ライフサイエンスコーパス: endocardial

1 Endocardial ablation could abolish all Epi-LAVA in 4 ICM

2 lly epicardial access is only performed when endocardial ablation has failed.

3 Epicardial mapping was helpful in guiding endocardial ablation in 2 patients (9.5%), showing that

4 endocardial+epicardial ablation versus only endocardial ablation in the first procedure in patients

5 Success of anatomically guided endocardial ablation may be identified by a short GCV-no

6 ss rate to achieve bidirectional block using endocardial ablation only with minimal need for epicardi

7 All patients received endocardial ablation targeting local abnormal ventricula

8 Endocardial ablation was able to eliminate Epi-LAVA at l

9 procedures, especially in IVT patients with endocardial ablation.

10 open-chest surgery after failing epicardial/endocardial ablation.

11 le to injury where it is closest to areas of endocardial ablation.

12 From a total of 173 endocardial ablations targeting Epi-LAVA at the facing s

13 f IVT procedures, and 50% of procedures with endocardial access only.

14 Previous studies showed that endocardial activation during long-duration ventricular

15 Endocardial activation mapping and local EGM assessment

16 rfused hearts, the calculated epicardial and endocardial activation patterns showed good qualitative

17 Endocardial activation patterns were classified as chaot

18 during sympathetic stimulation, and regional endocardial activation recovery interval patterns were s

19 The inducibility and earliest presystolic endocardial activation sites of VT as well as voltage an

20 troanatomic mapping in 12 patients showed an endocardial activation time significantly longer in pati

21 We ruled out defects in endocardial activation, epicardial activation, and dedif

22 ought to determine the long-term outcomes of endocardial and adjuvant epicardial CA in nonischemic di

23 h nonischemic dilated cardiomyopathy and VT, endocardial and adjuvant epicardial CA is effective in a

24 The latest activation times (LATs) for LV endocardial and biventricular epicardial tissue were cal

25 hyaluronan and versican and is expressed in endocardial and endocardially-derived cells in the devel

26 CCM deficiency dramatically alters endocardial and endothelial gene expression, including i

27 o had failed ablation attempts from multiple endocardial and epicardial (1 patient) sites.

28 ion of the VAs when the distance between the endocardial and epicardial ablation sites was >8 mm and

29 technique was evaluated that estimates both endocardial and epicardial activation from body surface

30 LV endocardial and epicardial activation recovery intervals

31 he purpose of this study was to characterize endocardial and epicardial dispersion of repolarization

32 ry intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathe

33 Healthy swine underwent endocardial and epicardial linear ablation using a novel

34 ere midrange between those of the idiopathic endocardial and epicardial LVOT VAs, and more similar to

35 l LVOT VAs when compared with the idiopathic endocardial and epicardial LVOT VAs.

36 We assessed CF in different endocardial and epicardial regions during ventricular ta

37 sometimes require catheter ablation from the endocardial and epicardial sides for their elimination,

38 ed unipolar radiofrequency ablation from the endocardial and epicardial sides for their elimination,

39 imes require catheter ablation from both the endocardial and epicardial sides for their elimination,

40 ar radiofrequency catheter ablation from the endocardial and epicardial sides in treating intramural

41 required simultaneous ablation from both the endocardial and epicardial sides.

42 s rhythm and ventricular stimulation from 27 endocardial and epicardial sites.

43 tial maps during sinus rhythm and localizing endocardial and epicardial stimulation sites.

44 y2(+) cardiomyocytes, respectively, from the endocardial and epicardial zones of the ventricular wall

45 Endocardial and myocardial progenitors originate in dist

46 e Periostin Cre (Postn-Cre) lineage includes endocardial and neural crest derived mesenchymal cells o

47 compared the resulting lineage pattern with endocardial and proepicardial contributions to the coron

48 ression and active proliferation of adjacent endocardial and smooth muscle cells.

49 METHOD AND In 7 sheep, left ventricular endocardial and transmural mapping was performed 84 week

50 djustments applied for covariables, midwall, endocardial, and epicardial GLS were significant predict

51 variable adjusted hazard ratios for midwall, endocardial, and epicardial GLS, while accounting for fa

52 Global, endocardial, and epicardial MBF were calculated by using

53 Inhibition of endocardial angiogenesis results in reduced endocardial

54 quent application E-4031 increasing mid- and endocardial APD80 more significantly than in the epicard

55 A new attempt by endocardial approach was successful in a significant num

56 icardial AT and QRS vectors were minimal and endocardial AT vector indicated LV preexcitation.

57 impulse and rotor modulation (FIRM) with an endocardial basket catheter was used in all cases.

58 The defects in endocardial behavior in tal1-deficient embryos originate

59 Endocardial bipolar DS area >22.5 cm(2) best predicted s

60 Endocardial bipolar DS area >7 cm(2) and endocardial bip

61 ltage areas, whereas 18% had no identifiable endocardial bipolar DS areas.

62 We performed endocardial bipolar EVM-guided EMBs in 29 patients and w

63 Endocardial bipolar DS area >7 cm(2) and endocardial bipolar scar density >0.35 predicted epicard

64 endor independent and uses speckle tracking (endocardial border detection) on ultrasound (MRI) imagin

65 ejection fraction (EF) by manual tracing of endocardial borders is time consuming and operator depen

66 correlated better with epicardial than with endocardial bundles (% angles<20 degrees between directi

67 e perpendicular orientation of epicardial to endocardial bundles.

68 apped anisotropic conduction correlated with endocardial but not with epicardial bundles.

69 At sites with endocardial BV >1.50 mV, the optimal endocardial UV cuto

70 are associated with transmural scar with low endocardial BV, the additional use of endocardial UV at

71 Endocardial capillary density was reduced with evidence

72 bipolar radiofrequency instruments, required endocardial catheter ablation to complete the linear abl

73 so determined the ability of clinically used endocardial catheters to identify AF mechanisms using cl

74 served an initial decrease in myocardial and endocardial cavity volumes at day 3, followed by ventric

75 to demonstrate its ability to identify each endocardial cell and chamber-specific CM.

76 g cardiac sarcomeric Z-disks and endothelial/endocardial cell integrity in zebrafish and may also hel

77 f cardiac sarcomeric Z-disks and endothelial/endocardial cell integrity, partly through regulating F-

78 ebrafish heart valve formation, we show that endocardial cells are converging to the valve-forming ar

79 Hbegf expression in embryonic endocardial cells could be readily activated through a R

80 ata show that lineage conversion of neonatal endocardial cells during trabecular compaction generates

81 of endocardial morphogenesis: tal1-deficient endocardial cells fail to generate a cohesive monolayer

82 Here we show in mouse that endocardial cells form a primitive vascular plexus surro

83 Haemogenic activity arises from a subset of endocardial cells in the outflow cushion and atria earli

84 essively increasing number of tal1-deficient endocardial cells initiate myocardial gene expression.

85 9b expression is similarly restricted to the endocardial cells overlying the developing heart valves

86 Here we show that loss of CCM signaling in endocardial cells results in mid-gestation heart failure

87 action-responsive transcriptional changes in endocardial cells to regulate cardiac chamber maturation

88 ive transcription factor KLF2 is required in endocardial cells to regulate the mesenchymal cell respo

89 However, endocardial cells were present and retained expression o

90 s and flow directionality on the behavior of endocardial cells, the specialized endothelial cells of

91 e the fractal dimension, a unitless index of endocardial complexity calculated from endocardial conto

92 MR imaging data should expect slightly less endocardial complexity in Chinese American patients and

93 analysis of cardiac MR imaging data measures endocardial complexity, which helps to differentiate nor

94 fractal dimension (FD), which is a marker of endocardial complexity.

95 tissue anisotropy, and the presence of fast endocardial conduction on myocardial activation during E

96 Adding fast endocardial conduction to this model altered %dLV and %d

97 was used to assess the relationship between endocardial contact electrogram amplitude and histologic

98 of IMAT on scar tissue identification during endocardial contact mapping and optimal voltage-based ma

99 ex of endocardial complexity calculated from endocardial contours after segmentation.

100 endocardial angiogenesis results in reduced endocardial contribution to the liver vasculature and de

101 interval): cyanotic CHD (6.44, 3.95-10.50), endocardial cushion defects (5.47, 2.89-10.36), and left

102 truncus arteriosus, transposition complexes, endocardial cushion defects, and univentricular hearts.

103 ch Tbx20 regulates the Wnt pathway to direct endocardial cushion maturation and valve elongation, and

104 proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stra

105 endoderm, outflow tract and atrioventricular endocardial cushions and post-migratory neural crest der

106 chymal transition that supplies cells to the endocardial cushions and repositions cardiac neural cres

107 factor Tbx20 is expressed in the developing endocardial cushions and valves throughout heart develop

108 During valvulogenesis, globular endocardial cushions elongate and remodel into highly or

109 Fusion of the sternum and endocardial cushions is impaired in the mutant mice asso

110 rgeted mutant mice, we find that endothelial/endocardial deletion of Mib1-Dll4-Notch1 signaling, poss

111 ta demonstrate that physical separation from endocardial-derived factors prevents AVJ myocardium from

112 We propose that complementary SV-derived and endocardial-derived migratory routes unite to form the c

113 Dorsal (SV-derived) and ventral (endocardial-derived) coronary vessels developed in respo

114 There were no LV epicardial versus endocardial differences in activation recovery interval

115 Endocardial differentiation defects were rescued by myoc

116 ilbud stage resulted in severe inhibition of endocardial differentiation while there was little effec

117 on, and identify BMP as a signal involved in endocardial differentiation.

118 idate myocardium-derived signal required for endocardial differentiation.

119 t, apex-to-base, circumferential, epicardial-endocardial distribution, pattern, and type of MF in 30

120 Epicardial-endocardial distributions were as follows: trabecular 26

121 Endothelial/endocardial (EC) Raf1(L613V) causes cardiac hypertrophy

122 Additionally, the usefulness of unipolar endocardial electroanatomic mapping to identify epicardi

123 Endocardial electrogram amplitude correlated significant

124 Intramural electrograms during VA preceded endocardial electrograms (-29+/-34 versus -15+/-21 ms; P

125 High-density bipolar left ventricular endocardial electrograms were collected using CARTO3v4 i

126 plitude and duration correlated closely with endocardial electrograms, but were greater in amplitude

127 ntramural needle electrograms in relation to endocardial electrograms.

128 The novel noninvasive epicardial and endocardial electrophysiology system (NEEES) allows for

129 as well the percentage decrease in LATs for endocardial (en) versus epicardial (ep) LV pacing (defin

130 d need for antiarrhythmic drug therapy after endocardial (ENDO) and adjuvant epicardial (EPI) substra

131 rd potassium current (Ito) in EPI but not in endocardial (ENDO) cardiomyocytes of UNx rats led to a d

132 othelial to mesenchymal transition involving endocardial endothelial cells is caused by dysregulated

133 lly described in heart development where the endocardial endothelial cells that line the atrioventric

134 genic cells within EFE tissue originate from endocardial endothelial cells via aberrant endothelial t

135 Our aim was to compare the efficacy of endocardial+epicardial ablation versus only endocardial

136 In 2 other BrS patients, endocardial, epicardial RV (CARTO), and body surface map

137 A combined endocardial-epicardial ablation approach for initial VT

138 had epicardial-only ablation, whereas 3 had endocardial-epicardial ablation.

139 required in symptomatic cases refractory to endocardial-epicardial approach.

140 Of 6889 endocardial-epicardial mapping point pairs, 547 (8%) pai

141 (50+/-14 years; 79% men) underwent combined endocardial-epicardial right ventricular electroanatomic

142 nder antiarrhythmic drugs after unsuccessful endocardial/epicardial ablation.

143 +/-2 antiarrhythmic drugs and 2+/-1 previous endocardial/epicardial catheter ablation attempts underw

144 efore ablation, VT was inducible in 75%, and endocardial/epicardial LAVA were present in 88%/75%.

145 rigorously programmed process consisting of endocardial epithelial-mesenchymal transformation (EMT),

146 Endocardial fibroelastosis (EFE) is a unique form of fib

147 ity of endothelial cells and near regions of endocardial fibrosis/disruption.

148 Endocardial flowers are contiguous with coronary vessels

149 icity in the postinfarct heart, showing that endocardial flowers develop by arteriogenesis of Cx40(-)

150 Finally, endocardial flowers exhibit angiogenic features, includi

151 se previously undescribed structures, termed endocardial flowers, have a distinct endothelial phenoty

152 iest ventricular activation and discriminate endocardial from epicardial origin of activation with cl

153 re, we investigated how TBX20 interacts with endocardial gene networks to drive the mesenchymal and m

154 Apj-/- mice have greater endocardial Hdac4 and Hdac5 nuclear localization and red

155 tissue interactions involved in establishing endocardial identity are poorly understood.

156 he epicardium in 5 patients (63%) and in the endocardial inferolateral left ventricle in 3 patients (

157 Percutaneous delivery via endocardial injection was investigated with fluoroscopic

158 on patterning, whereby reciprocal myocardial-endocardial interactions coordinate the processes of val

159 c valve, and septal defects, indicating that endocardial Jag1 to Notch1 signaling is required for pos

160 Mice lacking endocardial Jag1, Notch1, or RBPJ displayed enlarged val

161 Endocardial Klf2 deficiency results in defective valve f

162 ate potentials tended to be more common than endocardial late potentials (53.6% versus 35.7%; P=0.12)

163 in showed a similar trend from epicardial to endocardial layers (epiwall: -16.0 +/- 2.9%; midwall: -1

164 gher for IPL compared with right ventricular endocardial leads (0.75+/-0.33 V; P=0.001) but not diffe

165 One hundred twenty endocardial left ventricular ablation lesions (conventio

166 as multisite pacing, His bundle pacing, and endocardial left ventricular pacing.

167 erence between linear (n=22) and focal (n=7) endocardial line length or volume.

168 ), we identified accessible chromatin within endocardial lineages and intersected these data with TBX

169 ides insight into the chromatin landscape of endocardial lineages during septation.

170 n enhancer drove reporter gene expression in endocardial lineages in a TBX20-binding site-dependent m

171 Selective ablation of Tbx20 in murine endocardial lineages reduced the expression of extracell

172 The WT <5 mm area was smaller than the endocardial low-voltage area (54 cm(2) [Q1-Q3, 46-92] ve

173 Endocardial LP abolition was associated with reduced VT

174 The most common indications for endocardial LV pacing were difficult CS anatomy (n =12),

175 s with CC undergoing detailed epicardial and endocardial LV tachycardia mapping and ablation were inc

176 pacing, QRS duration (187+/-29 ms; P=NS) and endocardial LV total activation time (91+/-23 ms; P=NS)

177 ic conduction, QRS duration was 185+/-30 ms, endocardial LV total activation time 92+/-27 ms, and tra

178 There was no significant difference in endocardial LV total activation time between LVendo and

179 from the coronary venous system and multiple endocardial LV/right ventricular sites.

180 and more similar to those of the idiopathic endocardial LVOT VAs than those of the idiopathic epicar

181 ogram thresholds for IMAT delineation during endocardial mapping and to describe the use of endocardi

182 docardial mapping and to describe the use of endocardial mapping for delineation of IMAT dense region

183 e (16 patients and 58 VTs), left ventricular endocardial mapping was performed in sinus rhythm.

184 ions of myocardium reliably identified using endocardial mapping with thresholds of <3.7 and <0.6 mV,

185 uring left ventricular and right ventricular endocardial mapping, 94% of VO were adequate.

186 ents (23.8%) underwent a successful repeated endocardial mapping, and ablation after epicardial mappi

187 Twenty-eight epicardial and 63 endocardial maps, obtained from 64 CRT patients undergoi

188 roaortic approach), and 12 right ventricular endocardial maps.

189 Endocardial margins of the RV were manually contoured on

190 docardial voltage signals and 314 epicardial/endocardial matched pairs of points were analyzed.

191 ntricular canal undergo an EndMT to form the endocardial mesenchymal cushion that later gives rise to

192 The transmural extent and intramural types (endocardial, midwall, epicardial, patchy, transmural) of

193 Deployment of an endocardial mitral isthmus line (MIL) with the end point

194 indicate that the myocardium is crucial for endocardial morphogenesis and differentiation, and ident

195 st for a potential role of the myocardium in endocardial morphogenesis, we used two different zebrafi

196 le is known about the molecules that control endocardial morphogenesis.

197 bryos originate during the earliest steps of endocardial morphogenesis: tal1-deficient endocardial ce

198 d universal increment from the epicardial to endocardial myocardial wall (epiwall: -15.4 +/- 1.9%; mi

199 lts in trunk vessel deficiencies, disordered endocardial-myocardial contact and impaired heart functi

200 0.69; P<0.001) with readings obtained in the endocardial myocardium performing better than those in t

201 Heat-shock-induced bmp2b expression rescued endocardial nfatc1 expression in hand2 mutants and in my

202 for apoptosis, which resulted in the loss of endocardial nfatc1 expression.

203 Region-specific endocardial Notch activity regulates heart morphogenesis

204 Although previous studies have shown that endocardial Notch signalling non-cell-autonomously promo

205 a RBPJ-binding site, identifying Hbegf as an endocardial Notch target.

206 Thirteen patients underwent endocardial-only ablation, 2 had epicardial-only ablatio

207 ecurrent VT or persistent inducibility after endocardial-only ablation.

208 ited by intramural substrate not amenable to endocardial or epicardial ablation.

209 cedure duration and help choosing between an endocardial or epicardial approach.

210 ablation catheter safely delivers contiguous endocardial or epicardial lesions without gaps in a sing

211 tricular activation and best pace map on the endocardial or epicardial side.

212 bxiphoid approach can be an alternative when endocardial or epicardial transvenous mapping has failed

213 approach is an alternative when conventional endocardial or transvenous epicardial ablation fails in

214 hteen goats were instrumented with an atrial endocardial pacemaker lead and a burst pacemaker.

215 ial pacing (BIVepi) with LV (LVendo) and BIV endocardial pacing (BIVendo) in patients with chronic he

216 py (CRT) delivered via left ventricular (LV) endocardial pacing (ENDO-CRT) is associated with improve

217 entional CRT underwent implantation of an LV endocardial pacing electrode and a subcutaneous pulse ge

218 pacing via a wireless left ventricular (LV) endocardial pacing electrode.

219 model and offers a potential alternative to endocardial pacing leads.

220 nized LV pacing, multisite LV pacing, and LV endocardial pacing offer promise as novel pacing options

221 LV endocardial pacing through a ventricular septal puncture

222 LV endocardial pacing through the interventriuclar septum m

223 ced ATs and increased synchrony arising from endocardial pacing.

224 nce using a transmural atrial (epicardial to endocardial) pacing approach in patients with congenital

225 Endocardial perfusion parameters obtained by semiautomat

226 singularities between the epicardial and the endocardial planes was significantly >0 with a median di

227 Endocardial plus adjuvant EPI ablation was performed in

228 At the optimal endocardial position, the acute hemodynamic response (AH

229 However, the precise identification of the endocardial precursors and the mechanisms they require f

230 on of Jun in Tie2-expressing endothelial and endocardial precursors does not result in aortic arch ar

231 Endocardial progenitors acquire a molecular identity dis

232 Because they do not depend on ELA-APJ, endocardial progenitors are able to expand and compensat

233 We show that in hand2 mutants endocardial progenitors migrate to the midline but fail

234 nhanced open chromatin states at endothelial/endocardial promoters.

235 ety of epicardial substrate elimination with endocardial radiofrequency (RF) delivery in patients wit

236 Sustained obesity results in global biatrial endocardial remodeling characterized by LA enlargement,

237 (NaviStar ThermoCool Catheter for Endocardial RF Ablation in Patients With Ventricular Tac

238 Elimination of Epi-LAVA with endocardial RF delivery is feasible and might be used fi

239 rS-ECG with data from various epicardial and endocardial right ventricular activation mapping procedu

240 mporary LVendo and BIVendo pacing with an LV endocardial roving catheter.

241 decremental preexcitation of the RVOT before endocardial RV mapping.

242 mapping demonstrated larger epicardial than endocardial scar and core-dense (</=0.5 mV) scar areas (

243 There was a linear correlation between endocardial scar area (<1.5 mV) and filtered QRS (r=0.41

244 ate the signal-averaged ECG (SAECG) with the endocardial scar characteristics in patients with ischem

245 ematic characterization of the LV epicardial/endocardial scar distribution and density in CC has not

246 Endocardial scar extension and density predict scar tran

247 ding of the confounding influence of IMAT on endocardial scar mapping.

248 nt correlation between the surface SAECG and endocardial scar size in patients with ischemic VTs.

249 lay and exceeded the region of corresponding endocardial scar.

250 erformed on the epicardial side in 9 VAs and endocardial side in 5 VAs.

251 sites anatomically opposite to the earliest endocardial site of activation under direct intracardiac

252 ultaneously recorded from 2 epicardial and 1 endocardial site of coronary-perfused canine left ventri

253 electrograms were recorded at epicardial and endocardial sites of coronary-perfused canine RV wedge p

254 al epicardial electrograms had corresponding endocardial sites with BV <1.50 mV, and the remaining co

255 ries and a remote approach from the adjacent endocardial sites.

256 An upregulation of endocardial SOX17 accompanied compensation in Apj mutant

257 n defects were rescued by myocardial but not endocardial-specific expression of hand2.

258 mesenchymal cells, a phenotype reproduced by endocardial-specific loss of Wnt9b.

259 gest that LV pacing alone may offer a viable endocardial stimulation strategy to achieve cardiac resy

260 e impaired 12-month outcome of patients with endocardial structural defects.

261 The mean endocardial surface area of these potentials was 18+/-4%

262 Lateral catheter sliding over target endocardial surface can lead to poor tissue contact and

263 tion were driven by rapid activations on the endocardial surface that blocked and broke up transmural

264 n of a native or prosthetic heart valve, the endocardial surface, or an indwelling cardiac device.

265 Regional patterns of LV endocardial sympathetic innervation are similar to that

266 ut our understanding of the contributions of endocardial TBX20 to heart development remains incomplet

267 ultaneously acquired from the epicardial and endocardial tissue during acute fibrillation in ovine is

268 ct that patients with viable fast-conducting endocardial tissue or distal Purkinje network or both, a

269 f discordance between the epicardial and the endocardial tissue.

270 ked and broke up transmurally, leading to an endocardial to epicardial activation rate gradient as LD

271 An endocardial-to-epicardial gradient existed at rest (nons

272 r beta-catenin are proposed to contribute to endocardial-to-mesenchymal transformation (EMT) through

273 1 (5.5-9 weeks) were detected, indicative of endocardial-to-mesenchymal transformation (EndMT) in val

274 Biplane ventriculographic and endocardial tracings were recorded.

275 ography was high on the RV when using either endocardial unipolar or epicardial bipolar data (kappa=0

276 versus 36%), associated with more extensive endocardial unipolar scar (41 [22-83] versus 9 [1-29] cm

277 Low endocardial unipolar voltage (UV) at sites with normal b

278 Endocardial unipolar voltage mapping serves to character

279 The endocardial unipolar voltage value (with a newly propose

280 Based on endocardial unipolar voltage, 44 were classified as pred

281 ing could be identified by corresponding low endocardial UV <3.7 mV.

282 th low endocardial BV, the additional use of endocardial UV at normal BV sites improves the diagnosti

283 es with endocardial BV >1.50 mV, the optimal endocardial UV cutoff for identification of epicardial B

284 ion of epicardial right ventricular scar, an endocardial UV cutoff value of 3.9 mV is more accurate t

285 This study aimed to define endocardial UV cutoff values using computed tomography-d

286 c/pharmacodynamic (PK/PD) model of simulated endocardial vegetations (SEVs) and by exposure to vancom

287 n=5) during sinus rhythm, and epicardial and endocardial ventricular pacing (65 records in total).

288 pproach from the anatomically opposite side (endocardial versus epicardial or above versus below the

289 hy (echo), cardiac MRI (CMR) offers improved endocardial visualization and potential to assess scar.

290 (CMR) signal intensity and left atrial (LA) endocardial voltage after LA ablation.

291 ity was associated with reduced posterior LA endocardial voltage and infiltration of contiguous poste

292 nt-by-point relationship between LGE CMR and endocardial voltage in patients undergoing repeat LA abl

293 e group (p < 0.001), consistent with reduced endocardial voltage in this region.

294 Sixty endocardial voltage maps (360+/-147 points) were perform

295 Detailed bipolar endocardial voltage maps (398 +/- 152 points) from 24 pa

296 A total of 8494 epicardial and 6331 endocardial voltage signals and 314 epicardial/endocardi

297 mines the correlation between atrial CMR and endocardial voltage.

298 Bipolar epicardial and endocardial voltages within scar were low (0.4 [0.2-0.55

299 Patients who underwent only an endocardial VT ablation in their first procedure (Endo-G

300 acing lead was successfully delivered to the endocardial wall of the lateral LV in all patients (9 me