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 heart failure in the setting of ventricular dyssynchrony.

4 th ventricles and thereby avoids ventricular dyssynchrony.

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

6 ogic changes may result in electromechanical dyssynchrony.

7 mass, regional left ventricular function and dyssynchrony.

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

9 delayed contraction and increased extent of dyssynchrony.

10 myocardial contraction and greater extent of dyssynchrony.

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

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

13 in patients with narrow QRS and evidence of dyssynchrony.

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

15 entricular conduction delays and ventricular dyssynchrony.

16 mportance of mechanical delay or ventricular dyssynchrony.

17 ventricular systolic dysfunction and cardiac dyssynchrony.

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

19 systolic heart failure (HF) and ventricular dyssynchrony.

20 ass III and IV heart failure and ventricular dyssynchrony.

21 nce for sustained improvement in ventricular dyssynchrony.

22 evere systolic heart failure and ventricular dyssynchrony.

23 volunteers, leading to ventilator-volunteer dyssynchrony.

24 associated with significant interventricular dyssynchrony.

25 ters as well as directly assessed mechanical dyssynchrony.

26 aluable for treating DCM patients with basal dyssynchrony.

27 uscle activity in causing patient-ventilator dyssynchrony.

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

29 in those patients with the greatest baseline dyssynchrony.

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

31 only BiVP significantly decreased electrical dyssynchrony.

32 and BiVP, despite differences in electrical dyssynchrony.

33 rom CRT in the presence of marked mechanical dyssynchrony.

34 hocardiographic evidence of left ventricular dyssynchrony.

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

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

37 sponse differs between indices of mechanical dyssynchrony.

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

39 c for LBBB and results from intraventricular dyssynchrony.

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

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

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

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

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

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

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

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

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

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

50 Mechanical dyssynchrony analysis has been particularly useful in ca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 We compared mechanical dyssynchrony and the impact of cardiac resynchronization

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

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

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

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

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

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

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

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

86 Dyssynchrony assessed by longitudinal motion is less sen

87 Dyssynchrony assessment based on the timing of regional

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

89 Typical electromechanical dyssynchrony associated with mechanical inefficiency, re

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

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

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

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

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

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

96 Dyssynchrony before CRT was defined as tissue Doppler ve

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

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

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

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

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

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

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

104 Flow dyssynchrony can be improved by increasing ventilator fl

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

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

107 LV dyssynchrony cannot be attributed to prematurity or abno

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

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

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

111 LV dyssynchrony correlated inversely with LV ejection fract

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

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

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

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

116 Heart failure with dyssynchrony displays decreased myocyte and myofilament

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

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

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

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

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

122 Dyssynchrony from timing of speckle-tracking peak radial

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

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

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

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

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

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

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

130 Dyssynchrony imposes high pressure loads on ventilator m

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

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

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

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

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

136 LV dyssynchrony in failing hearts generates myocardial prot

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

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

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

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

141 Cardiac dyssynchrony in the failing heart worsens global functio

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

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

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

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

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

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

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

149 Dyssynchrony indexes based on time to peak tissue veloci

150 Several echocardiographic dyssynchrony indexes have been proposed to identify resp

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

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

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

154 6%; QRS width, 170 +/- 22 ms), 4 mechanical dyssynchrony indices (septal systolic rebound stretch [S

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

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

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

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

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

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

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

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

163 Mechanical dyssynchrony is a potential means to predict response to

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

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

166 Mechanical LV dyssynchrony is best shown by evolving echocardiographic

167 Mechanical dyssynchrony is considered an independent predictor for

168 for quantifying left ventricular mechanical dyssynchrony is increasingly appreciated.

169 Left ventricular dyssynchrony is independently associated with increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Increased dyssynchrony may mediate the association of myocardial d

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

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

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

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

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

191 Cardiac dyssynchrony, measured by echocardiography prior to impl

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

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

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

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

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

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

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

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

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

201 Patients with intraventricular dyssynchrony on echocardiography were randomly assigned

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

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

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

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

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

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

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

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

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

211 Mechanical LV dyssynchrony potentially treatable by ventricular resync

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

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

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

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

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

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

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

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

220 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

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

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

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

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

225 Often termed dyssynchrony, this further decreases systolic function a

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

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

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

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

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

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

232 Radial dyssynchrony was assessed by speckle-tracking radial str

233 Dyssynchrony was assessed from both temporal and regiona

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

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

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

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

238 LV dyssynchrony was greater during long-coupled rather than

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

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

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

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

243 LV pacing region dyssynchrony was not predictive of response.

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

245 Lack of radial dyssynchrony was particularly associated with unfavorabl

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

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

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

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

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

251 Dyssynchrony was quantified by measuring the esophageal

252 This dyssynchrony was significantly reduced by both the VI st

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

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

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

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

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

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

259 mptomatic heart failure and left ventricular dyssynchrony were selected.

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

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

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

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

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

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

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

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

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

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

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

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

272 The CDOO worsened dyssynchrony with prolonged DeltaIVT and PSC.