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

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

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

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

21 PET subendocardial and subepicardial CFR were in good agreem

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

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

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

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

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

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

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

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

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

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

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

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

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

35 Subendocardial blood flow per beat was normal in both re

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

37 a) current density between subepicardial and subendocardial cells.

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

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

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

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

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

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

44 Locally, subendocardial end-diastolic strains occurred: Longitudi

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

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

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

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

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

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

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

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

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

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

55 0.03 ml/min/g, p < 0.01), critically reduced subendocardial flow reserve (adenosine flow: 1.04+/-0.09

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

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

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

59 Reductions in subendocardial flow were visually apparent in MRFP image

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

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

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

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

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

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

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

67 Post-gadolinium subendocardial hyperenhancement suggested focal involvem

68 tolic myocardial velocities did not identify subendocardial hypoperfusion.

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

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

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

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

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

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

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

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

77 njured myocardium associated with reperfused subendocardial infarctions.

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

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

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

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

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

83 Transcatheter subendocardial infusion can be used to reversibly impair

84 lar myocardium with the use of transcatheter subendocardial infusion.

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

86 Subendocardial injection of ethanol can predictably abla

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

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

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

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

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

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

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

94 Global subendocardial late gadolinium enhancement was found in

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

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

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

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

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

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

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

102 Subendocardial longitudinal shortening at base and subep

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

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

105 esults from complex activation involving the subendocardial muscle network.

106 o preferential propagation in the underlying subendocardial muscle structures.

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

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

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

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

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

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

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

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

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

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

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

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

119 larization in subepicardial myocytes than in subendocardial myocytes.

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

121 Subendocardial myofibers normally run in parallel along

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

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

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

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

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

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

128 receded pacing-induced triggered activity at subendocardial PCs.

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

130 analyzed quantitatively for the presence of subendocardial perfusion deficits.

131 Although subendocardial perfusion failed to increase during grade

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

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

134 compression in systole that likely benefits subendocardial perfusion.

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

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

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

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

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

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

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

142 ting myocardial function, especially for the subendocardial region.

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

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

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

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

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

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

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

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

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

152 4 transduction compared to LacZ (9.1%+/-0.9% subendocardial segment shortening in AAV2.9.LacZ vs. 15.

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

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

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

156 Regional LV function was assessed with subendocardial sonomicrometry crystals.

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

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

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

160 tly transmural and requires participation of subendocardial structures.

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

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

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

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

165 Subendocardial systolic shear strains were also perturbe

166 Subendocardial T1 in amyloid patients was shorter than i

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

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

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

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

171 AP propagation from subendocardial to subepicardial myocytes required less G

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

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

174 Two subendocardial viability defects were detected, which co

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

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

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

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

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

180 geographic dominance of ischemia within the subendocardial zones.