221 judicated as per the universal definition of myocardial infarction.

222 educes infarct size in rat and pig models of myocardial infarction.

223 as associated with increased risk of CAD and myocardial infarction.

224 erbated anterior wall thinning 28 days after myocardial infarction.

225 als (60801 CAD cases [approximately 70% with myocardial infarction] and 123504 noncases), the 6 SNPs

226 Acute CHD events included myocardial infarctions (MIs; nonfatal and fatal) and acu

227 patients with anterior ST-segment-elevation myocardial infarctions resulting in LV dysfunction.

228 deoff between increased bleeding and reduced myocardial infarctions with prolonged dual antiplatelet

229 During follow-up, 62 strokes or TIAs, 42 myocardial infarctions, 156 HF events, and 38 cardiovasc

230 ells significantly contribute to age-related myocardial inflammation and functional decline.

231 to differentiate reversible and irreversible myocardial injury and its predictive value for left vent

232 ins were validated in an independent planned myocardial injury cohort (n=15; P<1.33E-04, 1-way repeat

233 The magnitude of myocardial injury correlated with mortality.

234 vels revealed the presence of ongoing minute myocardial injury even in patients with stable ICM.

235 atients with type 2 myocardial infarction or myocardial injury have a similar crude rate of major adv

236 gnificantly inhibits TRAF3IP2 expression and myocardial injury in wild type mice post-I/R.

237 e density and diversity and the magnitude of myocardial injury is responsible for the resolving and n

238 n those with type 2 myocardial infarction or myocardial injury were because of noncardiovascular caus

239 t were increased within 1 hour after planned myocardial injury, 29 were also elevated in patients wit

240 g differentiates reversible and irreversible myocardial injury, and it is a strong predictor of left

241 ty for biomarker and pathway discovery after myocardial injury.

242 significantly improve recovery from ischemic myocardial injury.

243 tients with type 2 myocardial infarction and myocardial injury.

244 ) in individuals with no clinically manifest myocardial injury.

245 eans of restoring cardiac function following myocardial injury.

246 detected in cardiomyopathies, heart failure, myocardial ischaemia, and hypertrophy.

247 ement activation is a recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardio

248 Report of myocardial ischemia before or after onset of ocular cond

249 g DSE are more likely to have stress-induced myocardial ischemia compared with those with normal or h

250 ly implicating MerTK in cardiac repair after myocardial ischemia reperfusion.

251 e by resident and recruited phagocytes after myocardial ischemia reperfusion.

252 up to develop a consensus on the syndrome of myocardial ischemia with no obstructive coronary arterie

253 ve (FFR-CT) is a novel, noninvasive test for myocardial ischemia.

254 d to profile transcriptome remodeling during myocardial ischemia.

255 eads to heart failure and death during acute myocardial ischemia.

256 in atherogenesis and its major complication, myocardial ischemia; and summarizes LOX-1 modulation by

257 o have cardioprotective capabilities against myocardial ischemic injury.

258 boside treatment also robustly increases the myocardial levels of 3 metabolites, nicotinic acid adeni

259 Dietary fat overconsumption leads to myocardial lipid accumulation through mechanisms that ar

260 forms that incorporate diverse cues from the myocardial microenvironment are expected to lead to more

261 emical mechanisms responsible for modulating myocardial mPTP opening remain unclear.

262 or-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mous

263 myocardial efficiency defined as stroke work/myocardial oxygen consumption (r=0.63-0.65; all P<0.01).

264 rterial impedance (ie, global afterload) and myocardial oxygen consumption were reduced by -11% and -

265 elated with lower valvuloarterial impedance, myocardial oxygen consumption, and improved myocardial e

266 coronary circulation that combine to reduce myocardial oxygen demand and to increase supply, thereby

267 not been systemically validated for absolute myocardial perfusion and coronary flow reserve (CFR) by

268 atic analysis of dynamic computed tomography myocardial perfusion imaging may permit robust discrimin

269 tery disease (CAD) is ambiguous, but nuclear myocardial perfusion imaging with single-photon emission

270 with low event rates in patients with normal myocardial perfusion.

271 Research, Cardiac Failure, Cardiomyopathies/Myocardial & Pericardial Diseases, Congenital Heart Dise

272 behavior were measured in chemically skinned myocardial preparations isolated from human donor and he

273 unique roles for epicardium-derived Shha in myocardial proliferation during heart development and re

274 a possible mechanism by which BSJYD provides myocardial protection from hypertension.

275 sample to develop new insights for achieving myocardial regeneration.

276 We show how myocardial region-specific heterogeneity in cell functio

277 -induced changes in cardiac metabolism cause myocardial remodeling.

278 timulating neovascularization, and promoting myocardial remodeling.

279 Increased myocardial rupture in the absence of both Cd36 and Mertk

280 cluded cardiac magnetic resonance-determined myocardial salvage and creatine kinase kinetics.

281 Myocardial salvage index and microvascular obstruction (

282 st STEMI and early QW in the ECG had smaller myocardial salvage index and more extensive MVO than non

283 o retrospectively delineate MaR and quantify myocardial salvage.

284 DNA methylation on global gene expression in myocardial samples from end-stage CCC patients, compared

285 The authors obtained myocardial samples from patients with end-stage heart fa

286 factors, left ventricular ejection fraction, myocardial scar and ischemia, rate-pressure product, typ

287 with heart failure are shown, demonstrating myocardial slice viability, maximum contractility, Ca(2+

288 e followed in order to prepare highly viable myocardial slices.

289 ed a marker that is expressed in response to myocardial strain and possibly fibrosis.

290 cally relevant, disease-based perspective on myocardial strain imaging in patients with acute myocard

291 men and tissue Doppler echocardiography with myocardial strain measured by speckle tracking.

292 ft ventricular (LV) hypertrophy and abnormal myocardial strain predict mortality.

293 ribution characteristics of left-ventricular myocardial strain using a novel cine MRI based deformati

294 ability and provides exquisite detail about myocardial structure and composition, abnormalities of w

295 ether immunological activity would influence myocardial structure and function in elderly mice.

296 cardium based on both decreased function and myocardial T2.

297 ardiac amyloidosis (CA) from other causes of myocardial thickening with, however, scarce data on thei

298 multiple stem cell populations from a single myocardial tissue sample to develop new insights for ach

299 Only strain obtained from the inferior myocardial wall provided incremental prognostic informat

300 contribute to this process, forming a hybrid myocardial zone that is composed of cells derived from b