ライフサイエンスコーパス: dyssynchrony

1 control group and patients without systolic dyssynchrony).

2 9%; p < 0.02; p < 0.004 for correlation with dyssynchrony).

3 sponse differs between indices of mechanical dyssynchrony.

4 ction fraction, and a CMR-derived measure of dyssynchrony.

5 c for LBBB and results from intraventricular dyssynchrony.

6 en all 12 segments were used as a measure of dyssynchrony.

7 ogic changes may result in electromechanical dyssynchrony.

8 mass, regional left ventricular function and dyssynchrony.

9 sion, strain and strain rate, and mechanical dyssynchrony.

10 delayed contraction and increased extent of dyssynchrony.

11 myocardial contraction and greater extent of dyssynchrony.

12 03) compared with ARVD/C patients without RV dyssynchrony.

13 in patients with narrow QRS and evidence of dyssynchrony.

14 heart failure in the setting of ventricular dyssynchrony.

15 no data on the effects of medical therapy on dyssynchrony.

16 entricular conduction delays and ventricular dyssynchrony.

17 mportance of mechanical delay or ventricular dyssynchrony.

18 th ventricles and thereby avoids ventricular dyssynchrony.

19 ventricular systolic dysfunction and cardiac dyssynchrony.

20 ation (>/=120 ms) is a marker of ventricular dyssynchrony.

21 systolic heart failure (HF) and ventricular dyssynchrony.

22 ass III and IV heart failure and ventricular dyssynchrony.

23 nce for sustained improvement in ventricular dyssynchrony.

24 evere systolic heart failure and ventricular dyssynchrony.

25 jection fraction, left atrial volume, and LV dyssynchrony.

26 volunteers, leading to ventilator-volunteer dyssynchrony.

27 associated with significant interventricular dyssynchrony.

28 ters as well as directly assessed mechanical dyssynchrony.

29 aluable for treating DCM patients with basal dyssynchrony.

30 uscle activity in causing patient-ventilator dyssynchrony.

31 re then employed in an attempt to reduce the dyssynchrony.

32 in those patients with the greatest baseline dyssynchrony.

33 ent with age-related AN disengagement and AN dyssynchrony.

34 e, suggesting an interventricular mechanical dyssynchrony.

35 easures of deformation: strain, torsion, and dyssynchrony.

36 % of Hu-NSG mice exhibited LV dyskinesia and dyssynchrony.

37 only BiVP significantly decreased electrical dyssynchrony.

38 and BiVP, despite differences in electrical dyssynchrony.

39 rom CRT in the presence of marked mechanical dyssynchrony.

40 hocardiographic evidence of left ventricular dyssynchrony.

41 d to be more dependent on heart rate than on dyssynchrony.

42 ential network remodeling and Ca(2+) release dyssynchrony.

43 , p < 0.001) and intraventricular mechanical dyssynchrony (15 +/- 26 ms to 57 +/- 41 ms, p < 0.001),

44 o IV over several years; 4) major mechanical dyssynchrony; 5) no known etiology of cardiomyopathy; an

45 ate lead position (21%), or lack of baseline dyssynchrony (9%).

46 LV apical pacing is associated with less dyssynchrony, a more physiological LV contraction patter

47 eart failure, and had significant electrical dyssynchrony, all before CRT implant.

48 Mechanical dyssynchrony also correlated directly with %DeltadP/dt(m

49 We tested whether dyssynchrony also induces localized disparities in the e

50 Mechanical dyssynchrony also occurs in patients with a narrow QRS c

51 believed to be due principally to relief of dyssynchrony, although we recently showed that relief of

52 SRSsept and IVMD better represent LV dyssynchrony amenable to CRT and better predict CRT resp

53 tionships of LV mass and age with myocardial dyssynchrony among asymptomatic participants of the Mult

54 Mechanical dyssynchrony analysis has been particularly useful in ca

55 The new imaging and regional dyssynchrony analysis methods provide quantitative asses

56 Quantitative echocardiography, including dyssynchrony analysis, was performed at baseline.

57 ac resynchronization therapy depends both on dyssynchrony and (regional) contractility.

58 of patients with widened QRS who do not have dyssynchrony and accordingly do not respond to cardiac r

59 The VAQRS reflects electric interventricular dyssynchrony and accurately predicts optimal timing of L

60 ardiography for the assessment of mechanical dyssynchrony and as a possible aid for selecting patient

61 presence and precise location of mechanical dyssynchrony and be able to find the technical location

62 rameters of mechanical left ventricular (LV) dyssynchrony and correlated it with clinical outcomes in

63 circulatory, and basic myocardial effects of dyssynchrony and CRT in the failing heart, and we highli

64 ese observations support the relationship of dyssynchrony and CRT response.

65 aluable tool in the treatment of ventricular dyssynchrony and dilated cardiomyopathy in pediatric and

66 are a common clinical destiny of ventricular dyssynchrony and dilated cardiomyopathy.

67 ments include treatment of electromechanical dyssynchrony and dysrhythmia by cardiac resynchronisatio

68 Basal dyssynchrony and effects of single and BiV CRT on left v

69 pain and anxiety, improve patient-ventilator dyssynchrony and ensure patient safety.

70 Furthermore, the magnitude of dyssynchrony and impact of CRT in pure RBBB versus LBBB

71 ular septal (LVS) pacing reduces ventricular dyssynchrony and improves cardiac function relative to r

72 ck is associated with specific RV mechanical dyssynchrony and inefficient contraction.

73 s excellent performance in a canine model of dyssynchrony and is strongly associated with CRT respons

74 ventricular pacing induced electromechanical dyssynchrony and its reversal (resynchronization).

75 riability imaging (CVI), to quantify cardiac dyssynchrony and magnitude of resynchronization achieved

76 phic evidence of left ventricular mechanical dyssynchrony and may also benefit from CRT.

77 but also clinical outcomes in patients with dyssynchrony and narrow QRS duration (resynchronization

78 Speckle-tracking radial strain can quantify dyssynchrony and predict immediate and long-term respons

79 ographic image speckle tracking can quantify dyssynchrony and predict response to CRT.

80 n be used to infer integrated information on dyssynchrony and regional contractility, and thereby pre

81 This method provides evidence of dyssynchrony and regional myocardial dysfunction that oc

82 The data on dyssynchrony and resynchronization in ischemia/reperfusi

83 h impaired cardiac function have ventricular dyssynchrony and seek cardiac resynchronization therapy

84 entricle (LV) for both evaluation of cardiac dyssynchrony and the efficacy of resynchronization thera

85 We compared mechanical dyssynchrony and the impact of cardiac resynchronization

86 a major role in the assessment of mechanical dyssynchrony and the selection of patients for cardiac r

87 olically healthy obese had lower LS, greater dyssynchrony, and early diastolic dysfunction, supportin

88 ram (VCG) reflects electric interventricular dyssynchrony, and that the QRS vector amplitude (VAQRS),

89 to tolerate rapid rates or atrioventricular dyssynchrony, and the patient's ability to tolerate the

90 ies at the LVLP together with CMR mechanical dyssynchrony are strongly associated with echocardiograp

91 now support direct assessment of mechanical dyssynchrony as a method to better identify CRT responde

92 ging CMR acquisition methods for quantifying dyssynchrony as well as the potential role of CMR to imp

93 h the segmental wall motion abnormalities or dyssynchrony, as defined by echocardiography and other i

94 Induced baseline flow dyssynchrony, as measured by the pressure time product,

95 Dyssynchrony assessed by longitudinal motion is less sen

96 Dyssynchrony assessment based on the timing of regional

97 dy was to determine the use of RV strain and dyssynchrony assessment in ARVC using feature-tracking C

98 nt of a first HHF, possibly due to increased dyssynchrony associated with HF progression.

99 Typical electromechanical dyssynchrony associated with mechanical inefficiency, re

100 st year of follow-up demonstrated increasing dyssynchrony at 1 year compared with those who had no HH

101 jection fraction, left atrial volume, and LV dyssynchrony at 1-year in CRT-D patients by comorbidity

102 k, maximum pressure derivative, and systolic dyssynchrony at individually optimized AVD.

103 pler echocardiograms showed major mechanical dyssynchrony at left atrioventricular, interventricular,

104 riance at time of maximal shortening indexed dyssynchrony, averaging 28.0+/-7.1% in normal subjects v

105 ction similarly and correlated with improved dyssynchrony based on epsiloncc-based metrics.

106 Twelve echocardiographic parameters of dyssynchrony, based on both conventional and tissue Dopp

107 Dyssynchrony before CRT was defined as tissue Doppler ve

108 nger cycles were characterized by increasing dyssynchrony between follicle-stimulating hormone and lu

109 ation therapy continues to grow, the role of dyssynchrony beyond the ECG is being re-evaluated.

110 s an alternative method to assess myocardial dyssynchrony but these methods are relatively underdevel

111 severe heart failure and markers of cardiac dyssynchrony, but not all patients respond to a similar

112 When both longitudinal dyssynchrony by 2-site TDI (> or =60 ms) and radial dyss

113 y by tissue Doppler imaging (TDI) and radial dyssynchrony by speckle-tracking strain may predict left

114 echocardiographic assessment of longitudinal dyssynchrony by tissue Doppler imaging (TDI) and radial

115 Flow dyssynchrony can be improved by increasing ventilator fl

116 Combined patterns of longitudinal and radial dyssynchrony can be predictive of LV functional response

117 If sufficiently severe, flow dyssynchrony can produce significant imposed loads on ve

118 LV dyssynchrony cannot be attributed to prematurity or abno

119 In patients with heart failure and cardiac dyssynchrony, cardiac resynchronization improves symptom

120 Left bundle branch block-like dyssynchrony caused by DDD pacing could be acutely rever

121 Left ventricular (LV) dyssynchrony caused by premature ventricular contraction

122 In contrast, when ventricular dyssynchrony causes functional MR attributable to unequa

123 SE) provides high-quality strain for overall dyssynchrony (circumferential uniformity ratio estimate

124 a more detailed quantification of electrical dyssynchrony compared with conventional electrocardiogra

125 LV dyssynchrony correlated inversely with LV ejection fract

126 mposite parameter of electric and mechanical dyssynchrony correlated with RV end-diastolic volume (r=

127 omatic systolic heart failure and electrical dyssynchrony, CRT was associated with improved heart tra

128 Of 210 patients (89) with dyssynchrony data available, there were 62 events: 47 de

129 rmal conduction (AAI pacing), whereas during dyssynchrony (DDD pacing), the lateral wall was more loa

130 ircumferential, and radial RV strains and RV dyssynchrony (defined as the SD of the time-to-peak stra

131 LVS and IVS are novel measures of LV dyssynchrony derived from ERNA planar analysis.

132 Heart failure with dyssynchrony displays decreased myocyte and myofilament

133 modeling in our animal model with reversible dyssynchrony due to pacing.

134 cohort of 64 patients who were referred for dyssynchrony evaluation.

135 Furthermore, we suggest that ventricular dyssynchrony exacerbates subcellular remodeling in heart

136 by longitudinal motion is less sensitive to dyssynchrony, follows different time courses than those

137 d to determine the interaction of ventilator dyssynchrony frequency to cause clinically meaningful ch

138 f CRT in narrow QRS patients with mechanical dyssynchrony from a multicenter study--ESTEEM-CRT).

139 emodynamics may be attenuated by ventricular dyssynchrony from right ventricular apical pacing.

140 Dyssynchrony from timing of speckle-tracking peak radial

141 anteroseptal to posterior wall radial strain dyssynchrony >200 ms, lack of severe left ventricular di

142 hrony by 2-site TDI (> or =60 ms) and radial dyssynchrony (> or =130 ms) were positive, 95% of patien

143 Patients with RV dyssynchrony had a larger RV end-diastolic area (22 +/-

144 tients with narrower QRS duration who lacked dyssynchrony had the least favorable long-term outcome.

145 ure for 6 weeks, concurrent with ventricular dyssynchrony (HF(dys)) or CRT.

146 ds for quantitative assessment of mechanical dyssynchrony, highlighting newer acquisition and analysi

147 for delayed mechanical activation, known as dyssynchrony, imaging techniques have identified a subse

148 Dyssynchrony imposes high pressure loads on ventilator m

149 recent data show that measures of mechanical dyssynchrony improve the sensitivity and specificity of

150 The TDI-derived strain rate showed minimal dyssynchrony in AOO as seen by isovolumic tensing (IVT)

151 mechanisms underlying right ventricular (RV) dyssynchrony in arrhythmogenic right ventricular dysplas

152 The prevalence of systolic and diastolic dyssynchrony in DHF patients is unknown with no data on

153 ine the prevalence of systolic and diastolic dyssynchrony in diastolic heart failure (DHF) patients a

154 LV dyssynchrony in failing hearts generates myocardial prot

155 ld serve as a marker of diastolic mechanical dyssynchrony in LBBB hearts.

156 fy global and regional RV dysfunction and RV dyssynchrony in patients with ARVC and provides incremen

157 of pathophysiologically relevant mechanical dyssynchrony in patients with heart failure and normal E

158 timing index appears to be more specific for dyssynchrony in patients with systolic dysfunction and l

159 vely larger left ventricular (LV) electrical dyssynchrony in smaller hearts contributes to the better

160 Greater electrical dyssynchrony in smaller hearts contributes, in part, to

161 Cardiac dyssynchrony in the failing heart worsens global functio

162 Both spatial and temporal dyssynchrony in the LV declined nearly 40% with LV or Bi

163 techniques have emerged to quantify regional dyssynchrony, in hopes of improving patient selection an

164 hic methods for the assessment of myocardial dyssynchrony including quantitative assessment of circum

165 A systolic dyssynchrony index (SDI) was derived from the dispersion

166 n optimal tissue velocity- or strain-derived dyssynchrony index requires a large prospective clinical

167 Systolic dyssynchrony index was greater in PHT (0.14 +/- 0.06 vs.

168 gitudinal study was designed with predefined dyssynchrony indexes and outcome variables to test the h

169 Dyssynchrony indexes based on time to peak tissue veloci

170 Several echocardiographic dyssynchrony indexes have been proposed to identify resp

171 normal subjects have tissue velocity-derived dyssynchrony indexes higher than the cutoff value propos

172 e tissue velocity-derived and strain-derived dyssynchrony indexes in patients with or without systoli

173 RV mechanical dyssynchrony, indicated by early septal activation (righ

174 6%; QRS width, 170 +/- 22 ms), 4 mechanical dyssynchrony indices (septal systolic rebound stretch [S

175 ere used to assess the relationships between dyssynchrony indices and CRT response within wide ranges

176 variability of predictive power between the dyssynchrony indices can be explained by differences in

177 The power of echocardiographic dyssynchrony indices to predict response to cardiac resy

178 ian with the capability to assess mechanical dyssynchrony indices, as well as cardiac function and el

179 Left ventricular (LV) mechanical dyssynchrony induces regional heterogeneity of mechanica

180 ne the appropriate role of echocardiographic dyssynchrony information in patient selection for cardia

181 -These results show that although mechanical dyssynchrony is a key predictor for pacing efficacy in D

182 CMR assessment of myocardial dyssynchrony is a logical alternative to echocardiograph

183 Mechanical dyssynchrony is a potential means to predict response to

184 riables to test the hypothesis that baseline dyssynchrony is associated with long-term survival after

185 Mechanical LV dyssynchrony is associated with response to CRT; however

186 Mechanical LV dyssynchrony is best shown by evolving echocardiographic

187 Mechanical dyssynchrony is considered an independent predictor for

188 for quantifying left ventricular mechanical dyssynchrony is increasingly appreciated.

189 Left ventricular dyssynchrony is independently associated with increased

190 Less mechanical dyssynchrony is induced by RBBB than LBBB in failing hea

191 Cs may cause a more severe cardiomyopathy if dyssynchrony is the leading mechanism responsible for PV

192 eneous loading conditions, such as during LV dyssynchrony, is an adaptive process that helps to equil

193 r contractility by decreasing areas of focal dyssynchrony, is gaining wide acceptance.

194 anical discoordination, often referred to as dyssynchrony, is often observed in patients with heart f

195 retch [SRSsept], interventricular mechanical dyssynchrony [IVMD], septal-to-lateral peak shortening d

196 plete atrioventricular block, pacing-induced dyssynchrony lasting for decades might be especially del

197 Left ventricular (LV) mechanical dyssynchrony (LVMD) has emerged as a therapeutic target

198 ationship between gating-error magnitude and dyssynchrony magnitude was observed.

199 magnitude of the postcorrection increase in dyssynchrony magnitude was proportional to the magnitude

200 cause a spurious reduction in SPECT assay of dyssynchrony magnitude.

201 d gating error caused a spurious decrease in dyssynchrony magnitude.

202 ients with a reduced ejection fraction, this dyssynchrony may be especially detrimental.

203 ysis, no single echocardiographic measure of dyssynchrony may be recommended to improve patient selec

204 uggest that direct assessments of mechanical dyssynchrony may better predict chronic response.

205 t echocardiographic parameters of mechanical dyssynchrony may improve patient selection for cardiac r

206 Increased dyssynchrony may mediate the association of myocardial d

207 Left ventricular (LV) dyssynchrony may occur as a result of right ventricular

208 An RV dyssynchrony may occur in up to 50% of ARVD/C patients,

209 unique flow-specific measures of mechanical dyssynchrony may serve as an additional tool for conside

210 However, what all this dyssynchrony means clinically, and how or whether it sho

211 ither the QRS interval on the surface ECG or dyssynchrony measured by imaging is of any practical val

212 Cardiac dyssynchrony, measured by echocardiography prior to impl

213 as to evaluate global and regional gated MPS dyssynchrony measurements by comparing parameters obtain

214 des [DeltaM(W) and DeltaM(S), respectively]) dyssynchrony measures were calculated by Fourier harmoni

215 Mechanical interventricular dyssynchrony (MIVD) was determined as the time delay bet

216 Systolic dyssynchrony occurs in 33% of DHF patients, and diastoli

217 occurs in 33% of DHF patients, and diastolic dyssynchrony occurs in 58%.

218 Patient-ventilator flow dyssynchrony occurs when ventilator flow delivery is ins

219 anization index, the model predicted greater dyssynchrony of Ca(2+) release, which exceeded that obse

220 dices and CRT response within wide ranges of dyssynchrony of LV activation and reduced contractility.

221 th a QRS duration <120 ms and no evidence of dyssynchrony on conventional criteria and assessed the e

222 Patients with intraventricular dyssynchrony on echocardiography were randomly assigned

223 ymptoms, narrow QRS duration, and mechanical dyssynchrony on echocardiography.

224 We examined the influence of mechanical dyssynchrony on outcome in patients with left ventricula

225 and myeloid precursors, nuclear/cytoplasmic dyssynchrony, or dysmegakaryopoiesis with abnormalities

226 ine, there was no difference in MR grade, LV dyssynchrony, or LV volumes in those with QLV above vers

227 tern was superior to time-to-peak indexes of dyssynchrony (p < 0.01 for all).

228 volume and dP/dtmax despite more pronounced dyssynchrony (P<0.001).

229 was large variability in the analysis of the dyssynchrony parameters.

230 al delay decreased (P<0.001) and signs of RV dyssynchrony pattern were significantly abolished.

231 This has stimulated studies of dyssynchrony per se, and the phenomenon now appears to b

232 Mechanical LV dyssynchrony potentially treatable by ventricular resync

233 after CRT, baseline speckle-tracking radial dyssynchrony predicted a significant increase in ejectio

234 Combined longitudinal and radial dyssynchrony predicted EF response with 88% sensitivity

235 To test whether basal mechanical dyssynchrony predicted responsiveness to LV pacing, circ

236 evaluated not only how well imaging predicts dyssynchrony (Predictors of Response to Cardiac Resynchr

237 The degree of interventricular dyssynchrony present in normal sinus rhythm correlated w

238 The degree of interventricular dyssynchrony present in sinus rhythm correlated with the

239 and QRS duration, Yu Index and radial strain dyssynchrony remained independently associated with outc

240 causes cardiac remodeling due to mechanical dyssynchrony, reversible by biventricular stimulation.

241 ed by 4 weeks pacing at the right ventricle (dyssynchrony), right atrium (synchrony), or for 2 weeks

242 er LS (SE, 0.3%; P<0.001) and 7.8 ms greater dyssynchrony (SE, 1.5 ms; P<0.001) when compared with co

243 iable-adjusted analyses) and 10.8 ms greater dyssynchrony (SE, 3.3 ms; P=0.002), and OB/MS+ had 1.0%

244 Right ventricular pacing-induced dyssynchrony substantially reduced heart and myocyte fun

245 ced minipigs exhibited significantly more LV dyssynchrony than LV apex-paced animals, which was accom

246 e, women (n=228) displayed larger electrical dyssynchrony than men (QRS area, 132 55 versus 123 58 uV

247 e, women (n=228) displayed larger electrical dyssynchrony than men (QRS area, 132+/-55 versus 123+/-5

248 t pressure overload resulted in LV segmental dyssynchrony that was attenuated with return of the afte

249 hocardiographic evidence of left ventricular dyssynchrony, the primary outcome (death from any cause

250 Often termed dyssynchrony, this further decreases systolic function a

251 ability of baseline speckle-tracking radial dyssynchrony (time difference in peak septal wall-to-pos

252 y echocardiographic techniques in evaluating dyssynchrony to clinical practice at the present time.

253 The ability of echocardiographic dyssynchrony to predict response to cardiac resynchroniz

254 on therapy in patients with interventricular dyssynchrony, transcatheter mitral valve repair in patie

255 nce suggests that the analysis of mechanical dyssynchrony using gated myocardial perfusion SPECT (MPS

256 ll describe advanced methods for quantifying dyssynchrony, ventricular function and perfusion, and hy

257 Longitudinal dyssynchrony was assessed by color TDI for time to peak

258 LV dyssynchrony was assessed by dispersion of QRS-to-peak s

259 Radial dyssynchrony was assessed by speckle-tracking radial str

260 Dyssynchrony was assessed from both temporal and regiona

261 The absence of echocardiographic dyssynchrony was associated with significantly less favo

262 An RV dyssynchrony was defined as the difference in T(SV) betw

263 Mechanical interventricular dyssynchrony was determined as the time delay between up

264 Baseline electrical dyssynchrony was evaluated using the QRS area and the co

265 were measured in 12 segments, and myocardial dyssynchrony was expressed as the SD of time to peak str

266 LV dyssynchrony was greater during long-coupled rather than

267 Despite this, mechanical dyssynchrony was less in RBBB (circumferential uniformit

268 sed, LV dimensions normalized and mechanical dyssynchrony was nearly resolved in all patients, and me

269 The EF response rate was lowest (10%) when dyssynchrony was negative using 12-site TDI and radial s

270 Significant RV dyssynchrony was not noted in any of the control subject

271 LV pacing region dyssynchrony was not predictive of response.

272 The SD of TAUlocal as a measure of dyssynchrony was not related to the amplitude or the tim

273 Lack of radial dyssynchrony was particularly associated with unfavorabl

274 When either longitudinal or radial dyssynchrony was positive (but not both), 59% had an EF

275 Systolic dyssynchrony was present in 20 patients (33%) with DHF a

276 d on a cutoff value of 56 ms, significant RV dyssynchrony was present in 26 ARVD/C patients (50%).

277 Diastolic dyssynchrony was present in 35 patients (58%) with DHF a

278 Flow dyssynchrony was produced by reducing the set flow by 50

279 Dyssynchrony was quantified by measuring the esophageal

280 This dyssynchrony was significantly reduced by both the VI st

281 error alone could affect the measurement of dyssynchrony, we performed a prospective study in which

282 d be repaired for the purpose of quantifying dyssynchrony, we tested a correction algorithm on the pa

283 obal longitudinal strain (LS) and time-based dyssynchrony were assessed by speckle tracking.

284 Systolic and diastolic dyssynchrony were assessed by tissue Doppler and defined

285 Three indexes of electrical dyssynchrony were derived from intrinsic maps: right and

286 ts with heart failure and markers of cardiac dyssynchrony were randomly assigned to receive or not re

287 mptomatic heart failure and left ventricular dyssynchrony were selected.

288 sion with timing of strain, strain rate, and dyssynchrony were studied.

289 rse systolic mechanics as assessed by LS and dyssynchrony when compared with nonobese controls.

290 , as well as cardiac function and electrical dyssynchrony, when considering a pediatric or congenital

291 rease in TAT and mechanical interventricular dyssynchrony, whereas LV EDV hardly changed.

292 ing intervals demonstrate more pronounced LV dyssynchrony, whereas PVC location has minimal impact.

293 e a single reliable parameter for predicting dyssynchrony, whereas the latter trials did not demonstr

294 ch block (LBBB) causes left ventricular (LV) dyssynchrony which is often associated with heart failur

295 atients with predominantly right ventricular dyssynchrony who respond to CRT without reverse remodeli

296 ventricular systolic dysfunction and cardiac dyssynchrony who were receiving standard pharmacologic t

297 ived strain rate showed worsened ventricular dyssynchrony with CDOO and improvement with BDOO.

298 vere LV systolic dysfunction had significant dyssynchrony with normal QRS durations (SDI, 14.7+/-1.2%

299 We assessed ventricular dyssynchrony with parameters derived from the first harm

300 The CDOO worsened dyssynchrony with prolonged DeltaIVT and PSC.