ライフサイエンスコーパス: subendocardial

1 common LGE pattern was ischemic (transmural/subendocardial).

2 (0.16+/-0.15 versus 0.09+/-0.08; P<0.05) and subendocardial (0.45+/-0.40 versus 0.19+/-0.18; P<0.05)

3 utions were as follows: trabecular 26.1% and subendocardial 20.2%, midwall 33.4%, and subepicardial 2

4 Amyloid was dominantly subendocardial (42%) compared with midwall (29%) and sub

5 We found that subendocardial (6.8+/-2.9 mV) and transmural (4.6+/-1.9

6 as 26 did (Group III: 12 papillary muscle, 7 subendocardial, 7 transmural).

7 LGE was always typical for amyloidosis (29% subendocardial, 71% transmural), including right ventric

8 Missed infarcts were generally small or subendocardial (87%).

9 Subendocardial ablation at the apical LV markedly decrea

10 We tested the hypothesis that subendocardial ablation at this early site would decreas

11 (4) Chemical subendocardial ablation does not affect the incidence, l

12 The dog without subendocardial ablation had similar results.

13 al and endocardial optical mapping, chemical subendocardial ablation with Lugol's solution, and patch

14 complex tachyarrhythmias has revealed focal subendocardial activation whose mechanism remains unexpl

15 al reduction in subendocardial flow reserve (subendocardial adenosine flow, 0.53 +/- 0.20 vs. 3.96 +/

16 Basal subendocardial and apical subepicardial regions deform t

17 sensitivity for detecting pMI, particularly subendocardial and lateral infarcts.

18 2a) expression was significantly less in the subendocardial and midmyocardial layers compared with th

19 Fibrosis also increased in the subendocardial and midwall regions of LVH and LVD rats c

20 Purkinje fiber recruitment is restricted to subendocardial and periarterial sites but not those juxt

21 Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter

22 PET subendocardial and subepicardial CFR were in good agreem

23 s and a loss in the natural gradient between subendocardial and subepicardial layers in LVH.

24 phy, and region-specific analysis to compare subendocardial and subepicardial mechanics.

25 to quantitatively demonstrate differences in subendocardial and subepicardial microcirculation and to

26 the feasibility and accuracy of quantifying subendocardial and subepicardial myocardial blood flow (

27 lly significant (P<0.05) smaller I(pNa) than subendocardial and subepicardial myocytes.

28 The comparison of mean subendocardial and subepicardial SI within groups reveal

29 The mean difference between subendocardial and subepicardial TOTv values versus that

30 Fibrosis in POH-DCM was severe, subendocardial and subepicardial, in contrast with suben

31 ography angiography images were analyzed for subendocardial and transmural attenuation and the corres

32 e normalized to the segment with the highest subendocardial and transmural attenuation, respectively

33 at rest and during dobutamine stimulation in subendocardial and transmural experimental infarcts.

34 ECG did not detect 72.6% and 48.0% of subendocardial and transmural pMIs, respectively.

35 ifferentiating normal myocardial tissue from subendocardial and transmural scar tissue by using elect

36 LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated wi

37 gradient: subepicardial, midmyocardial, and subendocardial APD80 were 383+/-21, 455+/-20, and 494+/-

38 The segment with the lowest subendocardial attenuation and transmural attenuation we

39 We sought to investigate if subendocardial attenuation using coronary computed tomog

40 ss, and afterload as well, thereby improving subendocardial blood flow in patients with HF.

41 A difference in subendocardial blood flow per beat between the left vent

42 Subendocardial blood flow per beat was normal in both re

43 tal defects and failure to increase perfused subendocardial capillaries postnatally.

44 In subendocardial cells, ACh activates little or no IK,ACh

45 a) current density between subepicardial and subendocardial cells.

46 The construction of subendocardial channels to perfuse ischemic areas of the

47 Seven dogs were studied; six underwent subendocardial chemical ablation procedures.

48 er chronotropic stress and restores impaired subendocardial coronary flow and vasodilator reserve in

49 Enalaprilat also restored subendocardial coronary flow reserve (CFR) (baseline CFR

50 to 0.92+/-7 during hyperemia (P<0.005), and subendocardial CVR (1.43+/-3) was lower than subepicardi

51 We hypothesized that delayed onset of subendocardial diastolic thinning will functionally iden

52 en proposed, the latter of which may produce subendocardial dysfunction that is masked by larger sube

53 Locally, subendocardial end-diastolic strains occurred: Longitudi

54 Myocytes were isolated from basal subendocardial (endo), basal midmyocardial (mid), and ap

55 thologic condition, while more specifically, subendocardial enhancement is a feature expected in pati

56 At 1 month, subendocardial FDG deposition by excised tissue counting

57 At 2 months, subendocardial FDG deposition was increased (0.084+/-0.0

58 stmortem hearts revealed an abrupt change in subendocardial fiber orientation along a line following

59 Studies attribute subendocardial fibrosis in POH to ischaemia, and reduced

60 ocardial and subepicardial, in contrast with subendocardial fibrosis in POH-CLVH and nearly no fibros

61 rly interesting was the presence of abundant subendocardial fibrous tissue expressing smooth muscle a

62 Resting subendocardial flow (LAD 0.75+/-0.14 versus 1.19+/-0.14

63 nterline score, -1.9+/-0.1), reduced resting subendocardial flow (LAD: 0.85+/-0.03 vs. normal: 1.02+/

64 There was a critical limitation in subendocardial flow during vasodilation to 0.78+/-0.20 m

65 0.03 ml/min/g, p < 0.01), critically reduced subendocardial flow reserve (adenosine flow: 1.04+/-0.09

66 min/g, P < 0.05) and a critical reduction in subendocardial flow reserve (subendocardial adenosine fl

67 in FDG uptake were inversely related to LAD subendocardial flow reserve during adenosine (3.5+/-0.6

68 usion was most likely due to the presence of subendocardial flow reserve during dobutamine in dogs wi

69 Reductions in subendocardial flow were visually apparent in MRFP image

70 P < 0.001), with reductions in resting flow (subendocardial flow, 0.81 +/- 0.11 vs. 1.20 +/- 0.18 mL/

71 o the basic beats were consistently due to a subendocardial focal activity (SFA).

72 TdP was initiated by subendocardial focal activity that infringed on TDR, res

73 reas subsequent beats were due to successive subendocardial focal activity, reentrant excitation, or

74 tial beat of all VTs consistently arose as a subendocardial focal activity, whereas subsequent beats

75 This study was performed to evaluate subendocardial function using strain rate imaging (SRI).

76 More subtle contraction bands, subendocardial hemorrhage, and signs of acute myocardial

77 Post-gadolinium subendocardial hyperenhancement suggested focal involvem

78 tolic myocardial velocities did not identify subendocardial hypoperfusion.

79 midwall-subepicardial in 23.3%, and midwall-subendocardial in 20%.

80 dentified 100 of the 109 segments (92%) with subendocardial infarction (<50% transmural extent of the

81 ntly the most sensitive method for detecting subendocardial infarction (MI).

82 d low-dose dobutamine in canine stunning and subendocardial infarction (SEMI).

83 nversion times can enhance discrimination of subendocardial infarction and blood pool, but with incre

84 nary arteries, with histological evidence of subendocardial infarction identified in 50% of animals.

85 However, of the 181 segments with subendocardial infarction, 85 (47%) were not detected by

86 diagnosis of a previous MI and MI coded as a subendocardial infarction, leaving n = 1563 transmural i

87 njured myocardium associated with reperfused subendocardial infarctions.

88 l at MR imaging, and most of the unsuspected subendocardial infarcts (15 of 28 [54%]) had no associat

89 ble deformation was found in outer layers of subendocardial infarcts (p < 0.01 for Ecc and Err) but a

90 However, CMR systematically detects subendocardial infarcts that are missed by SPECT.

91 er patient basis, six (13%) individuals with subendocardial infarcts visible by CMR had no evidence o

92 as observed in inner layers of segments with subendocardial infarcts.

93 Transcatheter subendocardial infusion can be used to reversibly impair

94 lar myocardium with the use of transcatheter subendocardial infusion.

95 has been performed at bypass surgery and by subendocardial injection in the catheterization laborato

96 Subendocardial injection of ethanol can predictably abla

97 er zone cardiomyocytes via catheter-mediated subendocardial injection.

98 tructurally abnormal mitochondria; extensive subendocardial interstitial fibrosis; and marked hypertr

99 e that compounds the disease process through subendocardial ischaemia and fibrosis.

100 We discuss the central role played by subendocardial ischaemia and impaired lusitropy in the d

101 schemia for LCX and LAD occlusion but not in subendocardial ischemia (associated with mild ST depress

102 that higher spatial resolution detects more subendocardial ischemia and leads to greater diagnostic

103 the hypothesis that TID represents transient subendocardial ischemia rather than physical dilation fr

104 n=70), more segments were determined to have subendocardial ischemia with high-resolution than with s

105 r zone explained arrhythmic vulnerability in subendocardial ischemia, especially in LAD occlusion, as

106 reasing arrhythmic risk in transmural versus subendocardial ischemia, for both LAD and LCX occlusion.

107 lectrolyte concentrations ultimately lead to subendocardial ischemia, increased left ventricular wall

108 ing location (LAD/LCX occlusion), transmural/subendocardial ischemia, size, and normal/slow myocardia

109 ulnerability to reentry in transmural versus subendocardial ischemia.

110 le- and multivessel disease and detects more subendocardial ischemia.

111 CMR shows a characteristic pattern of global subendocardial late enhancement coupled with abnormal my

112 Global subendocardial late gadolinium enhancement was found in

113 e number of capillaries was increased in the subendocardial layer (46+/-4 vessels/field versus 17+/-3

114 ocardial flow was significantly lower in the subendocardial layer (P<0.05) in all animals, whereas vi

115 more, examination of medium-sized vessels in subendocardial layer in the heart demonstrated successfu

116 roup had increased numbers of vessels in the subendocardial layer of the infarct; the number of capil

117 est at epicardial layers and most delayed at subendocardial layers (p = 0.004), resulting in transmur

118 with hibernation are most pronounced in the subendocardial layers and vary in relation to local coro

119 me (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to

120 The remaining 22 had transmural or subendocardial LGE.

121 Subendocardial longitudinal shortening at base and subep

122 ential effects on the spatial density of the subendocardial microvasculature that may play a role in

123 ower compared to the subendocardial portion (subendocardial, mid-portion, and subepicardial activity:

124 Subendocardial, mid-portion, and subepicardial ROIs were

125 ircumferential strain (GCS) were assessed at subendocardial, midmyocardial, and subepicardial layers.

126 ded in acutely dissociated subepicardial and subendocardial murine left ventricular (LV) myocytes usi

127 esults from complex activation involving the subendocardial muscle network.

128 cycling cardiomyocytes are positioned in the subendocardial muscle of the left ventricle, especially

129 o preferential propagation in the underlying subendocardial muscle structures.

130 nnected to a pectinate muscle suggested that subendocardial muscles lead to epicardial breakthrough p

131 d for paired comparison of subepicardial and subendocardial MVD and SI within groups.

132 ported during the study, one attributable to subendocardial myocardial infarction (secondary to gastr

133 thrombi that are associated with evidence of subendocardial myocardial infarction in mice transgenic

134 tribution and was found predominantly in the subendocardial myocardium (9.8 +/- 4.6%) and rarely in t

135 te delivery are predominantly reduced in the subendocardial myocardium in the early stages of progres

136 APD75 is shortened in subendocardial myocytes but is prolonged in subepicardia

137 PD prolongation was significantly greater in subendocardial myocytes compared with subepicardial myoc

138 l duration (APD) was significantly longer in subendocardial myocytes compared with subepicardial myoc

139 Under control unoperated conditions, subendocardial myocytes exhibited significantly less tra

140 l characteristics of LV subepicardial versus subendocardial myocytes in different species.

141 ght ventricular Purkinje fibers and adjacent subendocardial myocytes were ablated with Lugol solution

142 Subepicardial, midmyocardial, and subendocardial myocytes were enzymatically dissociated f

143 y reflective of a loss of organization among subendocardial myocytes.

144 larization in subepicardial myocytes than in subendocardial myocytes.

145 tly larger in subepicardial myocytes than in subendocardial/myocytes.

146 Subendocardial myofibers normally run in parallel along

147 ved transmural viability in 10 dogs and thin subendocardial necrosis in 2 dogs.

148 nd 4 of these 6 had small scattered areas of subendocardial necrosis in the risk region on triphenyl

149 patients and were characterized by areas of subendocardial necrosis surrounded by a rim of fibrosis.

150 The first beats of induced VT arose from subendocardial or subepicardial sites distant from areas

151 ccurately distinguished from myocardium with subendocardial or transmural infarcts on the basis of un

152 sfunction and CAD had enhancement, which was subendocardial or transmural.

153 or epicardial pacing, clockwise rotation for subendocardial pacing, and dual rotation for midmyocardi

154 receded pacing-induced triggered activity at subendocardial PCs.

155 METHODS AND Global and regional subendocardial peak-systolic Lagrangian longitudinal (LS

156 segment was defined as ischemic if it had a subendocardial perfusion defect with no infarction.

157 analyzed quantitatively for the presence of subendocardial perfusion deficits.

158 Although subendocardial perfusion failed to increase during grade

159 Resting subendocardial perfusion was reduced to 0.65+/-0.08 (mea

160 maging techniques such as magnetic resonance subendocardial perfusion, and spectroscopic imaging will

161 compression in systole that likely benefits subendocardial perfusion.

162 tic abnormalities, with a marked decrease in subendocardial phosphocreatine/ATP (31P magnetic resonan

163 nsplantation of allogeneic pMultistem cells (subendocardial phosphocreatine/ATP to 1.34+/-0.29; n=7;

164 0.2% of all transmural pMIs and 12.3% of all subendocardial pMIs were detected.

165 In the mouse only the subendocardial population of lacZ-positive cells could b

166 take was significantly lower compared to the subendocardial portion (subendocardial, mid-portion, and

167 Aggregates (n=12) were dispersed from the subendocardial Purkinje fiber network of normal canine l

168 icardial, M-region, and endocardial sites or subendocardial Purkinje fibers.

169 rom epicardial, M region, and endocardial or subendocardial Purkinje sites in isolated arterially per

170 lar magnetic resonance, MVI was defined as a subendocardial recess of myocardium with low signal inte

171 ting myocardial function, especially for the subendocardial region.

172 ere larger than those in the less innervated subendocardial region.

173 were present in septal and thickened fibrous subendocardial regions, most apparent in the youngest fe

174 group), and 46 patients underwent map-guided subendocardial resection (surgical group).

175 morrhaphy, was performed with mapping-guided subendocardial resection for recurrent ventricular tachy

176 ricardial patch combined with mapping-guided subendocardial resection frequently cures recurrent vent

177 e predictive of functional recovery, but the subendocardial response was not.

178 Regionally, the decline in subendocardial %S was greater in adjacent (19 +/- 5% to

179 aptations responsible for this phenomenon in subendocardial samples from swine instrumented with a ch

180 e segments were divided into normal (n=211), subendocardial scar (n=49), and transmural scar (n=15).

181 myocardium was compared with myocardium with subendocardial scar, the threshold for differentiating b

182 4 transduction compared to LacZ (9.1%+/-0.9% subendocardial segment shortening in AAV2.9.LacZ vs. 15.

183 consistently arose as focal activity from a subendocardial site, whereas subsequent beats were due t

184 APD) were studied in canine left ventricular subendocardial slabs using microelectrode techniques.

185 us with coronary vessels and associated with subendocardial smooth muscle cell accumulation.

186 Regional LV function was assessed with subendocardial sonomicrometry crystals.

187 pericytes, and other cell populations in the subendocardial space.

188 HC animals showed an increase in subendocardial spatial density of microvessels compared

189 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) o

190 tly transmural and requires participation of subendocardial structures.

191 ons, [3H]ryanodine ligand binding revealed a subendocardial/subepicardial gradient in normal dogs.

192 e receptor binding and a loss in the natural subendocardial/subepicardial gradient, which roughly cor

193 inducible ischemia was defined as hyperemic subendocardial:subepicardial perfusion ratio <1.0.

194 Global myocardial blood flow and subendocardial:subepicardial perfusion ratio were quanti

195 at all transmural depths by inhibiting: (1) subendocardial systolic fiber shortening (-0.10+/-0.05 v

196 kening in the anterobasal region by reducing subendocardial systolic fiber shortening and laminar she

197 Subendocardial systolic shear strains were also perturbe

198 Subendocardial T1 in amyloid patients was shorter than i

199 essive coronary stenosis, a delayed onset of subendocardial thinning suggests an early stage of hypop

200 ique form of fibrosis, which forms a de novo subendocardial tissue layer encapsulating the myocardium

201 the patients with most severe AS (n=15), the subendocardial to subepicardial MBF ratio decreased from

202 failing heart, preferential conduction from subendocardial to subepicardial myocytes is lost, and fa

203 AP propagation from subendocardial to subepicardial myocytes required less G

204 Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at

205 ied as (1) no LGE, (2) ischemic-pattern LGE: subendocardial/transmural, (3) nonischemic LGE: midmyoca

206 tening at rest were greater in segments with subendocardial versus transmural infarcts, both in subep

207 Two subendocardial viability defects were detected, which co

208 ability triangular index (+15%; P=0.01), and subendocardial viability ratio (+12%; P=0.01x10(-4)) wer

209 peremia index (0.38 +/- 0.14, p = 0.009) and subendocardial viability ratio (7.7 +/- 3.1, p = 0.04),

210 entation index (beta = -0.11, p = 0.03), and subendocardial viability ratio (beta = 0.18, p = 0.001).

211 sure-time integral (r = 0.95, P < 0.05), and subendocardial viability ratio (r = 0.86, P < 0.05).

212 metry-derived central augmentation index and subendocardial viability ratio were measured to assess a

213 augmentation index, central blood pressure, subendocardial viability ratio, and additional measures

214 ditions, and the location of the infarction (subendocardial vs. transmural).

215 tude is largely derived from endocardial and subendocardial wall layers.

216 geographic dominance of ischemia within the subendocardial zones.