ライフサイエンスコーパス: myocardial

1 PET images showed focal myocardial (18)F-FOL uptake colocalizing with inflammato

2 Metabolic signatures of myocardial and vascular health in young adulthood specif

3 In addition to myocardial architecture disruption, this effect can be a

4 Rat tissue sections and myocardial autopsy samples from 6 patients with cardiac

5 with creatine kinase and/or creatine kinase-myocardial band (CK-MB) post-procedure were included.

6 Measurement of myocardial blood flow (MBF) with single photon emission

7 gmentation and flow measures for mean stress myocardial blood flow (MBF; 2.25 mL/min/g +/- 0.59 vs 2.

8 rticle discusses evolving methods to measure myocardial blood flow with positron emission tomography

9 rigid, elastic image registration, and blood myocardial border tracing).

10 Strategies to restore disrupted myocardial calcitonin signalling thus may offer therapeu

11 addition to oxidative stress, inflammation, myocardial cell death pathways, and neurohumoral mechani

12 re protected from persistent immune-mediated myocardial damage and decline of cardiac function, likel

13 Myocardial damage due to acute ST-segment elevation myoc

14 expression of hypoxia-sensitive proteins and myocardial damage due to ischemia alone.

15 ated with improved cardiac function, reduced myocardial damage, shock, lung injury and improved survi

16 .01) strains but not ventricular function or myocardial damage.

17 Studies have shown intrinsic myocardial defects but do not sufficiently explain devel

18 conditions include thrombotic complications, myocardial dysfunction and arrhythmia, acute coronary sy

19 Myocardial dysfunction has been demonstrated in MFS pati

20 ed bodyweight loss, behavioral sickness, and myocardial dysfunction.

21 Within the test set, myocardial end-systolic circumferential Green strain err

22 more, we demonstrate the correlation between myocardial energetics and measures of contractile functi

23 This therapeutic strategy may alter myocardial energy metabolism in a manner that reverses t

24 in all metrics of contractility, as well as myocardial energy production and utilization.

25 ischemic injury before reperfusion, improves myocardial energy substrate use, and preserves mitochond

26 Myocardial FDG uptake in patients suspected of having CS

27 conclusion, SGLT2 inhibition did not affect myocardial FFA uptake, but channeled myocardial substrat

28 The mechanisms sustaining myocardial fibrillation remain disputed, partly due to a

29 non-HIV-infected women) exhibited increased myocardial fibrosis (extracellular volume fraction, 0.34

30 Myocardial fibrosis is a major determinant of clinical o

31 nic PDE9a inhibition, with no differences in myocardial fibrosis or cardiac morphometry.

32 es) which were either healthy or affected by myocardial fibrosis using X-ray microtomography.

33 exercise-induced cardiac biomarker release, myocardial fibrosis, and atrial fibrillation.

34 Myocardial function and myocardial mass remained stable.

35 d improved postcardiopulmonary resuscitation myocardial function, neurologic outcomes, and survival.

36 l PDE10A deficiency significantly attenuated myocardial hypertrophy, cardiac fibrosis, and dysfunctio

37 ous disease in cats, and is characterized by myocardial hypertrophy, disarray and fibrosis, as in hum

38 al and flavoprotein oxidation, and prevented myocardial hypertrophy.

39 th a risk of ischemic stroke, and functional myocardial imaging has offered novel insights on its pat

40 d subgroup analysis of elderly patients with myocardial infarction (>=75 years) from the VALIDATE-SWE

41 versus 3.11%; HR, 0.88 [95% CI, 0.77-1.02]), myocardial infarction (1.08% versus 1.27%; HR, 0.85 [95%

42 5 [95% CI, 2.38-3.32]), or family history of myocardial infarction (2.71 [95% CI, 2.38-3.05]).

43 cardiac arrest (3.0-fold, 95% CI 2.64-3.46), myocardial infarction (2.9-fold, 95% CI 2.43-3.42) and m

44 CI, 1.23-5.18]; P=0.009), and target vessel myocardial infarction (8% versus 14%; hazard ratio, 1.92

45 plaque burden was the strongest predictor of myocardial infarction (adjusted hazard ratio, 1.60 (95%

46 recent decades, the rates of incident acute myocardial infarction (AMI) have declined in the United

47 The diagnosis of acute myocardial infarction (AMI) is missed more frequently in

48 ency department discharge diagnosis of acute myocardial infarction (AMI) or stroke using Internationa

49 In patients with shock after acute myocardial infarction (AMI), the optimal level of pharma

50 f platelet inhibition in patients with acute myocardial infarction (AMI).

51 on (HR, 0.78 [95% CI, 0.63-0.95]), and fatal myocardial infarction (HR, 0.50 [95% CI, 0.26-0.97]) but

52 ociated with significant reductions in total myocardial infarction (HR, 0.72 [95% CI, 0.59-0.90]), pe

53 initiation of BEP treatment were as follows: myocardial infarction (HR, 6.3; 95% CI, 2.9 to 13.9), ce

54 , but with CIs including the null value, for myocardial infarction (incidence rate, 3.9 versus 1.8 pe

55 ular events in stable patients with previous myocardial infarction (MI) and elevated high-sensitivity

56 Secondary analysis included myocardial infarction (MI) and fatal CHD.

57 Genetic risk scores (GRSs) for myocardial infarction (MI) and stroke were calculated to

58 with the association between post-discharge myocardial infarction (MI) and subsequent mortality.

59 , and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale.

60 Adverse cardiac remodeling after myocardial infarction (MI) causes structural and functio

61 e consequences of CMC administration on post myocardial infarction (MI) immune responses in vivo and

62 The formation of new blood vessels after myocardial infarction (MI) is essential for the survival

63 ice exhibit natural heart regeneration after myocardial infarction (MI) on postnatal day 1 (P1), but

64 ventricular dilation in mice one week after myocardial infarction (MI) surgery.

65 Acute myocardial infarction (MI) triggers a local and systemic

66 of intravenous statin administration during myocardial infarction (MI) with oral administration imme

67 s significantly reduce mortality after acute myocardial infarction (MI), a large number of patients w

68 cardiovascular diseases, particularly acute myocardial infarction (MI), is one of the leading causes

69 onic obstructive pulmonary disease, previous myocardial infarction (MI), ischemic heart disease (IHD)

70 diovascular disease (CVD) outcomes including myocardial infarction (MI), ischemic stroke (IS), and pe

71 Despite improvements in prognosis following myocardial infarction (MI), racial disparities persist.

72 dicted five-year risk of heart failure (HF), myocardial infarction (MI), stroke (ST), cardiovascular

73 ion (SCAD) is a non-atherosclerotic cause of myocardial infarction (MI), typically in young women.

74 In a mouse model of myocardial infarction (MI), wild-type EPC-derived exosom

75 renol-, transverse aortic constriction-, and myocardial infarction (MI)-induced heart failure mouse m

76 gina (UA) or non-ST-segment elevation (NSTE) myocardial infarction (MI).

77 biomarker of recurrence and mortality after myocardial infarction (MI).

78 ociated with better long-term outcomes after myocardial infarction (MI).

79 case-control study of 55 PWH with first-time myocardial infarction (MI; cases) and 182 PWH with no CV

80 mortality (RD, 0.001 [CI, -0.011 to 0.013]), myocardial infarction (RD, 0.003 [CI, -0.010 to 0.017]),

81 7 patients (14.8%) and clinically recognized myocardial infarction (RMI) in 358 patients (15.2%).

82 essel disease following ST-segment-elevation myocardial infarction (RR, 0.84 [95% CI, 0.69-1.04]; P=0

83 Circulating EPA in ST-segment elevation myocardial infarction (STEMI) relates to smaller infarct

84 ial damage due to acute ST-segment elevation myocardial infarction (STEMI) remains a significant glob

85 Admissions were classified as ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), myoca

86 were retrospectively classified into type 1 myocardial infarction (T1MI, atherothombotic event), T2M

87 et Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38), which randomized patients to

88 ation in Atrial Fibrillation-Thrombolysis in Myocardial Infarction 48) demonstrated noninferiority of

89 ect on Cardiovascular Events-Thrombolysis in Myocardial Infarction 58) studied the efficacy and safet

90 jury (troponin rise not meeting criteria for myocardial infarction [MI]) using the universal definiti

91 (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass.

92 lications such as cardiac regeneration after myocardial infarction and gene correction for inherited

93 ap junctions have been associated with acute myocardial infarction and heart failure.

94 tery atheroma, cardiac hypertensive disease, myocardial infarction and ischaemic stroke.

95 increased risks, although nonsignificant, of myocardial infarction and ischemic stroke.

96 The coprimary end points were myocardial infarction and major bleeding, which constitu

97 Shock), patients with CS complicating acute myocardial infarction and multivessel coronary artery di

98 nd men presenting with CS complicating acute myocardial infarction and multivessel coronary artery di

99 re important mediators of inflammation after myocardial infarction and of allograft injury after hear

100 The number of patients with myocardial infarction and severe obesity is increasing a

101 at are active in atherosclerosis and lead to myocardial infarction and stroke.

102 to the pathogenesis of deep vein thrombosis, myocardial infarction and stroke.

103 Hospitalizations after acute myocardial infarction are commonly underreported in inte

104 rategies, morbidity and mortality from acute myocardial infarction are still substantial.

105 subjects free of lipid-lowering therapy and myocardial infarction at study entry.

106 g stents, whereas extended-term DAPT reduces myocardial infarction at the expense of more bleeding ev

107 ementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4471), type 2 myocardi

108 cardial infarction by 11% (510/4471), type 2 myocardial infarction by 22% (205/916), and acute and ch

109 improves heart function in adult mice after myocardial infarction by a cardioprotective effect.

110 Thus, cardiomyocyte death as occurs during myocardial infarction has very detrimental consequences

111 d by primary CR-qualifying event type (acute myocardial infarction hospitalization; coronary artery b

112 commendations of the Universal Definition of Myocardial Infarction identified patients at high-risk o

113 y end point occurred in 104 (4.0%) patients, myocardial infarction in 9 (0.4%), cerebrovascular accid

114 n in ST-Segment and Non-ST-Segment Elevation Myocardial Infarction in Patients on Modern Antiplatelet

115 Reliable methods for predicting myocardial infarction in patients with established coron

116 ely young women and is an important cause of myocardial infarction in young patients without traditio

117 inical hypothyroidism in patients with acute myocardial infarction is associated with poor prognosis.

118 dial infarction (STEMI), non-STEMI (NSTEMI), myocardial infarction of unknown type, or other acute co

119 CAD events were defined by myocardial infarction or CAD mortality.

120 events (a composite of cardiovascular death, myocardial infarction or other acute coronary syndrome,

121 Those who had myocardial infarction or stroke in the previous 6 months

122 rt failure hospitalization), its components, myocardial infarction or stroke, and a renal composite o

123 Myocardial infarction patients receiving reperfusion the

124 uded 1653 patients with ST-segment-elevation myocardial infarction randomized to receive ticagrelor o

125 asure for patients with ST-segment-elevation myocardial infarction requiring inter-hospital transfers

126 atients presenting with ST-segment-elevation myocardial infarction scheduled for pPCI.

127 findings were sensitive to the definition of myocardial infarction that was used.

128 a 57-year-old man with a history of anterior myocardial infarction three years earlier.

129 arison in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous co

130 [95% CI 0.74-1.59]; p=0.68); non-procedural myocardial infarction was estimated in 8% after PCI vers

131 e hundred patients with ST-segment-elevation myocardial infarction were randomized to therapy (50 pat

132 Myocardial infarction with nonobstructive coronary arter

133 by qualifying event type (range: 7.1% [acute myocardial infarction without procedure] to 55.3% [coron

134 I trial (Omega-3 Fatty acids in Elderly with Myocardial Infarction) is an investigator-initiated, mul

135 l safety end point was TIMI (Thrombolysis in Myocardial Infarction) major bleeding, with Internationa

136 reatening/moderate and TIMI (Thrombolysis in Myocardial Infarction) major/minor bleeding with time-de

137 One death possibly related to treatment (myocardial infarction) occurred after 11 days of treatme

138 se limb events, 0.60 (95% CI, 0.48-0.74) for myocardial infarction, 0.94 (95% CI, 0.75-1.18) for isch

139 t failure, 1.76 (95% CI 1.51-2.05) for acute myocardial infarction, 1.78 (95% CI 1.53-2.07) for perip

140 ve heart failure or non-ST-segment-elevation myocardial infarction, and had multivessel or left main

141 , HRs were adjusted for age, sex, history of myocardial infarction, and history of chronic obstructiv

142 e composite of all-cause mortality, nonfatal myocardial infarction, and nonfatal stroke).

143 or adverse cardiovascular events, fatal CVD, myocardial infarction, and stroke.

144 dence of distal embolization, periprocedural myocardial infarction, and target lesion revascularizati

145 ent heart repair and function after neonatal myocardial infarction, and that cardiac delivery of RELN

146 heart failure/cardiomyopathy, hypertension, myocardial infarction, atrial fibrillation, valvular dis

147 e myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure wi

148 return to pre-infarct activities after acute myocardial infarction, but the trial lacked statistical

149 Heart failure, induced via myocardial infarction, causes a decrease of the cGMP lev

150 luded cardiovascular disease (a composite of myocardial infarction, cerebrovascular accident, heart f

151 composite outcome was cardiovascular death, myocardial infarction, coronary revascularization, and s

152 Myocardial infarction, following heart ischemia and repe

153 ents eccentric cardiac remodeling induced by myocardial infarction, in each case improving cardiac fu

154 acy of current classical risk predictors for myocardial infarction, including stenosis severity.

155 nary artery disease, particularly with prior myocardial infarction, is associated with greatest risk

156 confidence intervals for the study outcomes (myocardial infarction, ischemic stroke, heart failure, a

157 oint (MACE) comprised death of CAD, nonfatal myocardial infarction, ischemic stroke, or unstable angi

158 tervention in patients presenting with acute myocardial infarction, multivessel disease, and cardioge

159 In a mouse model of myocardial infarction, nanoparticle-mediated inhibition

160 ar diagnoses such as heart failure and acute myocardial infarction, need frequently arises for advanc

161 intraabdominal leak, unplanned reoperation, myocardial infarction, or infectious complications.

162 events (MACE; a composite of cardiac death, myocardial infarction, or ischemia-driven target lesion

163 t of cardiovascular death, all-cause stroke, myocardial infarction, or rehospitalization for heart fa

164 ed to have higher adjusted risk of CV death, myocardial infarction, or stroke (adjusted hazard ratio

165 erse cardiovascular events (all-cause death, myocardial infarction, or stroke).

166 utcome was death from cardiovascular causes, myocardial infarction, or stroke.

167 site of cardiac death, target vessel-related myocardial infarction, or target lesion revascularizatio

168 he composite of cardiac death, target vessel myocardial infarction, or target vessel revascularizatio

169 (SCAD) has emerged as an important cause of myocardial infarction, particularly among younger women.

170 cute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial in

171 atients presenting with ST-segment-elevation myocardial infarction, percutaneous coronary interventio

172 d, particularly for non-ST-segment-elevation myocardial infarction, reflecting a more conservative ap

173 All-cause mortality and the composite of myocardial infarction, repeat revascularization, stroke,

174 te-targeted strategy, after acute or chronic myocardial infarction, resulted in increased cardiomyocy

175 tcomes were MACE (cardiovascular [CV] death, myocardial infarction, stroke), CV death/HHF, and progre

176 end point of major CVD events (composite of myocardial infarction, stroke, and CVD mortality; hazard

177 Post-ACS death, myocardial infarction, stroke, and overall major adverse

178 tiology of many serious conditions including myocardial infarction, stroke, deep vein thrombosis, and

179 major adverse cardiovascular events (death, myocardial infarction, stroke, heart failure) and COVID-

180 lifetime risk of CVD (composite of incident myocardial infarction, stroke, heart failure, or CVD dea

181 ts (MACE) (composite of all-cause mortality, myocardial infarction, stroke, or emergency cardiovascul

182 t failure, unstable angina, non-ST-elevation myocardial infarction, syncope).

183 neumonia, pneumothorax, respiratory failure, myocardial infarction, thyrotoxicosis, alcohol, pericard

184 MACE as a composite of cardiovascular death, myocardial infarction, unstable angina with revasculariz

185 We investigated 2 individual manifestations (myocardial infarction, unstable angina) as secondary out

186 % CI, 0.37-0.93) were particularly linked to myocardial infarction, whereas high HDL oxidative-inflam

187 on how sex influences the outcomes of acute myocardial infarction-cardiogenic shock (AMI-CS) in youn

188 type using the Third Universal Definition of Myocardial Infarction.

189 atory and the reparatory immune responses to myocardial infarction.

190 study of patients hospitalized with an acute myocardial infarction.

191 conditions, during atherosclerosis and after myocardial infarction.

192 sms to enhance myocardial regeneration after myocardial infarction.

193 ease, leading to ischaemic heart disease and myocardial infarction.

194 ochondrial function in swine models of acute myocardial infarction.

195 o regenerate functional myocardium following myocardial infarction.

196 on improves outcomes in ST-segment-elevation myocardial infarction.

197 ective use of CMR after ST-segment-elevation myocardial infarction.

198 ears of follow-up, 1,816 were diagnosed with myocardial infarction.

199 tively, fulfilled criteria for a biochemical myocardial infarction.

200 independent prediction of fatal or nonfatal myocardial infarction.

201 atients presenting with ST-segment-elevation myocardial infarction.

202 otential immunomodulatory treatment in acute myocardial infarction.

203 ronary intervention for ST-segment-elevation myocardial infarction.

204 troponin for accelerated diagnosis of acute myocardial infarction: a systematic review and meta-anal

205 ary arteries (MINOCA) occurs in 6% to 15% of myocardial infarctions (MIs) and disproportionately affe

206 ion at chromosome 9p21.3 accounts for 20% of myocardial infarctions (MIs) in several populations.

207 Myocardial infarctions occurring in this short term risk

208 ction of 10-year first CHD events (including myocardial infarctions, fatal coronary events, silent in

209 lecular imaging methods for the detection of myocardial infiltration, device infection, and cardiovas

210 Thus, controlling liver and/or myocardial inflammation (e.g., with selective CB(2) -R a

211 hronic inflammatory cardiomyopathy indicates myocardial inflammation with established dilated cardiom

212 dary to the collateral damage from sustained myocardial inflammation within the infarct zone.

213 pha levels and improved cardiac dysfunction, myocardial inflammation, and oxidative stress, underlini

214 tential approach for the detection of active myocardial inflammation.

215 exposures may trigger the onset of nonfatal myocardial infraction.

216 phenotype that arises following a variety of myocardial injuries.

217 -up of 10.2 years, mortality was highest for myocardial injury (45.6%), followed by type 2 MI (34.2%)

218 Episodes of acute myocardial injury (chest pain with troponin elevation an

219 vant clinical factors, even small amounts of myocardial injury (e.g., troponin I >0.03 to 0.09 ng/ml;

220 tion (T1MI, atherothombotic event), T2MI, or myocardial injury (troponin rise not meeting criteria fo

221 tion increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, parti

222 macrophage function in the context of acute myocardial injury and chronic disease.

223 l injury without TTE abnormalities, and with myocardial injury and TTE abnormalities.

224 tion by 22% (205/916), and acute and chronic myocardial injury by 36% (443/1233) and 43% (389/898), r

225 went PCI, the primary outcome of PCI-related myocardial injury did not differ between colchicine (n=2

226 ular disease, and >7% of patients experience myocardial injury from the infection (22% of critically

227 tients without myocardial injury, those with myocardial injury had more electrocardiographic abnormal

228 to identify clinical factors associated with myocardial injury in COVID-19.

229 Myocardial injury is common, but true myocarditis is rar

230 While postoperative myocardial injury remains a major driver of morbidity an

231 Myocardial injury was defined as any elevation in cardia

232 Overall, myocardial injury was observed in 190 patients (62.3%).

233 Moreover, MIS-C patients with myocardial injury were more affected than those without

234 um enhancement (90%), even in cases of acute myocardial injury with normal ventricular function (4/5,

235 injury were more affected than those without myocardial injury with respect to all functional paramet

236 in patients without myocardial injury, with myocardial injury without TTE abnormalities, and with my

237 ly available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular infla

238 cardiovascular complications including acute myocardial injury, myocarditis, arrhythmias, and venous

239 Compared with patients without myocardial injury, those with myocardial injury had more

240 e 5.2%, 18.6%, and 31.7% in patients without myocardial injury, with myocardial injury without TTE ab

241 ad type 1 MI, 32% had type 2 MI, and 13% had myocardial injury.

242 r of damaged sarcolemmal membranes following myocardial injury.

243 g young adults with type 1 MI, type 2 MI, or myocardial injury.

244 resent in nearly two-thirds of patients with myocardial injury.

245 nditioning strategies reduced both renal and myocardial injury.

246 and have the potential to result in profound myocardial injury.

247 severity of liver disease and the degree of myocardial involvement.

248 Myocardial ischaemia resulting from obstructive coronary

249 aded neutrophils in a human-disease-relevant myocardial ischemia reperfusion injury mouse model after

250 and cellular (caSMC and caEC) mechanisms in myocardial ischemic injury.

251 mmatory mediators which are generated during myocardial ischemic injury.

252 microwave catheter ablation can create deep myocardial lesions endocardially and epicardially though

253 Myocardial function and myocardial mass remained stable.

254 uced spectral changes, including the drop in myocardial NADH levels, the release of lipofuscin-like p

255 Normative data are presented for myocardial native T1 and ECV using the MOLLI T1 mapping

256 Empagliflozin did not change myocardial oxygen consumption or MEE.

257 Myocardial palmitate and glucose uptake were measured wi

258 tivity and specificity for identification of myocardial pathological substrates.

259 ction system degeneration or a reflection of myocardial pathology.

260 and reserve, provided the best estimation of myocardial performance following transplantation.

261 Vasodilator stress and rest myocardial perfusion CMR and LGE imaging had high diagno

262 tion fraction, risk area (before treatment), myocardial perfusion defect over time (infarct size), an

263 in were determined by quantitative real-time myocardial perfusion echocardiography and speckle tracki

264 The performance of SPECT myocardial perfusion imaging (MPI) may deteriorate in sm

265 xygen level-dependent (BOLD) cardiac MRI for myocardial perfusion is limited by inadequate spatial co

266 g with complementary murine studies revealed myocardial protection, improved angiogenesis, inflammato

267 pression of site IQ electron leak, decreased myocardial reactive oxygen species generation and improv

268 cell cycle regulatory mechanisms to enhance myocardial regeneration after myocardial infarction.

269 ed cardiomyocyte, its antagonistic effect on myocardial regeneration, and its potential contribution

270 primary end point (180-day all-cause death, myocardial reinfarction, or major bleeding), the individ

271 onsisting of a composite of all-cause death, myocardial reinfarction, or major bleeding, within 180 d

272 eals the biological basis for chronic atrial myocardial remodeling that paves the way of atrial fibri

273 s study was to examine the clinical profile, myocardial remodeling, and survival of patients with PPC

274 deficient-EPC-derived exosome dysfunction in myocardial repair and to investigate if modification of

275 Cardiac MRI LGE showed myocardial scar in three of 17 cases (18%, scar burden o

276 enables fast and accurate quantification of myocardial scar volume, outperforms a two-dimensional co

277 chanical properties of ischemic or infarcted myocardial segments.

278 We aimed to characterize myocardial steatosis and associated potential risk facto

279 LV myocardial stiffness in patients with LVH and elevated b

280 Although the LV myocardial stiffness of patients with LVH is greater tha

281 wedge pressure - right atrial pressure), LV myocardial stiffness was nearly 30% greater in LVH than

282 mine the prognostic relevance of MRI-derived myocardial strain for a combined end point (events) of h

283 es of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show signif

284 tracardiac pressure-volume relationships and myocardial structural alterations.

285 poptosis, glycolytic process and decrease in myocardial structural proteins were differentially expre

286 Significant improvements in myocardial structure and function have been reported in

287 defined as the presence of abnormalities in myocardial structure and function that occur in the abse

288 iopulmonary resuscitation and is mediated by myocardial stunning resulting from mitochondrial electro

289 affect myocardial FFA uptake, but channeled myocardial substrate utilization from glucose toward oth

290 d that absence of runx1 results in increased myocardial survival and proliferation, and overall heart

291 vely obtained paired left ventricular apical myocardial tissue from nonfailing donor hearts as well a

292 ndings suggest a previously unknown role for myocardial trabeculae in the function of the adult heart

293 l complexity and reveal the influence of the myocardial trabeculae on susceptibility to cardiovascula

294 Myocardial uptake of (68)Ga-FOL was 20-fold lower than t

295 There were 60 (25.8%) patients with diffuse myocardial uptake, 1 (0.4%) with regional uptake, and 17

296 ith regional uptake, and 172 (73.8%) with no myocardial uptake.

297 eline-directed medical therapies, imaging of myocardial viability failed to deliver effective guidanc

298 ogates of structural or tissue substrates of myocardial viability.

299 tibility changes associated with hypokinetic myocardial wall motion and microvascular obstruction, de

300 T-proBNP and cTnI, suggesting improvement in myocardial wall stress.