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1 %), activation mapping demonstrated residual endocardial (3/11; 27.2%) or epicardial (8/11; 72.7%) co
2 hythm was performed (2518 points [1615-3752] endocardial, 5049+/-2580 points epicardial) and identifi
3 velopment of a minimally invasive epicardial/endocardial ablation approach (Hybrid Convergent) to ach
4 ONVERGE trial (Convergence of Epicardial and Endocardial Ablation for the Treatment of Symptomatic Pe
5 lly epicardial access is only performed when endocardial ablation has failed.
6  endocardial+epicardial ablation versus only endocardial ablation in the first procedure in patients
7  fully characterize the AF mechanism and why endocardial ablation may not be sufficient.
8 ss rate to achieve bidirectional block using endocardial ablation only with minimal need for epicardi
9                  The addition of Bmp2 during endocardial ablation partially rescued myocyte different
10 y and Feasibility Study of the IOWA Approach Endocardial Ablation System to Treat Atrial Fibrillation
11 afety and Feasibility Study of the FARAPULSE Endocardial Ablation System to Treat Paroxysmal Atrial F
12 le to injury where it is closest to areas of endocardial ablation.
13  procedures, especially in IVT patients with endocardial ablation.
14                                              Endocardial ablations at 180 W reached depths of 10.7+/-
15                                              Endocardial ablations were performed at 140 to 180 W for
16                                              Endocardial abnormalities cause reduced cardiomyocyte pr
17 f IVT procedures, and 50% of procedures with endocardial access only.
18  Three apical LVS-VAs exhibited an eccentric endocardial activation pattern that was from the basal t
19 rfused hearts, the calculated epicardial and endocardial activation patterns showed good qualitative
20                                              Endocardial activation patterns were classified as chaot
21 during sympathetic stimulation, and regional endocardial activation recovery interval patterns were s
22                                              Endocardial activation slowing during SR may differentia
23 troanatomic mapping in 12 patients showed an endocardial activation time significantly longer in pati
24                                    A minimal endocardial activation velocity cutoff <=0.1 m/s differe
25 aled infarction, the spatial distribution of endocardial activation velocity was compared between SR
26 ow conduction and delayed quasi-simultaneous endocardial activation.
27           During a process we term "coronary-endocardial anchoring," new coronaries respond by sprout
28                               A total of 109 endocardial and 9 epicardial locations were paced in 9 p
29 ought to determine the long-term outcomes of endocardial and adjuvant epicardial CA in nonischemic di
30 h nonischemic dilated cardiomyopathy and VT, endocardial and adjuvant epicardial CA is effective in a
31    The latest activation times (LATs) for LV endocardial and biventricular epicardial tissue were cal
32 ve robust Notch signaling hyperactivation in endocardial and endothelial cells, including increased p
33           CCM deficiency dramatically alters endocardial and endothelial gene expression, including i
34 o had failed ablation attempts from multiple endocardial and epicardial (1 patient) sites.
35  technique was evaluated that estimates both endocardial and epicardial activation from body surface
36 standard criteria for mitral line block with endocardial and epicardial activation mapping.
37                                           LV endocardial and epicardial activation recovery intervals
38 he purpose of this study was to characterize endocardial and epicardial dispersion of repolarization
39 ry intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathe
40                      Healthy swine underwent endocardial and epicardial linear ablation using a novel
41 ere midrange between those of the idiopathic endocardial and epicardial LVOT VAs, and more similar to
42 l LVOT VAs when compared with the idiopathic endocardial and epicardial LVOT VAs.
43                                With combined endocardial and epicardial mapping, the isthmus could be
44 imes require catheter ablation from both the endocardial and epicardial sides for their elimination,
45 sometimes require catheter ablation from the endocardial and epicardial sides for their elimination,
46 required simultaneous ablation from both the endocardial and epicardial sides.
47 s rhythm and ventricular stimulation from 27 endocardial and epicardial sites.
48 tial maps during sinus rhythm and localizing endocardial and epicardial stimulation sites.
49 y2(+) cardiomyocytes, respectively, from the endocardial and epicardial zones of the ventricular wall
50 ion, and essential cell-cell interactions of endocardial and myocardial cells throughout heart develo
51 ind that the OFT expands via accrual of both endocardial and myocardial cells.
52                                              Endocardial and myocardial progenitors originate in dist
53 ed proliferation and impaired recruitment of endocardial and neural crest cells during the early stag
54 ression and active proliferation of adjacent endocardial and smooth muscle cells.
55      METHOD AND In 7 sheep, left ventricular endocardial and transmural mapping was performed 84 week
56                                     Although endocardial and vascular endothelium are molecularly sim
57 djustments applied for covariables, midwall, endocardial, and epicardial GLS were significant predict
58 variable adjusted hazard ratios for midwall, endocardial, and epicardial GLS, while accounting for fa
59                                Inhibition of endocardial angiogenesis results in reduced endocardial
60 quent application E-4031 increasing mid- and endocardial APD80 more significantly than in the epicard
61 ronic arrays in multilayer configurations on endocardial balloon catheters can establish conformal co
62  impulse and rotor modulation (FIRM) with an endocardial basket catheter was used in all cases.
63                                              Endocardial bipolar DS area >22.5 cm(2) best predicted s
64 ltage areas, whereas 18% had no identifiable endocardial bipolar DS areas.
65                                 We performed endocardial bipolar EVM-guided EMBs in 29 patients and w
66 endor independent and uses speckle tracking (endocardial border detection) on ultrasound (MRI) imagin
67  ejection fraction (EF) by manual tracing of endocardial borders is time consuming and operator depen
68 ithms that allow near automated detection of endocardial boundaries and measurement of LV volumes and
69 either manual or automated identification of endocardial boundaries followed by model-based calculati
70                                At sites with endocardial BV >1.50 mV, the optimal endocardial UV cuto
71 are associated with transmural scar with low endocardial BV, the additional use of endocardial UV at
72                                              Endocardial capillary density was reduced with evidence
73                 The limited effectiveness of endocardial catheter ablation (CA) for persistent and lo
74 bipolar radiofrequency instruments, required endocardial catheter ablation to complete the linear abl
75 so determined the ability of clinically used endocardial catheters to identify AF mechanisms using cl
76 served an initial decrease in myocardial and endocardial cavity volumes at day 3, followed by ventric
77 on modulates OFT morphogenesis by triggering endocardial cell accumulation that induces OFT lumen exp
78  to demonstrate its ability to identify each endocardial cell and chamber-specific CM.
79 g cardiac sarcomeric Z-disks and endothelial/endocardial cell integrity in zebrafish and may also hel
80 f cardiac sarcomeric Z-disks and endothelial/endocardial cell integrity, partly through regulating F-
81 the ECM (extracellular matrix) between the 2 endocardial cell monolayers, undergo endothelial-to-mese
82 cular phenotype by enhancing endothelial and endocardial cell proliferation and stabilizing endocardi
83 proaches, a population of human pre-valvular endocardial cells (HPVCs) can be derived from pluripoten
84 -type injury site consists of Runx1-positive endocardial cells and thrombocytes that induce expressio
85 ebrafish heart valve formation, we show that endocardial cells are converging to the valve-forming ar
86                Hbegf expression in embryonic endocardial cells could be readily activated through a R
87                   With this potential, human endocardial cells could provide unique therapeutic oppor
88                   Here we show in mouse that endocardial cells form a primitive vascular plexus surro
89 required for development of the hPSC-derived endocardial cells identified a novel role for BMP10 in t
90      We find that initially atrioventricular endocardial cells migrate collectively into the cardiac
91 9b expression is similarly restricted to the endocardial cells overlying the developing heart valves
92 action-responsive transcriptional changes in endocardial cells to regulate cardiac chamber maturation
93 ive transcription factor KLF2 is required in endocardial cells to regulate the mesenchymal cell respo
94                                     However, endocardial cells were present and retained expression o
95  receptor Acvrl1 is required for addition of endocardial cells, but not for their proliferation, indi
96 s and flow directionality on the behavior of endocardial cells, the specialized endothelial cells of
97                              To access human endocardial cells, we generated a human pluripotent stem
98 es with diphtheria toxin efficiently ablated endocardial cells, which significantly attenuated the pe
99 e identified: inflammatory, fibroblastic and endocardial cells.
100 me generates higher junctional forces within endocardial cells.
101 (cTSD; the difference between epicardial and endocardial circumferential strain) in a genotyped cohor
102  MR imaging data should expect slightly less endocardial complexity in Chinese American patients and
103 fractal dimension (FD), which is a marker of endocardial complexity.
104                                  Adding fast endocardial conduction to this model altered %dLV and %d
105  was used to assess the relationship between endocardial contact electrogram amplitude and histologic
106 of IMAT on scar tissue identification during endocardial contact mapping and optimal voltage-based ma
107  endocardial angiogenesis results in reduced endocardial contribution to the liver vasculature and de
108  de novo source of tissue macrophages in the endocardial cushion, the primordium of the cardiac valve
109  proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stra
110              During valvulogenesis, globular endocardial cushions elongate and remodel into highly or
111                                    Intrinsic endocardial defects contribute to abnormal endothelial-t
112                                              Endocardial deletion of Efnb2 phenocopies the coronary a
113 rgeted mutant mice, we find that endothelial/endocardial deletion of Mib1-Dll4-Notch1 signaling, poss
114 ciently explain developmental defects in the endocardial-derived cardiac valve, septum, and vasculatu
115 egulatory pathway is predominantly active in endocardial-derived vessels, whilst SOXF/RBPJ and BMP-SM
116           There were no LV epicardial versus endocardial differences in activation recovery interval
117 ilbud stage resulted in severe inhibition of endocardial differentiation while there was little effec
118 on, and identify BMP as a signal involved in 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   There was no mechanics-derived evidence of endocardial dysfunction with hypoxia at sea level or hig
122 stimulation), but does not appear to reflect endocardial dysfunction.
123                                  Endothelial/endocardial (EC) Raf1(L613V) causes cardiac hypertrophy
124     Additionally, the usefulness of unipolar endocardial electroanatomic mapping to identify epicardi
125                                              Endocardial electrogram amplitude correlated significant
126 tected by fragmentation/fractionation of the endocardial electrograms and by 3-dimensional anatomic l
127        High-density bipolar left ventricular endocardial electrograms were collected using CARTO3v4 i
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 rd potassium current (Ito) in EPI but not in endocardial (ENDO) cardiomyocytes of UNx rats led to a d
131 LNA) protein is expressed, in particular, in endocardial endothelia during fetal valve morphogenesis
132 ascular endothelium are molecularly similar, endocardial endothelial cells exhibit a distinct plastic
133 othelial to mesenchymal transition involving endocardial endothelial cells is caused by dysregulated
134 lly described in heart development where the endocardial endothelial cells that line the atrioventric
135 genic cells within EFE tissue originate from endocardial endothelial cells via aberrant endothelial t
136  ICM VTs, the isthmus could be identified by endocardial entrainment in 55 (62%), compared with only
137       Our aim was to compare the efficacy of endocardial+epicardial ablation versus only endocardial
138                     In 2 other BrS patients, endocardial, epicardial RV (CARTO), and body surface map
139                                   A combined endocardial-epicardial ablation approach for initial VT
140  had epicardial-only ablation, whereas 3 had endocardial-epicardial ablation.
141  required in symptomatic cases refractory to endocardial-epicardial approach.
142                                              Endocardial-epicardial dissociation and focal breakthrou
143                                   We defined endocardial-epicardial dissociation as phase difference
144 n persistent AF recordings shows significant Endocardial-epicardial dissociation marked temporal hete
145                                              Endocardial-epicardial dissociation was seen in 50.3% of
146                                      Of 6889 endocardial-epicardial mapping point pairs, 547 (8%) pai
147  (50+/-14 years; 79% men) underwent combined endocardial-epicardial right ventricular electroanatomic
148 nder antiarrhythmic drugs after unsuccessful endocardial/epicardial ablation.
149 efore ablation, VT was inducible in 75%, and endocardial/epicardial LAVA were present in 88%/75%.
150                                              Endocardial fibroelastosis (EFE) is a unique form of fib
151             Secondary outcomes included mild endocardial fibroelastosis (n = 1) and cutaneous neonata
152 cy, and secondary outcomes included isolated endocardial fibroelastosis, 1 degrees CHB at birth and s
153 ity of endothelial cells and near regions of endocardial fibrosis/disruption.
154 ine pigs underwent closed-chest placement of endocardial fiducial markers, computed tomography, and p
155                                              Endocardial flowers are contiguous with coronary vessels
156                                     Finally, endocardial flowers exhibit angiogenic features, includi
157 se previously undescribed structures, termed endocardial flowers, have a distinct endothelial phenoty
158                                        A low endocardial fraction shortening (eFS) was present in 17%
159 iest ventricular activation and discriminate endocardial from epicardial origin of activation with cl
160 logy and provide a rationale for considering endocardial function in regenerative strategies.
161 novo HLHS mutations associated with abnormal endocardial gene and fibronectin regulation.
162 re, we investigated how TBX20 interacts with endocardial gene networks to drive the mesenchymal and m
163 ver, when cardiac function is disrupted, OFT endocardial growth ceases, accompanied by reduced prolif
164                           Here, we show that endocardial hematopoiesis is critical for cardiac valve
165 tissue interactions involved in establishing endocardial identity are poorly understood.
166 ned lesion known as Quilty effect or nodular endocardial infiltrates.
167 ned lesion known as Quilty effect or nodular endocardial infiltrates.
168                    Percutaneous delivery via endocardial injection was investigated with fluoroscopic
169 ERF ablation is a promising new approach for endocardial intramural and full thickness ablation of ve
170                                              Endocardial Jag1 removal blocks SV capillary sprouting,
171 c valve, and septal defects, indicating that endocardial Jag1 to Notch1 signaling is required for pos
172                                 Mice lacking endocardial Jag1, Notch1, or RBPJ displayed enlarged val
173                                              Endocardial Klf2 deficiency results in defective valve f
174                              Upregulation of endocardial Kruppel-like factor 2 in Adamts19 knockout m
175 eflectance of the cardiac muscle beneath the endocardial layer.
176 in showed a similar trend from epicardial to endocardial layers (epiwall: -16.0 +/- 2.9%; midwall: -1
177 egarding the safety of DCCV in patients with endocardial left atrial appendage occlusion (LAAO) devic
178  as multisite pacing, His bundle pacing, and endocardial left ventricular pacing.
179 -like tube, from which it is separated by an endocardial-like layer.
180 erence between linear (n=22) and focal (n=7) endocardial line length or volume.
181 ), we identified accessible chromatin within endocardial lineages and intersected these data with TBX
182 ides insight into the chromatin landscape of endocardial lineages during septation.
183 n enhancer drove reporter gene expression in endocardial lineages in a TBX20-binding site-dependent m
184        Selective ablation of Tbx20 in murine endocardial lineages reduced the expression of extracell
185                                              Endocardial LP abolition was associated with reduced VT
186              The most common indications for endocardial LV pacing were difficult CS anatomy (n =12),
187 s with CC undergoing detailed epicardial and endocardial LV tachycardia mapping and ablation were inc
188 from the coronary venous system and multiple endocardial LV/right ventricular sites.
189  and more similar to those of the idiopathic endocardial LVOT VAs than those of the idiopathic epicar
190 sional interactions provide insight into why endocardial mapping alone may not fully characterize the
191 ogram thresholds for IMAT delineation during endocardial mapping and to describe the use of endocardi
192 docardial mapping and to describe the use of endocardial mapping for delineation of IMAT dense region
193 e (16 patients and 58 VTs), left ventricular endocardial mapping was performed in sinus rhythm.
194 ions of myocardium reliably identified using endocardial mapping with thresholds of <3.7 and <0.6 mV,
195 ents (23.8%) underwent a successful repeated endocardial mapping, and ablation after epicardial mappi
196 h comparable efficacy to currently available endocardial-mapping techniques but with 2 times higher a
197 docardial voltage signals and 314 epicardial/endocardial matched pairs of points were analyzed.
198 ntricular canal undergo an EndMT to form the endocardial mesenchymal cushion that later gives rise to
199                             Deployment of an endocardial mitral isthmus line (MIL) with the end point
200 ysiological signals (for example, for active endocardial monitoring).
201  indicate that the myocardium is crucial for endocardial morphogenesis and differentiation, and ident
202 st for a potential role of the myocardium in endocardial morphogenesis, we used two different zebrafi
203 d universal increment from the epicardial to endocardial myocardial wall (epiwall: -15.4 +/- 1.9%; mi
204 lts in trunk vessel deficiencies, disordered endocardial-myocardial contact and impaired heart functi
205 ur findings provide novel insight into early endocardial-myocardial interactions that can be explored
206 0.69; P<0.001) with readings obtained in the endocardial myocardium performing better than those in t
207  Heat-shock-induced bmp2b expression rescued endocardial nfatc1 expression in hand2 mutants and in my
208 for apoptosis, which resulted in the loss of endocardial nfatc1 expression.
209                              Region-specific endocardial Notch activity regulates heart morphogenesis
210    Although previous studies have shown that endocardial Notch signalling non-cell-autonomously promo
211 a RBPJ-binding site, identifying Hbegf as an endocardial Notch target.
212                  Thirteen patients underwent endocardial-only ablation, 2 had epicardial-only ablatio
213 ecurrent VT or persistent inducibility after endocardial-only ablation.
214 cedure duration and help choosing between an endocardial or epicardial approach.
215 ium where it is inaccessible to conventional endocardial or epicardial approaches.
216 ablation catheter safely delivers contiguous endocardial or epicardial lesions without gaps in a sing
217 tricular activation and best pace map on the endocardial or epicardial side.
218 bxiphoid approach can be an alternative when endocardial or epicardial transvenous mapping has failed
219 approach is an alternative when conventional endocardial or transvenous epicardial ablation fails in
220 ice alternatives that require intravascular, endocardial, or epicardial contact.
221 hteen goats were instrumented with an atrial endocardial pacemaker lead and a burst pacemaker.
222                                              Endocardial pacemaker leads and right ventricular (RV) p
223 py (CRT) delivered via left ventricular (LV) endocardial pacing (ENDO-CRT) is associated with improve
224 entional CRT underwent implantation of an LV endocardial pacing electrode and a subcutaneous pulse ge
225  pacing via a wireless left ventricular (LV) endocardial pacing electrode.
226  model and offers a potential alternative to endocardial pacing leads.
227 nized LV pacing, multisite LV pacing, and LV endocardial pacing offer promise as novel pacing options
228 acy was estimated using 552 left ventricular endocardial pacing sites pooled together and 25 VT-exit
229 0.495 muJ, which is higher than the required endocardial pacing threshold energy (0.377 muJ).
230 ced ATs and increased synchrony arising from endocardial pacing.
231 stages of myocardial differentiation rely on endocardial paracrine signaling mediated in part by Bmp2
232 docardial cell proliferation and stabilizing endocardial patterning.
233                                              Endocardial perfusion parameters obtained by semiautomat
234                               The effects of endocardial PFA and RFA on the phrenic nerve were also c
235  the scientific basis for the first-in-human endocardial PFA studies.
236 singularities between the epicardial and the endocardial planes was significantly >0 with a median di
237                                              Endocardial plus adjuvant EPI ablation was performed in
238 Here, we identify a developmentally impaired endocardial population in HLHS through single-cell RNA p
239   However, the precise identification of the endocardial precursors and the mechanisms they require f
240       Because they do not depend on ELA-APJ, endocardial progenitors are able to expand and compensat
241                We show that in hand2 mutants endocardial progenitors migrate to the midline but fail
242 o pathway transcriptional regulator Yap1 and endocardial proliferation.
243 nhanced open chromatin states at endothelial/endocardial promoters.
244 ovides therapeutic vagal denervation through endocardial radiofrequency ablation for these cases.
245 Sustained obesity results in global biatrial endocardial remodeling characterized by LA enlargement,
246            (NaviStar ThermoCool Catheter for Endocardial RF Ablation in Patients With Ventricular Tac
247 rS-ECG with data from various epicardial and endocardial right ventricular activation mapping procedu
248 decremental preexcitation of the RVOT before endocardial RV mapping.
249  mapping demonstrated larger epicardial than endocardial scar and core-dense (</=0.5 mV) scar areas (
250 e relationship between calcifications within endocardial scar and VTs is unclear.
251       There was a linear correlation between endocardial scar area (<1.5 mV) and filtered QRS (r=0.41
252 ate the signal-averaged ECG (SAECG) with the endocardial scar characteristics in patients with ischem
253 ematic characterization of the LV epicardial/endocardial scar distribution and density in CC has not
254                                              Endocardial scar extension and density predict scar tran
255 ding of the confounding influence of IMAT on endocardial scar mapping.
256 nt correlation between the surface SAECG and endocardial scar size in patients with ischemic VTs.
257 lay and exceeded the region of corresponding endocardial scar.
258 erformed on the epicardial side in 9 VAs and endocardial side in 5 VAs.
259 ation of a lead at the left ventricular (LV) endocardial side of the interventricular septum, referre
260  sites anatomically opposite to the earliest endocardial site of activation under direct intracardiac
261 al epicardial electrograms had corresponding endocardial sites with BV <1.50 mV, and the remaining co
262 ries and a remote approach from the adjacent endocardial sites.
263 lated from the great cardiac vein and remote endocardial sites.
264                           Regions of maximal endocardial slowing during SR corresponded to the VT ist
265                           An upregulation of endocardial SOX17 accompanied compensation in Apj mutant
266 t tubes and genetic lineage tracing with the endocardial specific Nfatc1-Cre mouse revealed that hemo
267      To test this, we generated an in vitro, endocardial-specific ablation model using the diphtheria
268 mesenchymal cells, a phenotype reproduced by endocardial-specific loss of Wnt9b.
269 ventricular tachycardia, >10% increase in RV endocardial surface area of bipolar voltage consistent w
270                                     The mean endocardial surface area of these potentials was 18+/-4%
271 s derived from manually drawn epicardial and endocardial surface contours.
272 tion were driven by rapid activations on the endocardial surface that blocked and broke up transmural
273 n of a native or prosthetic heart valve, the endocardial surface, or an indwelling cardiac device.
274 al strain was measured at the epicardial and endocardial surfaces; their difference yielded the circu
275 ut our understanding of the contributions of endocardial TBX20 to heart development remains incomplet
276 ct that patients with viable fast-conducting endocardial tissue or distal Purkinje network or both, a
277 f discordance between the epicardial and the endocardial tissue.
278 ked and broke up transmurally, leading to an endocardial to epicardial activation rate gradient as LD
279 r beta-catenin are proposed to contribute to endocardial-to-mesenchymal transformation (EMT) through
280 1 (5.5-9 weeks) were detected, indicative of endocardial-to-mesenchymal transformation (EndMT) in val
281                                          Low endocardial unipolar voltage (UV) at sites with normal b
282                                              Endocardial unipolar voltage mapping serves to character
283                                          The endocardial unipolar voltage value (with a newly propose
284 ing could be identified by corresponding low endocardial UV <3.7 mV.
285 th low endocardial BV, the additional use of endocardial UV at normal BV sites improves the diagnosti
286 es with endocardial BV >1.50 mV, the optimal endocardial UV cutoff for identification of epicardial B
287 ion of epicardial right ventricular scar, an endocardial UV cutoff value of 3.9 mV is more accurate t
288                   This study aimed to define endocardial UV cutoff values using computed tomography-d
289 signaling and intra-ventricular sprouting by endocardial Vegfa signaling.
290 n=5) during sinus rhythm, and epicardial and endocardial ventricular pacing (65 records in total).
291 nd chronic hypoxia and (2) elucidate whether endocardial versus epicardial mechanics respond differen
292 pproach from the anatomically opposite side (endocardial versus epicardial or above versus below the
293  (CMR) signal intensity and left atrial (LA) endocardial voltage after LA ablation.
294 ity was associated with reduced posterior LA endocardial voltage and infiltration of contiguous poste
295 e group (p < 0.001), consistent with reduced endocardial voltage in this region.
296                                        Sixty endocardial voltage maps (360+/-147 points) were perform
297 went 2 detailed sinus rhythm electroanatomic endocardial voltage maps (average 385+/-177 points per m
298                                              Endocardial voltage maps showed myocardial scar in 19 pa
299          A total of 8494 epicardial and 6331 endocardial voltage signals and 314 epicardial/endocardi
300 ping-guided endomyocardial biopsy showed low endocardial voltages and fibro-fatty replacement in area
301                       Bipolar epicardial and endocardial voltages within scar were low (0.4 [0.2-0.55

 
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