ライフサイエンスコーパス: ventricular pacing

1 n the group assigned to dual-chamber minimal ventricular pacing.

2 ing, His bundle pacing, and endocardial left ventricular pacing.

3 nd mechanical asynchrony in any patient with ventricular pacing.

4 ositioned across the valve ring during rapid ventricular pacing.

5 y frequent following temporary cessations of ventricular pacing.

6 Programming minimized ventricular pacing.

7 ormal pump function and in case of part-time ventricular pacing.

8 of TG and NTG rabbits was subjected to rapid ventricular pacing.

9 rimposed heart failure (HF) induced by rapid ventricular pacing.

10 CHF was produced in 2 groups of dogs by ventricular pacing.

11 duced AF were studied one week after ceasing ventricular pacing.

12 troke or improve survival when compared with ventricular pacing.

13 ol, n=5) and with HF (n=8) produced by rapid ventricular pacing.

14 es heart failure symptoms when compared with ventricular pacing.

15 We induced CHF in nine dogs by rapid ventricular pacing.

16 ers significant improvement as compared with ventricular pacing.

17 ase in the quality of life, as compared with ventricular pacing.

18 prove stroke-free survival, as compared with ventricular pacing.

19 ntricular apex were measured on cessation of ventricular pacing.

20 velopment of the dilated myopathy induced by ventricular pacing.

21 5% confidence interval, 0-3) required rescue ventricular pacing.

22 experimental heart failure produced by rapid ventricular pacing.

23 ents who had guideline-based indications for ventricular pacing.

24 ase of a normal action potential produced by ventricular pacing.

25 al status with dual-chamber pacing than with ventricular pacing.

26 alters the characteristics of IC neurons to ventricular pacing.

27 entricle in conditions of AV block and right ventricular pacing.

28 ntrol and AV junction ablation and permanent ventricular pacing.

29 other group underwent a period of rapid left ventricular pacing.

30 vascular resistance than does single-chamber ventricular pacing.

31 deteriorated LVEF requiring a high burden of ventricular pacing.

32 as a safe and effective alternative to right ventricular pacing.

33 arkedly decreased conduction velocity during ventricular pacing.

34 with RVAP in the setting of a high burden of ventricular pacing.

35 biventricular pacing and conventional right ventricular pacing.

36 x were obtained during all ectopic beats and ventricular pacing.

37 on fraction </=50% to biventricular or right ventricular pacing.

38 Three devices (0.3%) were replaced for right ventricular pacing.

39 tients who required permanent single-chamber ventricular pacing.

40 no systematic reverse remodeling with right ventricular pacing.

41 mal) and after induction of HF by rapid left ventricular pacing.

42 HCC at rest, but in only the HCW group under ventricular pacing.

43 ects exhibited cardiac memory in response to ventricular pacing.

44 0 ms in the absence of a documented need for ventricular pacing.

45 nd during delivery of biventricular and left ventricular pacing.

46 n, and was likely equivalent to, backup-only ventricular pacing.

47 5 versus 18.4+/-11.0 cm(2), P<0.001) or left ventricular pacing (12.3+/-10.5 versus 17.1+/-10.7 cm(2)

48 Stroke volume was altered by right ventricular pacing (160, 210, 260, and 305 beats/min).

49 vs. 19%, p < 0.012, OR 1.57) and to require ventricular pacing (18% vs. 11%, p = 0.006, OR 1.73).

50 Rapid ventricular pacing (180 to 230 bpm) was subsequently ini

51 anterior descending artery followed by right ventricular pacing (240 ppm) for 3 weeks to produce hear

52 Multiple extrasystoles were induced by right ventricular pacing (25% of heart beats).

53 However, 53 patients assigned to ventricular pacing (26 percent) were crossed over to dua

54 during NTP (-4.7+/-1.4 U/mm Hg) than during ventricular pacing (-3.4+/-1.1 U/mm Hg).

55 5 versus 27.6+/-16.3 cm(2), P=0.003) or left ventricular pacing (31.7+/-18.5 versus 27.0+/-19.2 cm(2)

56 raventricular conduction defect 5, and right ventricular pacing 5) referred for CRT in addition to LV

57 nd the decline was greater with AV than with ventricular pacing (60 beats/min -40 +/- 11% vs. -17 +/-

58 sinus rhythm, and epicardial and endocardial ventricular pacing (65 records in total).

59 After 1 month of left ventricular pacing, 8 mongrel dogs were monitored for he

60 on to dual-chamber pacing (1014 patients) or ventricular pacing (996 patients) and followed them for

61 mal activation sequence resulting from right ventricular pacing accounts for only part of the reducti

62 Asynchronous ventricular pacing, after the Fontan procedure, has acut

63 At 4 and 8 weeks of ventricular pacing, all LA strains were decreased and LA

64 observed in the control dogs that underwent ventricular pacing alone (n = 4) did not change.

65 Long-term right ventricular pacing alone does not appear to be associate

66 e parameters showed little change with right ventricular pacing alone, indicating no systematic rever

67 Right ventricular pacing also impaired hemodynamics and LV fun

68 Right ventricular pacing alters the ventricular activation seq

69 in the pattern of atrial activation between ventricular pacing and AVNRT in only 21 of 46 patients.

70 ned the short-term effects of single-chamber ventricular pacing and dual-chamber atrioventricular (AV

71 -blind, randomized, controlled comparison of ventricular pacing and dual-chamber pacing in 407 patien

72 art failure induced by 3 to 4 weeks of rapid ventricular pacing and from 16 nonpaced control dogs did

73 ctivation was recorded in 17 patients during ventricular pacing and in 26 patients during AVNRT.

74 f the triangle of Koch in 38 patients during ventricular pacing and in 43 patients during AVNRT.

75 During right ventricular pacing and inferior right septal pacing, act

76 SCaE was reproducibly induced by rapid ventricular pacing and inhibited by 3 mumol/L of ryanodi

77 -term memory (STM) was induced by 2 hours of ventricular pacing and long-term memory (LTM) by ventric

78 ct, septum, and apex were mapped during left ventricular pacing and MES recorded.

79 HF was induced in sheep by rapid ventricular pacing and recovered following termination o

80 Frequent nonphysiological ventricular pacing and resultant pacing-induced cardiomy

81 collected using CARTO3v4 in sinus rhythm or ventricular pacing and reviewed for ripple mapping condu

82 f the paced wall during prolonged rapid left ventricular pacing and that regional stunning contribute

83 al has raised concerns of conventional right ventricular pacing and the risk of heart failure in a su

84 isk of developing HF in the setting of right ventricular pacing and to determine whether these patien

85 induced: ventricular fibrillation (by rapid ventricular pacing) and, after successful defibrillation

86 sodes associated with a device intervention (ventricular pacing), and (3) symptomatic episodes associ

87 focal activation initiated by right or left ventricular pacing, and (iv) atrial flutter.

88 tic root angiogram during breath-hold, rapid ventricular pacing, and injection of 32 mL contrast medi

89 orded in each dog during sinus rhythm, right ventricular pacing, and pacing of the right septum throu

90 ed with dual-chamber pacing as compared with ventricular pacing are observed principally in the subgr

91 amber (atrioventricular) and single-chamber (ventricular) pacing are alternative treatment approaches

92 lation in patients with dual-chamber minimal ventricular pacing as compared with those with conventio

93 Dual-chamber minimal ventricular pacing, as compared with conventional dual-c

94 ine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial

95 clusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial

96 The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial

97 Of those, 988 patients with <20% right ventricular pacing at 1 week were randomized to DDDR AVS

98 ons: (1) twice at baseline; (2) during right ventricular pacing at 110 bpm; (3) during intravenous in

99 Epicardial ventricular pacing at 130 bpm was achieved by use of a p

100 Mild CHF was produced by rapid ventricular pacing at 180 bpm for 10 days and severe CHF

101 sure) was measured at 3 specific conditions: ventricular pacing at 200 and 300 beats per minute, and

102 l of which underwent simultaneous atrial and ventricular pacing at 220 beats per minute for 14 days.

103 in 21 HF dogs (subjected to 3 weeks of rapid ventricular pacing at 240 beats per minute).

104 CHF was induced by continuous ventricular pacing at 320 to 340 bpm for 3 weeks.

105 PVCs and PVCs at 375 ms compared with rapid ventricular pacing at 400 ms (P<0.0001), whereas no diff

106 n 30 patients during simultaneous atrial and ventricular pacing at 500 ms with S(2) coupling interval

107 erquartile range, -2 to -19 ms) during right ventricular pacing at 6 months (P<0.05).

108 for 1 week, with atrioventricular block and ventricular pacing at 80 bpm); (2) congestive heart fail

109 In 6 hearts, measurements during ventricular pacing at a basic cycle length (BCL) of 120

110 activation during AVNRT (337 +/- 43 ms) and ventricular pacing at a similar cycle length (352 +/- 51

111 refractory period extension by shocks during ventricular pacing at fast rates predict that all tissue

112 the novel possibility that continuous right ventricular pacing at least partially suppresses pacemak

113 echocardiography, or atrioventricular versus ventricular pacing at the same rate.

114 All dogs underwent 8 weeks of high-rate ventricular pacing (at 220 beats per minute for the firs

115 rial pacing (at 70 beats/min) versus minimal ventricular pacing (at 40 beats/min) and followed up for

116 Twenty-nine (65.9%) patients had right ventricular pacing before CRT upgrade.

117 have provoked interest in the utilization of ventricular pacing beyond maintenance of heart rate.

118 d MRI was markedly dyssynchronous with right ventricular pacing but synchronous with right atrial pac

119 ociation functional class, and percent right ventricular pacing, but it was independent of gender and

120 ical benefit as compared with single-chamber ventricular pacing, but the supporting evidence is mainl

121 adiofrequency ablation (AVNA) with permanent ventricular pacing can be used to control rate in patien

122 Although right ventricular pacing can contribute to cardiomyopathy, the

123 Ventricular pacing can improve hemodynamics in heart fai

124 ents who demonstrated a </=0.5 V increase in ventricular pacing capture threshold (100% MRI vs. 98.8%

125 The primary efficacy endpoints were ventricular pacing capture threshold and ventricular sen

126 , between tip and ring electrodes of a right ventricular pacing catheter, and unipolar, from tip to a

127 iac pacing and was greater with AV than with ventricular pacing (change in mean blood pressure +/- SE

128 Contact maps during right ventricular pacing correlated closely to inverse solutio

129 tion predictors were VVIR cumulative percent ventricular pacing (Cum%VP) >80 (HR, 3.58; 95% CI, 1.72-

130 utcome, the interaction of QRS duration with ventricular pacing (DDDR-70) independently contributed t

131 mmed in a manner that promoted more frequent ventricular pacing (DDDR-70), there was a significant ad

132 fraction <35%, left atrial diameter >60 mm, ventricular pacing dependency, and previous ablation.

133 filtration rate, LVEF, atrial fibrillation, ventricular pacing, diabetes, cardiac resynchronization

134 udy was to determine whether the response to ventricular pacing during tachycardia is useful for diff

135 e aim of this research was to evaluate right ventricular pacing effects on left ventricular function.

136 hose without low risk access for transvenous ventricular pacing (eg, single ventricle physiology or E

137 Pacing permitted (S-L-S sequences without ventricular pacing) episodes accounted for 6.4% (DDD/R),

138 delineation and mapping efficiency of right ventricular pacing+ES (RVp+ES) and sensed ES pacing stra

139 Ventricular desynchronization imposed by ventricular pacing even when AV synchrony is preserved i

140 Burst ventricular pacing excluded atrial tachycardia when the

141 us presumed to have a higher burden of right ventricular pacing, experienced an increased risk of new

142 heart failure were induced by chronic right ventricular pacing for 1 to 2 weeks, 3 to 4 weeks, and 7

143 CHF was induced by rapid ventricular pacing for 10 days.

144 tized dogs with experimental CHF produced by ventricular pacing for 10 days.

145 ricular pacing and long-term memory (LTM) by ventricular pacing for 21 days.

146 multiple comorbidities, AVNA with permanent ventricular pacing for rate control seems safe during fo

147 ent leadless pacemakers are limited to right ventricular pacing, future advanced, communicating, mult

148 in 190 of 342 patients (55.6%) in the right-ventricular-pacing group, as compared with 160 of 349 (4

149 entricular ejection fraction (LVEF) >40% and ventricular pacing >20%.

150 The site of ventricular pacing has a major impact on LV mechanical s

151 ed response amplitude (VERA) obtained during ventricular pacing have been correlated with the presenc

152 e over time than did those assigned to right ventricular pacing (hazard ratio, 0.74; 95% credible int

153 ure (HR 1.85, P < .001), lower percentage of ventricular pacing (HR 1.12), and age.

154 on therapy, which coordinates right and left ventricular pacing in a subset of patients with interven

155 The impact of prolonged right ventricular pacing in adults without structural heart di

156 a safe alternative to minimal (backup-only) ventricular pacing in defibrillator recipients with impa

157 Rapid ventricular pacing in dogs is characterized by a dilated

158 (Biventricular Versus Right Ventricular Pacing in Heart Failure Patients With Atriov

159 The BLOCK HF (Biventricular Versus Right Ventricular Pacing in Heart Failure Patients With Atriov

160 ilure], BLOCK-HF [Biventricular Versus Right Ventricular Pacing in Heart Failure Patients with Atriov

161 The Biventricular versus Right Ventricular Pacing in Heart Failure Patients with Atriov

162 te that electrical remodeling in response to ventricular pacing in human subjects results in action p

163 controlling SNA and arterial pressure during ventricular pacing in humans.

164 This should not imply that right ventricular pacing in NQRS patients is safe but rather t

165 (Electromechanically Optimized Right Ventricular Pacing in Obstructive Hypertrophic Cardiomyo

166 ORI-HCM (Electromechanically Optimized Right Ventricular Pacing in Obstructive Hypertrophic Cardiomyo

167 We assessed the effect of right ventricular pacing in patients who underwent pacemaker i

168 ar pacing was superior to conventional right ventricular pacing in patients with atrioventricular blo

169 By univariate analysis, ventricular pacing in patients with AVB appeared to be a

170 Single-site ventricular pacing in patients with heart failure, atria

171 imal model of heart failure induced by rapid ventricular pacing in pigs.

172 ient randomized trial of dual-chamber versus ventricular pacing in sinus node dysfunction.

173 The mean percent right ventricular pacing in the DDDR AVSH arm was 10% (median

174 set (S-L-S sequences actively facilitated by ventricular pacing including the terminal beat after a p

175 rter defibrillator (ICD) therapy with backup ventricular pacing increases survival in patients with l

176 Right ventricular pacing increases the risk of heart failure i

177 ivity and higher arterial pressure than does ventricular pacing, indicating that cardiac pacing mode

178 We then apply it to study right ventricular pacing induced electromechanical dyssynchron

179 Although chronic right ventricular pacing-induced cardiomyopathy has been recog

180 solated from normal dogs and dogs with rapid ventricular pacing-induced CHF.

181 Right ventricular pacing-induced dyssynchrony substantially re

182 are associated with regional dysfunction in ventricular pacing-induced heart failure, regional myoca

183 Right ventricular pacing is associated with modest hemodynamic

184 The percentage of ventricular pacing is used as an indicator of adequate b

185 We conclude that chronic epicardial ventricular pacing is well tolerated by the fetus, can b

186 reated with percutaneous drainage and a left ventricular pacing lead dislodgement with no deaths.

187 nted with cardiac dimension crystals, a left ventricular pacing lead, and a pacemaker.

188 Ventricular pacing leads to a dilated myopathy in which

189 c and electromechanical consequences of left ventricular pacing (LVP) and biventricular pacing (BiVP)

190 nderwent thoracotomy, and, during epicardial ventricular pacing, mapping was performed.

191 ges in ventricular function induced by right ventricular pacing may account for some of its associate

192 ds no clear advantage or disadvantage over a ventricular pacing mode that minimizes pacing altogether

193 CHF was produced in dogs by use of the rapid ventricular pacing model.

194 ppressed LA fibrosis in the canine high-rate ventricular pacing model.

195 During short AV delays (<300 ms) and right ventricular pacing, MVC occurred significantly later.

196 nd by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]).

197 ntaneous activity and following cessation of ventricular pacing (n = 5) to give similar features to W

198 as repeated with heart rate held constant by ventricular pacing (n=3).

199 elopment of CHF produced by 3 weeks of rapid ventricular pacing (n=9).

200 differences were found among the systems at ventricular pacing of 200 and 300 beats per minute, unde

201 We evaluated the effects of the site of ventricular pacing on left ventricular (LV) synchrony an

202 ffects of dual-chamber versus single-chamber ventricular pacing on subsequent stroke in patients with

203 ory (CM) refers to T-wave changes induced by ventricular pacing or arrhythmia that accumulate in magn

204 e QRS complex vector during prior periods of ventricular pacing or arrhythmia.

205 s to an altered T-wave morphology induced by ventricular pacing or arrhythmias that persist for varia

206 s with AVB, alternate single-site RV or left ventricular pacing or biventricular pacing may be superi

207 and were randomly assigned to standard right ventricular pacing or biventricular pacing.

208 that had been randomly programmed to either ventricular pacing or dual-chamber pacing.

209 aseline left ventricular conduction disease, ventricular pacing, or ventricular pre-excitation were e

210 ely abolished by both biventricular and left ventricular pacing (P<0.05).

211 ing post-MI (63% in control vs. 44% in MI to ventricular pacing; P < 0.01).

212 randomization (after 30 to 60 days of right ventricular pacing postimplant) and every 6 months throu

213 ntricular beat of one of the following three ventricular pacing protocols: constant ventricular rates

214 Comparison of NTP doses and ventricular pacing rates that produced comparable hypote

215 AV nodal ablation and bi-ventricular pacing remains another viable option.

216 for patients with a standard indication for ventricular pacing remains controversial.

217 Right ventricular pacing restores an adequate heart rate in pa

218 In all subjects, ventricular pacing resulted in a prolongation of the act

219 In 13 sheep, acute right ventricular pacing resulted in LBBB-1 (23%) and LBBB-2 (

220 CM induced by right ventricular pacing results in a distinctive T-vector pat

221 AVB patients receiving either LBBAP or right ventricular pacing (RVP) and to analyse predictors of mo

222 Twenty dogs underwent rapid ventricular pacing (RVP) for 4 weeks to create a model o

223 Right ventricular pacing (RVP) increases risk of atrial fibril

224 Seventeen dogs underwent rapid ventricular pacing (RVP) to create heart failure.

225 However, among HFrEF patients with right ventricular pacing (RVP), the efficacy of CRT-D upgrade

226 yopathy (oHCM) have devices capable of right ventricular pacing (RVP).

227 occur among some patients who receive right ventricular pacing (RVP).

228 llowing groups (12 per group): chronic rapid ventricular pacing (RVP; 400 bpm, 3 weeks), RVP and conc

229 ent in pacing mode in the very elderly, with ventricular pacing selected for sicker and older patient

230 o intraventricular conduction abnormalities, ventricular pacing should be avoided as much as possible

231 of right ventricular pacing, suggesting that ventricular pacing should be minimized whenever possible

232 imize detection enhancements and to minimize ventricular pacing, significantly decrease inappropriate

233 Left ventricular (LV) and right ventricular pacing site characteristics have been shown

234 cades of technological advances, the optimal ventricular pacing site to mimic normal human ventricula

235 Patient selection, left ventricular pacing site, and optimal device programming

236 Multiple LV and apical right ventricular pacing sites were assessed during an invasiv

237 high-rate episode is a high burden of right ventricular pacing, suggesting that ventricular pacing s

238 ly, was less evident during continuous right ventricular pacing, suggesting the novel possibility tha

239 were paced was lower in dual-chamber minimal ventricular pacing than in conventional dual-chamber pac

240 -term RV apical pacing, alternative sites of ventricular pacing that simulate normal biventricular el

241 During ventricular pacing, the peak amplitude of fast Fourier t

242 complex is wide and abnormal, such as during ventricular pacing, the T waves will also be abnormal an

243 then normalizes, such as after cessation of ventricular pacing, the T waves will normalize as well,

244 The ventricular pacing threshold (VPT) and ventricular fibri

245 ism for VER, dogs (n=6) underwent 4 weeks of ventricular pacing to induce VER.

246 Sheep underwent rapid right ventricular pacing to obtain moderate to severe function

247 imaging was used before and after 1 month of ventricular pacing to reconstruct epicardial activation

248 presents a new paradigm that aims to tailor ventricular pacing to the individual patient to achieve

249 g using an intracardiac electrogram during a ventricular pacing train.

250 Ang II, and activation of p53 function with ventricular pacing upregulates the myocyte RAS and the g

251 suggest that electric separation during left ventricular pacing varies within the right ventricle (RV

252 under normal sinus rhythm were compared with ventricular pacing (VDD) at varying sites and AV delays

253 tic and arterial pressure responses to VT or ventricular pacing (VP) in dogs with inducible VT.

254 ympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electro

255 in the group receiving dual-chamber minimal ventricular pacing vs. 5.4% in the group receiving conve

256 Eight mongrel dogs underwent demand ventricular pacing (VVI) at 250 beats/min for 3 weeks to

257 ial comparing dual-chamber pacing (DDDR) and ventricular pacing (VVIR) in sinus node dysfunction, dem

258 beats min(-1)) using ULFS-49, and atrial or ventricular pacing was achieved via an intra-oesophageal

259 These results persisted when incident ventricular pacing was included in the outcome and when

260 Ventricular pacing was performed adjacent to the His bun

261 gh altered ventricular activation from right ventricular pacing was presumed to be the likely cause f

262 The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricul

263 ed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infu

264 ade atrial activation during tachycardia and ventricular pacing were determined by intracardiac recor

265 edation, sodium channel-blocking agents, and ventricular pacing were effective in suppressing acute e

266 of intracardiac electrograms and atrial and ventricular pacing were performed.

267 synchrony but results in high percentages of ventricular pacing, which causes ventricular desynchroni

268 line (atrial antibradycardia pacing or right ventricular pacing with atrial fibrillation) to dual-cha

269 acing (535 patients) or dual-chamber minimal ventricular pacing with the use of new pacemaker feature

270 es were evaluated during sinus rhythm, right ventricular pacing without preceding atrial contraction,

271 (no pacing, no S-L-S) and pacing associated (ventricular pacing without S-L-S) onset accounted for 44

272 er beta-adrenergic stimulation or programmed ventricular pacing, without significant proarrhythmic ef

273 Right ventricular pacing worsens LV function in patients with

274 ar activities (LAVAs) during sinus rhythm or ventricular pacing would be a useful and effective end p

275 r), we hypothesized that CM induced by right ventricular pacing would manifest a TWI pattern differen