ライフサイエンスコーパス: diastole

1 heads, and bifid PM mobility (in systole and diastole).

2 cytoplasmic Ca(2+) to relax the heart during diastole.

3 HFNEF is not an isolated disorder of diastole.

4 rogeneity of regional myocardial flow during diastole.

5 ated normalized ventricular elastance at end diastole.

6 asurement of balloon luminal pressure at end diastole.

7 t of global cardiac mechanics in systole and diastole.

8 ating active restoration of the LV cavity in diastole.

9 , VSA was greater than ASA during 75-100% of diastole.

10 alized ventricular elastance at arterial end diastole.

11 n inability to normalize cytosolic [Ca2+] in diastole.

12 he cardiac cycle and occurring at the end of diastole.

13 and sphericity index at end-systole and end-diastole.

14 blood flow velocity during late systole and diastole.

15 to inhibit cardiac muscle contraction during diastole.

16 ike a sail, between the 2 stay chords during diastole.

17 elastic recoil engendered by stretch during diastole.

18 lve time points covering systole and most of diastole.

19 tension during systole and relaxation during diastole.

20 ptor afferent firing is maximal, relative to diastole.

21 cite cells during the periods of depolarized diastole.

22 those without LBBB during early but not late diastole.

23 to the central aorta in systole rather than diastole.

24 action potential and during the depolarized diastole.

25 coincide with either the cardiac systole or diastole.

26 action, ejection, isovolumic relaxation, and diastole.

27 action, ejection, isovolumic relaxation, and diastole.

28 outside the circuit were rarely activated in diastole.

29 worsening chamber function, particularly in diastole.

30 segment of the circuits was activated during diastole.

31 ation of systole and forward flow throughout diastole.

32 s of the reentrant circuits activated during diastole.

33 ch increases cardiac minute work and shorten diastole.

34 al to the circuit were also activated during diastole.

35 05), indicating a less circular shape at end-diastole.

36 s then stimulated to contract during cardiac diastole.

37 hened, and its outer limit occurred later in diastole.

38 thickness is much less than that measured in diastole.

39 ere constructed from the MRI images at early diastole.

40 mass were calculated at end-systole and end-diastole.

41 asis for generating a hydraulic force during diastole.

42 ase in ventricular chamber compliance during diastole.

43 and to measure its thickness in systole and diastole.

44 ated little change in AR orifice size during diastole.

45 ting heart, similar to the value measured at diastole.

46 of EM flowmeters showed little change during diastole.

47 2+) leak via the mutant RyR2 channels during diastole.

48 mitral valve leaflets at end systole and end diastole.

49 ith similar T1 and ECV values in systole and diastole.

50 contraction contributed to the extension of diastole.

51 more rapid rise of free Ca in the SR during diastole.

52 dequately at normal filling pressures during diastole.

53 of electrogenic Na/Ca exchanger (NCX) during diastole.

54 e to changes in luminal [Ca(2+)] seen during diastole.

55 i be sufficiently high in systole and low in diastole.

56 rough its removal of cytosolic Ca(2+) during diastole.

57 ventricular systole, both known to affect LV diastole.

58 ents in generating subcellular strain during diastole.

59 n by spontaneous calcium (Ca) release during diastole.

60 ges, after balloon inflation, at systole and diastole.

61 0.425 [0.072]; P<0.001) because of shortened diastole.

62 to acquire myocardial T1 maps in systole and diastole.

63 ganization affects SR Ca(2+) handling during diastole.

64 arful faces presented at systole relative to diastole.

65 xcursion of the leaflets from the annulus in diastole.

66 ere rated as more intense at systole than at diastole.

67 e action potential (AP) and is absent during diastole.

68 ardiac function deterioration in systole and diastole.

69 ic dysfunction, has not been well studied in diastole.

70 load and the occurrence of Ca2+ waves during diastole.

71 mferential strain rates in early systole and diastole.

72 rd-traveling decompression (suction) wave in diastole.

73 , and filling rate during the first third of diastole (1/3FR) were obtained from MPI with SPECT softw

74 cardial wall thickness increased in both end diastole (11.5 +/- 2.7 to 13.7 +/- 2.4 mm, p = 0.03) and

75 y human control subjects, E2A increased from diastole (18 degrees ) to systole (65 degrees ; p < 0.00

76 ivery: left ventricular internal diameter in diastole, +19 7% versus HZ-CTRL; P<0.05), increased atri

77 -1.8 s(-1), P:<0.0001) but increased in late diastole (2.0+/-1.3 versus 1.1+/-0.9 s(-1), P:<0.01).

78 , 29 cm2, respectively; P<0.005), RV area in diastole (21, 27, 27 cm2, respectively; P<0.005), and pu

79 al annular A-P dimension in both systole and diastole (24.3+/-2.5 to 19.7+/-2.4 mm; P<0.03; 31.0+/-3.

80 2 uW/mL 1.6; P = .03), increased during late diastole (3.9 uW/mL 4.0 vs 2.2 uW/mL 1.6; P = .03), and

81 sions (left ventricular internal diameter in diastole = -3.4 mm vs. -0.3 mm, p < 0.001 and left ventr

82 sus 4.5+/-0.5 s(-1), P:<0.0001) and in early diastole (4.9+/-2.7 versus 8.8+/-1.8 s(-1), P:<0.0001) b

83 nary flow velocity time integral occurred in diastole (69% [41%-84% ]; P=0.047).

84 gnificantly lower in the Physio group at end diastole (8.4+/-3.8, 6.7+/-2.3, and 3.4+/-0.6 mm, respec

85 eries are best displayed during mid- to late diastole (80%).

86 T1 (984 msec +/- 28 [standard deviation] in diastole, 959 msec +/- 21 in systole) and all segmental

87 antly different when measured in systole and diastole (985 +/- 26 ms vs 988 +/- 29 respectively; p =

88 Additionally, during diastole a substantially larger left ventricular posteri

89 y in early diastole [E wave] to that in late diastole [A wave]) (P = .03) and LVMI (P = .04).

90 dly with no intervening period of electrical diastole; a shock defibrillates by interacting with the

91 During diastole, AL twice crossed the virtual plane formed by t

92 D patients compared with control subjects in diastole (all P<0.05).

93 left atrial pressure and produce nonfilling diastoles, allowing measurement of fully relaxed pressur

94 hysio (23+/-11%, 24+/-7%, and 12+/-2% at end diastole and 42+/-17%, 37+/-17%, and 21+/-10% at end sys

95 increases infarct coronary flow by extending diastole and augmenting coronary driving pressure.

96 igh-frequency electrograms spanning electric diastole and completing reentrant circuits in activation

97 ity zone, extending its outer limit later in diastole and comprising an increasing component of the t

98 ardiocytes to resist changes in shape during diastole and contribute to diastolic dysfunction.

99 ed left ventricular internal diameter at end-diastole and decreased fractional shortening.

100 velocity of the mitral annulus during early diastole and decreased propagation velocity mitral inflo

101 erence in capillary blood volume between end diastole and end systole at baseline.

102 were also projected onto the MA plane at end diastole and end systole to assess PM dynamics.

103 d contours, and a correspondence between end diastole and end systole was computed with a novel algor

104 triggering performed separately at both end diastole and end systole.

105 lus and LV base-apex length increased at end-diastole and end-systole (all +1 mm, P<0.05).

106 MR severity, LV volumes at end-diastole and end-systole, and LA volumes were measured a

107 o the cardiac cycle that started during late diastole and ended during the systolic period, but which

108 ed to the AV junction only during electrical diastole and for a total of 30 seconds.

109 r sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and increased propensity to arrhythmias under s

110 ium contributes to accelerated relaxation in diastole and increased rates of force development in sys

111 tion of diameter changes between systole and diastole and is therefore preferable to standard single-

112 Reduction of LV volumes at end-diastole and LA volumes, but not LV volumes at end-systo

113 lower than during wakefulness (p < 0.001 for diastole and p < 0.01 for systole), but did not differ s

114 entifies microstructural alterations in both diastole and systole after STEMI, enabling detection of

115 systole) and all segmental T1 values between diastole and systole differed significantly (P < .001).

116 tion with other ACP nodules; and (5) leaflet diastole and systole flexure causing nodules to twist, f

117 Methods DT-CMR was performed at diastole and systole in 20 CA, 11 hypertrophic cardiomyo

118 myocardial microstructure and strain between diastole and systole in patients with dilated cardiomyop

119 pillary blood volume does not change between diastole and systole in vivo.

120 The diagnostic accuracies at diastole and systole were similar (area under the ROC cu

121 erfilament spacing was not different between diastole and systole within 1%; this was true also over

122 t ventricular function was decreased in both diastole and systole, nondipping was more prevalent, and

123 ions are 368 +/- 68 nM and 654 +/- 164 nM in diastole and systole, respectively.

124 ion and reduced left ventricular diameter at diastole and systole.

125 T(MAX)) under all conditions was observed in diastole and temporally correlated with peak annular SL

126 nchrony of cytosolic [Ca(2)(+)] decay during diastole and the impact of cardiac remodeling.

127 w much blood fills the left ventricle during diastole and thus in the etiology of heart disease.

128 e sinuses, while at the same time prolonging diastole and vasodilating with acetylcholine (ACh) to ma

129 ection fraction: 24.8% versus 6.8% (P<.001) (diastole) and 25.7% versus 5.3% (P<.001) (systole).

130 w FRET states were most populated in low Ca (diastole), and were indicative of an open, disordered st

131 ted leaflet motion has also been observed in diastole, and attributed to reduced mitral inflow.

132 lsatility index, percent time in systole and diastole, and change in vascular blood volume over a car

133 ecreases the duration of systole relative to diastole, and enhances coronary blood flow.

134 Ts, the isolated potential occurred later in diastole, and in these cases, the QRS configuration duri

135 s had increased LV dimensions in systole and diastole, and increased indexed LV mass.

136 Maximum MA area occurred in early diastole, and minimum MA area near end-diastole; maximum

137 D are better imaged in systole and others in diastole, and therefore, the dual-phase approach allows

138 tagged MRI results during systole and early diastole (apical and basal rotation, r=0.87 and 0.90, re

139 Between 1 and 3 minutes, diastole appeared primarily as the result of APD(100) sh

140 hat not all spontaneous RyR2 openings during diastole are associated with Ca(2+) sparks.

141 The two principal processes responsible for diastole are relaxation and passive pressure-volume prop

142 tex formation in the blood flow during early diastole, as measured by a dimensionless numerical index

143 cellular Ca(2+) handling in both systole and diastole, as well as mean blood pressure, were more comp

144 reflection would only be construed to be in diastole at an extrapolated age of -221 years.

145 etecting systole at the first micropulse and diastole at the last, during cuff deflation.

146 The percent diastole at which relaxation is complete was increased i

147 measured in a parasternal long-axis view, in diastole, at the level of the sinus of Valsalva.

148 al intensity and homogeneity in systole than diastole because of greater systolic myocardial thicknes

149 Coronary flow peaks in diastole because of the dominance of a "suction" wave ge

150 ich causes intervening periods of electrical diastole between fibrillation action potentials and, thu

151 n during fibrillation, leading to electrical diastole between fibrillation action potentials.

152 In end diastole, both the ostial and distal intramural sections

153 based indexes indicated resynchronization in diastole but much less in systole and had a lower dynami

154 DCM, E2A was similar to control subjects in diastole, but systolic values were markedly lower (40 de

155 unit increase in peak velocity flow in late diastole by atrial contraction (MV A Peak) indicating po

156 used on optimizing myocardial performance in diastole by control of blood pressure, restoration or ma

157 pressure and volume, and ratio of systole to diastole can all be precisely manipulated to apply hemod

158 years of age, 70% male) underwent DT-CMR in diastole, cine, late gadolinium enhancement (LGE), and e

159 ng axis area measurements during systole and diastole compared to hyperglycemic MBL-null mice.

160 open probability under conditions simulating diastole compared with channels from control hearts, sug

161 nduced aberrant transient inward currents in diastole consistent with delayed after-depolarizations.

162 decreased stored energy at the beginning of diastole contributed to these impairments.

163 rated that failure of sheetlet relaxation in diastole correlated with extracellular volume in transth

164 tolic pressure and, coupled with a shortened diastole, could adversely influence myocardial supply.

165 t, time-dependent HCN current flowing during diastole decreases for both constructs during a train of

166 ce of electrical activity in all segments of diastole defined the evidence of having had recorded the

167 rrespondingly, greater angiographic (systole-diastole) Deltaangle at the stent edge or unstented lesi

168 Diastole developed progressively from 5% of VF cycles at

169 tic pressure during the complete duration of diastole (dPR), 25% to 75% of diastole (dPR25-75), and m

170 te duration of diastole (dPR), 25% to 75% of diastole (dPR25-75), and midpoint of diastole (dPRmid),

171 75% of diastole (dPR25-75), and midpoint of diastole (dPRmid), along with Matlab calculated iFR (iFR

172 from increased actin-myosin formation during diastole due to altered tropomyosin position, which bloc

173 fluences chamber pressures early and late in diastole due to viscoelasticity, with larger net effects

174 Fibrillation cycle length and diastole duration increased, whereas APD(100) shortened

175 the left ventricular posterior wall in early diastole during both isovolumic relaxation and rapid ven

176 slower heart rate increases the duration of diastole during which AR occurs.

177 stances and volumes (strain) from successive diastoles during caval occlusion were used to evaluate L

178 diastolic pressure, resulting in nonfilling diastoles during which the LV fully relaxed at its ESV.

179 Peak mitral flow velocity in early diastole (E) increased 13.3% during the first trimester

180 ar-filling peak blood flow velocity in early diastole [E wave] to that in late diastole [A wave]) (P

181 Baseline LV sphericity at end diastole (ED) (r = 0.13, p = 0.6) did not correlate with

182 three-dimensional marker coordinates at end diastole (ED) and end systole (ES) were computed.

183 At low arousal, systole contracted while diastole expanded time, but as arousal increased, this c

184 sence or absence of intraparenchymal forward diastole flow), splenic vein thrombus, and edema.

185 e of peak regurgitant flow (usually early in diastole) for each hemodynamic state.

186 exity of calcium handling during systole and diastole has made the prediction of its release at stead

187 ulation receives its perfusion mostly during diastole; hence, an excessive decrease in diastolic pres

188 rcoplasmic reticulum Ca(2+) depletion during diastole, identifying subcellular pathophysiological alt

189 ly diastole in 32 of 35 VTs (91.4%), in late diastole in 1 (2.9%), and in systole in 2 (5.7%).

190 intenance of reentry, was activated in early diastole in 32 of 35 VTs (91.4%), in late diastole in 1

191 excessive, LV trabeculation measured in end-diastole in asymptomatic population-representative indiv

192 s old) had reversed myocardial velocities in diastole in the RV free wall, which were associated with

193 However, the inherent complexity of LV diastole, in its electrical, muscular, and hemodynamic p

194 Ts, the isolated potential occurred early in diastole; in these cases, the QRS configuration during p

195 first was over the left ventricle at the end-diastole including the aortic valve plane area, and the

196 Diastole increased from 1% of cycle length at 5 seconds

197 Between 2 and 5 minutes, diastole increased primarily as the result of increased

198 ular resistance over the wave-free period of diastole increased significantly post-TAVI (pre-TAVI, 2.

199 corresponding to ventricular filling during diastole, increases the magnitude of the Ca2+ transient;

200 as the earliest marker of awareness for low (diastole/inhalation) and a perceptual component (visual

201 y, with activity occurring primarily in late diastole into isovolumetric contraction.

202 to wave reflection moving progressively from diastole into systole.

203 ysis-unavailable state characteristic of the diastole is adjusted to the sarcomere length-dependent s

204 cardial disease but should be preserved when diastole is impaired as a result of extrinsic causes.

205 the presence of a net hydraulic force during diastole is that the atrial short-axis area (ASA) is sma

206 Diastole is the summation of processes by which the hear

207 were constructed from the MRI images at end-diastole, isovolumic systole, peak-systole and end-systo

208 ed as [(lumen area at systole--lumen area at diastole)/(lumen area at diastole x pulse pressure)] x 1

209 ever, stroke volume, LV internal diameter in diastole (LVIDd), and LV internal diameter in systole (L

210 in left ventricular internal diameter at end-diastole (LVIDd; 95% CI, -0.92 to -0.67; P = 2.3 x 10-36

211 of structural (LV internal dimension at end-diastole [LVIDd]) and functional (LV ejection fraction [

212 stole (LVW(cr/s)) and the caudal wall during diastole (LVW(ca/d)) compared to CON; this was observed

213 velocities (over 25 to 40 points during each diastole) matched for each steady state.

214 early diastole, and minimum MA area near end-diastole; maximum area reduction was 12+/-1% (P< or =.00

215 cardial relaxation gradients at the onset of diastole may have a physiologic significance in facilita

216 The population diastole MDS was determined and two groups established (

217 e plane (n = 7), and loss of contrast during diastole (n = 5).

218 ymmetry caused the rise in [Ca(2+) ]m during diastole observed at elevated stimulation frequencies.

219 al and time-averaged AR orifice areas during diastole obtained by EM flowmeters ranged from 0.06 to 0

220 hich correlate respectively with systole and diastole of this multichambered heart.

221 -fixed region of interest (ROI) drawn at end-diastole, often underestimates the left ventricular ejec

222 e either just before electrical stimulation (diastole), or at the peak of the contraction (systole);

223 p = 0.012) and the degree of septal shift in diastole (p = 0.004) were predictors of a composite end

224 f heart rate and acquisition mode on FWHM at diastole (p-values < 0.001).

225 pectively, with insignificant differences at diastole (p-values < 0.01).

226 ansplantation recipient (all required atrial diastole pacing).

227 In diastole, patients had reduced and delayed untwisting, r

228 ause coronary perfusion occurs mainly during diastole, patients with coronary artery disease (CAD) co

229 to the base), and torsional recoil in early diastole (phi(5%), first 5% of filling) for each LV free

230 ble for reuptake of cytosolic calcium during diastole, plays a central role in the molecular mechanis

231 tio of passive filling to atrial kick during diastole, potentially as a result of increased mitral in

232 discriminating between systole-entrained and diastole-presented stimuli in a separate interoceptive a

233 quickly clears Ca under the cell membrane in diastole, preventing premature releases.

234 t end-systole (r = 0.91, p < 0.0001) and end-diastole (r = 0.86, p < 0.0001).

235 l with segmental myocardial T1 (R = 0.73 for diastole, R = 0.72 for systole).

236 ntricular filling tends to decrease in early diastole, reducing the mitral ratio of peak early to lat

237 in resistance to ventricular filling during diastole resulting from the prolonged force and Ca(2+) t

238 s, which causes incomplete relaxation during diastole resulting in hypertrophy and sarcomeric disarra

239 eanwhile, LV pressure was reduced throughout diastole resulting in significant and consistent elevati

240 he aged heart but rise rapidly during atrial diastole, resulting in a higher late atrial pressure and

241 cover to their previous levels at the end of diastole, resulting in a smaller SR Ca2+ release and AP

242 measurements of WT twitching muscles during diastole revealed stretch-induced increases in the inten

243 culated using volumetric measurements at end diastole ([right atrial+atrialized right ventricular vol

244 During ventricular diastole shocks as low as 10 V produced ventricular exci

245 imiting energy loss during repeated stretch (diastole)-shortening (systole) cycles of the heart.

246 ascular reserve over the wave-free period of diastole significantly improved post-TAVI (pre-TAVI 1.88

247 +) concentration be reduced to low levels in diastole so that the ventricle can relax and refill with

248 ion ([Ca(2+) ]i ) must be sufficently low in diastole so that the ventricle is relaxed and can refill

249 ea, randomized jet ventilation (systole- and diastole-synchronized); b) postjet ventilation apnea, be

250 ial movement of the myosin motors during the diastole-systole cycle under sarcomere length control.

251 d the rate of Ca(i) transient decline during diastole (tauCa).

252 patients showed significantly greater E2A in diastole than control subjects did (48 degrees ; p < 0.0

253 MPR was greater in diastole than systole in all segment groups (P < .05).

254 Stress MBF was greater in diastole than systole in normal, remote, and stenosis-de

255 imates of stress MBF and MPR were greater in diastole than systole in patients with and patients with

256 oss the belly region at midsystole and early diastole, the CC curvature of the AML along the M(CC) fl

257 During diastole, the heart fills with blood and the heart chamb

258 As the heart fills with blood during diastole, the myocardium is stretched and oxidants are p

259 This article reviews the physiology of diastole, the pathogenesis of diastolic heart failure, a

260 trength and timing of each heartbeat, and at diastole, the period between heartbeats when barorecepto

261 e percent change in the cavity area from end diastole to end systole (fractional area change [FAC]),

262 vers during phase 3 repolarization and early diastole to initial values.

263 The percent change in leaflet width from diastole to systole (% delta W), an index of the contrib

264 ynamic reorientation of sheetlets (E2A) from diastole to systole during myocardial thickening, and ma

265 Sphericity change from diastole to systole was also significantly reduced in MR

266 the normal decrease in tethering length from diastole to systole was eliminated (P < 0.01).

267 Lateral shortening of the IPMD from diastole to systole was severely reduced in patients wit

268 e interpapillary muscle distance (IPMD) from diastole to systole, and adversely affect mitral valve g

269 o activate contraction and then fall, during diastole, to allow the myofilaments to relax and the hea

270 f intracellular Ca(2+) concentrations during diastole, together with the appearance of spontaneous Ca

271 olic -diastolic at same volume) during early diastole (UNCOUP_ED) and late diastole (UNCOUP_LD).

272 ) during early diastole (UNCOUP_ED) and late diastole (UNCOUP_LD).

273 e sections which covered systole and most of diastole using twelve equally incremented time points th

274 a(2+) stores depolarizes the membrane during diastole via activation of the Na(+)-Ca(2+) exchanger.

275 he entry of Ca2+ into the cell occurs during diastole (via Na+-Ca2+ exchange) rather than in systole

276 hological response compared with overload in diastole (volume overload).

277 unctional MR, reduction in LV volumes at end-diastole was associated with degree of residual MR at 12

278 LV internal dimension in diastole was increased in PTU-S and PTU-L rats, but only

279 The area of the coronary sinus during diastole was larger in the atrial fibrillation group tha

280 Coronary artery blood flow velocity (BFV) in diastole was not different but left pulmonary artery BFV

281 e of antegrade pulmonary artery flow in late diastole was present in 38% of the patients.

282 Interestingly, the duration of diastole was prolonged with LV support.

283 NC (noncompacted/compacted ratio >2.3 in end-diastole) was confirmed in all patients.

284 In addition, MR angiography (in systole and diastole) was repeated in those 10 subjects after reposi

285 Measures of IVS cross-sectional area at diastole were a strong proxy for the 3-dimensional volum

286 mation during early (E(SR)) and late (A(SR)) diastole were comparable between stunned and remote wall

287 nd torsional profiles throughout systole and diastole were compared with those by tagged MRI at isoch

288 strain and strain rate of the early phase of diastole were improved in BNP-treated compared with untr

289 yocardial T1 distribution characteristics in diastole were similar to those in systole.

290 series reconstructed at end systole and end diastole were used to measure LV-LAS.

291 racings for a given ventricle at systole and diastole) were quantified and compared by using paired t

292 Coronary blood flow peaks in diastole when aortic blood pressure has fallen.

293 e brain that the heart has contracted, or in diastole when baroreceptors are silent.

294 osure time was defined as the time after end diastole when the distance between leaflet edge markers

295 oreceptors fire signals to the brain, and to diastole, when the heart relaxes, and baroreceptors are

296 During diastole, when the mitral leaflets are slack and unstres

297 rimarily manifests as defects in relaxation (diastole) while preserving contractile performance.

298 ally from the lateral right atrium, scanning diastole with a 10-ms decrement until AT termination or

299 tole--lumen area at diastole)/(lumen area at diastole x pulse pressure)] x 1000, was compared between

300 l wall thickness (interventricular septum in diastole Z value, +0.45 +/- 0.49, P < 0.001) and more di