ライフサイエンスコーパス: VT

1 VT activation mappings using the GMC were performed in 4

2 VT carriage prevalence half-life is similar among PCV-va

3 VT circuits were complex with 41.7% exhibiting discontin

4 VT episodes or PVC burden were reduced in 17/18 evaluabl

5 VT occurred in 3 (1.2%) patients, including 1 (0.4%) wit

6 VT recurred in 5 patients (15%) in whom the ICD-electrog

7 VT recurrences were documented in 25 patients (20%) by 1

8 VT required cardioversion in 2 patients and new implanta

9 VT-1161 (otesaconazole) is an oral agent with increased

10 All 14 VT channel/exit sites (0.88 +/- 0.74 mV) were localized

11 were included in VT diastolic pathway in 17 VTs, the other 6 VTs showed mismatching of them.

12 Results Fifty-six paced maps and 23 VT circuits were mapped in 22 patients.

13 ocardial pacing sites pooled together and 25 VT-exit sites identified by contact mapping.

14 For the 25 VT-exit sites, localization error of the population-base

15 bolished at least 1 inducible VT in 19 of 26 VT patients (73%), and suppressed ambient arrhythmia in

16 A total of 29 VTs were available for comparison.

17 mappings using the GMC were performed in 40 VTs, visualizing the full diastolic pathway in 22 (55%)

18 VT diastolic pathway in 17 VTs, the other 6 VTs showed mismatching of them.

19 Ps were present in 60% of the patients and a VT was either inducible or sustained/incessant in 85% of

20 patients had a cardiac CT performed before a VT ablation procedure.

21 Of these, 70.8% were from a VT background.

22 s with NICM (523 procedures) who underwent a VT ablation from 2010 to 2016 were included.

23 int for a successful long-term outcome after VT ablation.

24 Significant effectiveness against VT IPD in infants was observed, although the impact on n

25 duced ventricular fibrillation/VT (29%), and VT could not be induced in 2 patients (9%).

26 We investigated whether LP abolition and VT noninducibilty have a similar impact on the outcomes

27 nalysis, the combination of LP abolition and VT noninducibilty was independently associated with free

28 T ablation, the strategy of LP abolition and VT noninducibilty were associated with better outcomes i

29 olition was achieved in 79% of the cases and VT noninducibility in 80%.

30 11%; p < 0.001) and polymorphic VA (NSVT and VT: 19% vs. 2%; p = 0.002; premature ventricular complex

31 s reveal different electronic structures and VT behavior for the four cobalt complexes; one-step one-

32 he D-VTd group (3.8 [95% CI 1.6 to 6.0]) and VTd group (2.9 [0.7 to 5.1]; p=0.43), or from baseline t

33 D-VTd and VTd were associated with on-treatment health-related qua

34 n calcifications within endocardial scar and VTs is unclear.

35 ished patients with calcification-associated VT from patients without calcification-associated VTs (a

36 om patients without calcification-associated VTs (area under the curve, 0.87; sensitivity, 0.87; spec

37 Eyes with DME had larger AVC, VT, FAZ-A, and FAZ-CI and lower VD than those in the con

38 was to assess the effect of substrate-based VT ablation targeting local abnormal ventricular activit

39 The BERLIN VT study (Preventive Ablation of Ventricular Tachycardia

40 icular ejection fraction, 30+/-10%) had both VT and VF and met inclusion criteria.

41 ced Parkinson's disease, loss of 11C-BU99008 VT in the frontal (r = 0.79; P = 0.001), temporal (r = 0

42 The greatest 11C-BU99008 VT increase in patients with early Parkinson's disease w

43 tively enrolled in the University of Chicago VT Ablation Registry between 2016 and 2018.

44 ing of the diastolic pathway of the clinical VT was achieved in 24/85 (28.2%) patients.

45 ing of the diastolic pathway of the clinical VT was feasible in 25/85 patients (29.4%).

46 Clinical VTs and computed tomography-defined target volume areas

47 s possible in all 13 with inducible clinical VTs.

48 argeted documented but noninducible clinical VTs based on stored implantable cardioverter-defibrillat

49 he second 33 patients, noninducible clinical VTs were also targeted by pace-mapping based on stored I

50 The lack of inducibility of clinical VTs during ablation procedures remains problematic and m

51 The clinical VTs were inducible in 13 patients (62%), whereas 6 patie

52 serotypes 3, 6A and 19F were the most common VT and non-typeable isolates, the most common NVT.

53 In conclusion, VT after inhibition of antithrombin and protein C is dep

54 ients with cardiogenic shock and concomitant VT refractory to antiarrhythmic drugs on mechanical supp

55 D-VTd and VTd were associated with on-treatment health-rel

56 tients were enrolled and randomly assigned D-VTd (n=543) or VTd (n=542).

57 ortezomib, thalidomide, and dexamethasone (D-VTd) significantly improved rates of stringent complete

58 post-consolidation between the two groups (D-VTd group, 9.7 (95% CI 7.4 to 11.9) vs VTd group, 8.7 (6

59 t-induction were not different between the D-VTd group (3.8 [95% CI 1.6 to 6.0]) and VTd group (2.9 [

60 an sites and were randomly assigned to the D-VTd group (n=543) or the VTd group (n=542).

61 antation, 157 (29%) of 543 patients in the D-VTd group and 110 (20%) of 542 patients in the VTd group

62 211 (39%) patients in the D-VTd group versus 141 (26%) in the VTd group achieved a c

63 pain (-23.3 [95% CI -26.6 to -20.0] in the D-VTd group vs -19.7 [-23.0 to -16.3] in the VTd group; p=

64 high at baseline (511 [94%] of 543 in the D-VTd group vs 510 [94%] of 542 in the VTd group).

65 le myeloma were randomly assigned (1:1) to D-VTd or VTd.

66 lement the clinical benefits observed with D-VTd versus VTd, and support the addition of daratumumab

67 o 0.9] vs 1.8 [-2.4 to 6.0]; p=0.025) with D-VTd versus VTd.

68 This study sought to describe VT ablation results and identify factors associated with

69 bortezomib, thalidomide, and dexamethasone (VTd) in patients with newly diagnosed multiple myeloma.

70 Design flexibility for dinuclear VT complexes confers an advantage over two-step spin cro

71 fraction between 30% and 50%, and documented VT were randomly assigned 1:1 to a preventive or deferre

72 d VT ablation guidance designed to eliminate VT inducibility following initial ablation.

73 Fast VT was defined as TCL <333 milliseconds (rate >180 bpm).

74 iseconds (306-443 milliseconds), and 24 fast VTs were characterized.

75 e. ventricular tachycardia and fibrillation (VT, VF)) on admission at one institution were included (

76 contraction-induced ventricular fibrillation/VT (29%), and VT could not be induced in 2 patients (9%)

77 Nineteen patients were enrolled (17 for VT, 2 for PVC cardiomyopathy).

78 h a decrease of 36.3% (95% CI 23.8-46.9) for VT IPD and an increase of 101.4% (95% CI 62.0-145.4) for

79 Patients were prospectively followed for VT recurrence and mortality.

80 cium exchanger as predominant phenotypes for VT/VF.

81 oblematic and may be in part responsible for VT recurrences.

82 tudies, histological findings after SBRT for VT are unknown.

83 sms of acute cellular injury during SBRT for VT, which may have an antiarrhythmic effect before the o

84 e ICD implantation to prevent ICD shocks for VT) and deferred ablation after 3 ICD shocks for VT.

85 and deferred ablation after 3 ICD shocks for VT.

86 Ventricular scar, the key substrate for VT, can be noninvasively defined with late gadolinium en

87 d may represent a potential novel target for VT ablation.

88 Fifty-four VTs with complete circuit delineation (>90% TCL) by high

89 ay was associated with a higher freedom from VT recurrence as compared with partial diastolic pathway

90 At a mean of 12.8 months, freedom from VT recurrence was 67% in the overall cohort.

91 At a mean of 12.8 months, freedom from VT recurrence was 88%, 50%, and 55% in patients who had

92 pendently associated with free survival from VT (hazard ratio, 0.45 [95% CI, 0.29-0.69], P=0.0002) an

93 nar chirality has been obtained through (1)H VT NMR studies and by addition of Pirkle's reagent.

94 However, VT recurrence can occur despite extensive ablation proce

95 erved within the reentrant path during human VT, the dimensions of the circuit were not predictive of

96 nalyze the determinants of the rate of human VT with comparison of circuit dimensions and conduction

97 isthmus could be identified in 56 (63%) ICM VTs and 12 (26%) NICM VTs ( P<0.01), whereas any critica

98 or exit) could be identified in 76 (85%) ICM VTs and 37 (79%) NICM VTs ( P=0.3).

99 Of 89 ICM VTs, the isthmus could be identified by endocardial entr

100 error of 7.2+/-4.1 mm for the 25 identified VT-exit sites.

101 es of mortality, defibrillator implantation, VT ablation (adjusted HR: 4.68; 95% CI: 2.45 to 8.92; p

102 PD alternans was greater (by 80%, P<0.05) in VT/VF(+) versus VT/VF(-) STIM1-KD hearts.

103 troduce a macroscopic polarization change in VT compounds.

104 zation schedule, there have been declines in VT pneumococcal colonization and disease in children age

105 latest late potential areas were included in VT diastolic pathway in 17 VTs, the other 6 VTs showed m

106 Despite evidence of reduction in VT carriage over the study period, there is high persist

107 rom a total of 686 patients with an incident VT ablation procedure targeting LAVAs, 21 patients (age,

108 nFAT substrate noninducible to VT, including VTs that arise postablation, were determined.

109 electron partial VT, two-step VT, incomplete VT, and temperature-invariant {Co(III)-cat-cat-Co(III)}

110 ances (median, 8%), the microarray increased VT detection by 31.5% over that by latex serotyping.

111 Sotalol significantly increased VT recurrence and ICD shocks compared with amiodarone.

112 digital-heart technology for individualized VT ablation guidance designed to eliminate VT inducibili

113 2 emulated clinical procedure with 2 induced VTs, the site of origin localization system achieved acc

114 echnology evaluated the rapid-pacing-induced VTs in each personalized inFAT-based substrate.

115 Inducible VT predicts mortality.

116 ent, ablation abolished at least 1 inducible VT in 19 of 26 VT patients (73%), and suppressed ambient

117 toffs for ruling-out and ruling-in inducible VT, RV LGE >10 cm(3) was 100% sensitive and >36 cm(3) wa

118 e-VT animals: 35 +/- 14 mm vs. non-inducible VT animal: 9.94 mm).

119 Univariable predictors of inducible VT included increased RV LGE (odds ratio [OR], 1.15; P=0

120 and 81% specificity for predicting inducible VT (area under the curve, 0.81; P<0.001).

121 ) was 100% specific for predicting inducible VT.

122 onance but whether this relates to inducible VT is unknown.

123 n is independently associated with inducible VT and may help refine patient selection for programmed

124 In case of inducible VTs, the GMC was used to create the VT activation maps f

125 33 patients (control group), only inducible VTs were targeted, and in the second 33 patients, nonind

126 han those detected in animals with inducible VTs (inducible-VT animals: 35 +/- 14 mm vs. non-inducibl

127 ted in animals with inducible VTs (inducible-VT animals: 35 +/- 14 mm vs. non-inducible VT animal: 9.

128 w insights for understanding the macro-level VT mechanism.

129 nt demonstrates that CardioInsight localizes VT circuits with sufficient accuracy to provide a region

130 tients with sepsis had a significantly lower VT (sepsis, 9.5 [7.8-11.9]; no sepsis, 11.8 [10.5-13.8]

131 ECGI mapped VT sites of origin onto the correct AHA segment with hig

132 quartile range); male 87%] achieved a median VT of 11.7 (9.7-13.4) mL.kg.min.

133 ified include CC5-MRSA-V (edinA+), CC5-MRSA-[VT + fusC], CC5-MRSA-IVa (tst1+), CC5-MRSA-[V/VT + cas +

134 (62%), compared with only 8 of 47 (17%) NICM VTs ( P<0.01).

135 tified in 56 (63%) ICM VTs and 12 (26%) NICM VTs ( P<0.01), whereas any critical component (defined a

136 tified in 76 (85%) ICM VTs and 37 (79%) NICM VTs ( P=0.3).

137 In contrast, among mappable NICM VTs, although some critical component can typically be i

138 No VT episodes were found after redo ablation was performed

139 crease of 101.4% (95% CI 62.0-145.4) for non-VT IPD.

140 s (OR, 3.5; P=0.02), history of nonsustained VT (OR, 3.5; P=0.02), and previous clinical sustained VT

141 During catheter ablation of VT, simultaneous mapping was performed using electroanat

142 The primary study endpoint was assessment of VT recurrences by 12-month follow-up.

143 ed phase mapping during the initial beats of VT/VF identified one or more rotors that were localized

144 Clearance of VT serotypes was consistent across different genetic bac

145 adults with treatment-refractory episodes of VT or cardiomyopathy related to premature ventricular co

146 ssue factor reduced the clinical features of VT, the coagulopathy in the head, and fibrin deposition

147 nsions of the circuit were not predictive of VT cycle length.

148 analysis, AM stage was the only predictor of VT recurrences by 12 months (hazard ratio: 9.5; 95% conf

149 Predictors of VT recurrences were retrospectively identified.

150 pharmacological option for the prevention of VT development.

151 ding has been associated with a high rate of VT termination during radiofrequency ablation as well as

152 is the principal determinant of the rate of VT.

153 r tachycardia (VT) reduces the recurrence of VT in patients with implantable cardioverter-defibrillat

154 Recurrences of VT were defined as appropriate implantable cardioverter

155 l study evaluated the efficacy and safety of VT-1161 versus fluconazole in subjects with moderate-to-

156 The median TCL of VT was 365 milliseconds (306-443 milliseconds), and 24 f

157 imensions, confirmed by rapid termination of VT during radiofrequency delivery.

158 The appropriate timing of VT ablation and its effects on mortality and heart failu

159 patient-specific proarrhythmic substrate of VTs and therapeutic planning.

160 er, the role of diastolic pathway mapping on VT recurrence has yet to be clearly elucidated.

161 lete diastolic pathway activation mapping on VT recurrence.

162 The incidence of CHB or VT presenting after 72 hours post-ASA was low.

163 ergoing premature ventricular contraction or VT ablation.

164 Only in PM patients with NSVT or VT, the dominant morphology (right-bundle branch block w

165 olled and randomly assigned D-VTd (n=543) or VTd (n=542).

166 oma were randomly assigned (1:1) to D-VTd or VTd.

167 alt complexes; one-step one-electron partial VT, two-step VT, incomplete VT, and temperature-invarian

168 The decrease in PCV13 VT that has occurred since the introduction of PCV13 app

169 We estimated the prevalence of PCV13 VT and NVT by age and compared these to earlier surveys

170 The prevalence of PCV13 VT carriage decreased during the 10 years between CSS0 a

171 Arrhythmic storm with recurrent polymorphic VT in patients with coronary disease responds to quinidi

172 ospective study of patients with polymorphic VT related to coronary artery disease, but without evide

173 ites in >1/3 of patients with postinfarction VT.

174 regional heterogeneities in the postischemic VT substrate not appreciated by any single modality alon

175 computed tomography to noninvasively predict VT ablation targets and assesses the capability of the t

176 DIFAT also predicted VTs targeted in redo procedures years later.

177 In CSS3, the most prevalent VTs were 7F in infants and 3 in mothers, and the most pr

178 Preventive VT ablation before ICD implantation did not reduce morta

179 antation, we compared outcomes of preventive VT ablation (undertaken before ICD implantation to preve

180 help refine patient selection for programmed VT-stimulation when applied to an at least intermediate

181 clinically scheduled for invasive programmed VT-stimulation were prospectively recruited for prior 3-

182 th: r=-0.3, P=0.047) and predictive of rapid VT termination by a single radiofrequency application (r

183 ode of VVC (n=55) were randomized to receive VT-1161 300 mg once daily (q.d.) for 3 days, 600 mg q.d.

184 ng AM, but is often of benefit for recurrent VT after the acute phase of myocarditis.

185 The primary outcome was recurrent VT.

186 ar tachycardia (VT) has been shown to reduce VT recurrence and decrease mortality.

187 ship between the dimensions of the reentrant VT circuit and tachycardia cycle length (TCL) has not be

188 3 remotes (67.8+/-17.0 mm from the reference VT-exit site), and then 5 close pacing sites, resulted i

189 all had multiple episodes of drug-refractory VTs.

190 Patients with scar-related VT were prospectively enrolled in the University of Chic

191 catheter ablation procedures of scar-related VT, site of origin localization accuracy was estimated u

192 ent 144 ablation procedures for scar-related VT.

193 high-income settings, there is high residual VT carriage 3.6-7.1 years after PCV introduction.

194 to fully understand dynamics of the residual VTs and replacement NVT serotypes post-PCV.

195 A trend toward worse SCD/VT/VF (p = 0.062) and DHF/HTx/VAD (p = 0.061) was found

196 By detecting additional vaccine serotype (VT) pneumococci carried at low relative abundances (medi

197 .2% (95% CI 26.7-46.1) for vaccine serotype (VT) pneumococci.

198 t Streptococcus pneumoniae vaccine-serotype (VT) carriage and transmission.

199 ned by the persistence of vaccine serotypes (VT) and the emergence of non-vaccine serotypes (NVT).

200 se (IPD) incidence due to vaccine serotypes (VT) has declined, partial replacement by non-vaccine ser

201 requency and diversity of vaccine serotypes (VTs) decreased significantly post-PCV, but no significan

202 to 179 beats/min) in 27%, and rarely severe (VT >=180 beats/min) in 9%.

203 her inhibitor, the triazole (S)-seviteronel (VT-464), with P450 17A1.

204 sthmus and path length between fast and slow VTs and between unstable and stable VTs.

205 he circuit was similar between fast and slow VTs and between unstable and stable VTs.

206 nce infrared Fourier transform spectroscopy (VT-DRIFTS) aided by ab initio plane wave density functio

207 Maps were generated for all stable VTs and with pacing from the atrium, right ventricular a

208 and slow VTs and between unstable and stable VTs.

209 and slow VTs and between unstable and stable VTs.

210 c parameters governing the one- and two-step VT behavior.

211 lear path to the next generation of two-step VT complexes through incorporation of mixed-valence clas

212 provide an avenue toward controlled two-step VT interconversions of the form {Co(III)-cat-cat-Co(III)

213 ; one-step one-electron partial VT, two-step VT, incomplete VT, and temperature-invariant {Co(III)-ca

214 were trained to 2 end points: (1) sustained VT/VF or (2) mortality at 3 years.

215 .5; P=0.02), and previous clinical sustained VT (OR, 12.8; P=0.003); only prior sustained VT (OR, 8.0

216 s yielded c-statistics of 0.90 for sustained VT/VF (95% CI, 0.76-1.00) and 0.91 for mortality (95% CI

217 The incidence and timing of CHB or sustained VT within 30 days post-ASA were assessed.

218 VT (OR, 12.8; P=0.003); only prior sustained VT (OR, 8.02; P=0.02) remained independent in bivariable

219 all cases, patients had recurrent sustained VT and had failed multiple antiarrhythmics and radiofreq

220 Here, we report on systematic VT and DOSY NMR studies, XRD analyses as well as DFT cal

221 block (CHB) and ventricular tachyarrhythmia (VT) after ASA to better understand when patients can be

222 carditis undergoing ventricular tachycardia (VT) ablation.

223 ie prematurely from ventricular tachycardia (VT) and sudden cardiac death.

224 mensional nature of ventricular tachycardia (VT) circuits.

225 Postinfarction ventricular tachycardia (VT) generally involves myocardial fibers surrounded by s

226 n of postinfarction ventricular tachycardia (VT) has been shown to reduce VT recurrence and decrease

227 ies for ablation of ventricular tachycardia (VT) have been described, but their impact on ventricular

228 quency ablation for ventricular tachycardia (VT) in patients with cardiogenic shock and concomitant V

229 atheter ablation of ventricular tachycardia (VT) in structural heart disease is challenging because o

230 atheter ablation of ventricular tachycardia (VT) in structurally abnormal hearts remains to be fully

231 omyopathy (ICM) and ventricular tachycardia (VT) is important for understanding the patient-specific

232 and postprocedural ventricular tachycardia (VT) noninducibility is known to be the desirable end poi

233 edure for sustained ventricular tachycardia (VT) or nonsustained VA with associated left ventricular

234 theter ablation for ventricular tachycardia (VT) reduces the recurrence of VT in patients with implan

235 c radioablation for ventricular tachycardia (VT) using stereotactic body radiation therapy, although

236 ilitate ablation of ventricular tachycardia (VT), an automated localization system to identify the si

237 cular fibrillation, ventricular tachycardia (VT), nonsustained ventricular tachycardia (NSVT), and Lo

238 In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location charact

239 ty to develop acute ventricular tachycardia (VT).

240 ment for refractory ventricular tachycardia (VT).

241 anatomic mapping in ventricular tachycardia (VT).

242 ost often moderate (ventricular tachycardia [VT]; 120 to 179 beats/min) in 27%, and rarely severe (VT

243 te for postinfarct ventricular tachycardias (VT) identifiable on contrast-enhanced computed tomograph

244 Fast ventricular tachycardias (VTs) have historically been attributed to shorter path l

245 ectrum of mappable ventricular tachycardias (VTs).

246 Valence tautomerism (VT) involves a reversible stimulated intramolecular elec

247 ch undergoes a two-step valence tautomerism (VT).

248 d with better outcomes in terms of long-term VT recurrences and cardiac survival.

249 Ablation lesions that terminated VTs were localized in areas of slow conduction on CV map

250 Poisson regression revealed that VT was a significant predictor for the number of septic

251 Our findings suggest that VT ablation should be avoided during AM, but is often of

252 The VT transition profile is rationalized by (1) the degree

253 ablation strategies were undertaken) and the VT noninducibilty.

254 nducible VTs, the GMC was used to create the VT activation maps focusing on the diastolic interval.

255 tion during ablation were used to define the VT site of origin (SoO).

256 with the change in dipole moments during the VT process.

257 s achieved therapeutic cure at Day 28 in the VT-1161 and fluconazole groups.

258 At 3 and 6 months, no subjects in the VT-1161 groups versus 28.5% and 46.1% of subjects in the

259 reentry and correlation to components of the VT circuit are unknown.

260 enefit of the LP abolition on preventing the VT recurrence in patients with ARVD and postmyocarditis

261 ation wavefront running perpendicular to the VT isthmus may increase sensitivity to detect arrhythmog

262 In addition, within the VT retina, i- and cRGC populations are born at distinct

263 s in the D-VTd group versus 141 (26%) in the VTd group achieved a complete response or better, and 34

264 d group and 110 (20%) of 542 patients in the VTd group in the intention-to-treat population had achie

265 n the D-VTd group vs 510 [94%] of 542 in the VTd group).

266 D-VTd group vs -19.7 [-23.0 to -16.3] in the VTd group; p=0.042), significantly smaller reductions in

267 y assigned to the D-VTd group (n=543) or the VTd group (n=542).

268 In the present study, we used this VT mouse model to investigate the involvement of tissue

269 ng diastolic activity may help predict those VTs employing intramural circuits and further optimize a

270 nfigurational lability was too high, through VT-HPLC analysis on the chiral stationary phase (DeltaG(

271 t render the inFAT substrate noninducible to VT, including VTs that arise postablation, were determin

272 Susceptibility to VT/VF (ventricular tachycardia/fibrillation) is difficul

273 likely related to enhanced susceptibility to VT/VF secondary to discordant APD alternans.

274 uated whether the addition of daratumumab to VTd before and after autologous stem-cell transplantatio

275 entrainment mapping of at least 1 tolerated VT was performed in 111 patients (ICM 71, NICM 40).

276 e total number of isolates and vaccine-type (VT) pneumococci decreased from PreVac to PostVac-II (n =

277 445 patients (ICM 228, NICM 217) undergoing VT ablation, detailed entrainment mapping of at least 1

278 We enrolled 6 patients with ICM undergoing VT ablation and 5 with structurally normal left ventricl

279 cutive patients with myocarditis, undergoing VT ablation.

280 In patients with NICM undergoing VT ablation, the strategy of LP abolition and VT nonindu

281 of patients with non-ICMs (NICM) undergoing VT ablation.

282 Patients undergoing VT ablation at our center were enrolled in a prospective

283 ghty-five consecutive patients who underwent VT ablation guided by high-density mapping were enrolled

284 fication of critical isthmuses in unmappable VTs.

285 Unstable VT was defined by hemodynamic deterioration with an intr

286 oss a wide range of both stable and unstable VTs delineated by high-resolution mapping.

287 V + fusC + tir], CC80-MRSA-IVa, CC121-MRSA-V/VT, CC152-MRSA-[V + fusC] (PVL+).

288 A-[V/VT + cas + fusC + ccrA/B-1], CC8-MRSA-V/VT, CC22-MRSA-[IV + fusC + ccrAA/(C)], CC45-MRSA-[IV + f

289 T + fusC], CC5-MRSA-IVa (tst1+), CC5-MRSA-[V/VT + cas + fusC + ccrA/B-1], CC8-MRSA-V/VT, CC22-MRSA-[I

290 greater (by 80%, P<0.05) in VT/VF(+) versus VT/VF(-) STIM1-KD hearts.

291 clinical benefits observed with D-VTd versus VTd, and support the addition of daratumumab to standard

292 .8 [-2.4 to 6.0]; p=0.025) with D-VTd versus VTd.

293 ps (D-VTd group, 9.7 (95% CI 7.4 to 11.9) vs VTd group, 8.7 (6.5 to 11.0; p=0.45).

294 nt calcification pattern was associated with VT target sites independent of calcification volume ( P=

295 Calcifications were associated with VT when compared with a control group.

296 ients (70%) in the postinfarction group with VT, compared with 6 of 56 patients (11%) in the control

297 eries describes outcomes for 5 patients with VT storm refractory to drug therapy treated with left st

298 technology by comparing its predictions with VT ablation procedure data from patients with ischemic c

299 patients (11%) in the control group without VT.

300 utive patients with prior infarction without VT who had cardiac CTs served as a control group.