ライフサイエンスコーパス: diastole

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

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

3 asis for generating a hydraulic force during diastole.

4 HFNEF is not an isolated disorder of diastole.

5 rogeneity of regional myocardial flow during diastole.

6 ated normalized ventricular elastance at end diastole.

7 asurement of balloon luminal pressure at end diastole.

8 mitral valve leaflets at end systole and end diastole.

9 t of global cardiac mechanics in systole and diastole.

10 ating active restoration of the LV cavity in diastole.

11 alized ventricular elastance at arterial end diastole.

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

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

14 and sphericity index at end-systole and end-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 of electrogenic Na/Ca exchanger (NCX) during diastole.

21 cite cells during the periods of depolarized diastole.

22 to the central aorta in systole rather than diastole.

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

24 action potential and during the depolarized diastole.

25 action, ejection, isovolumic relaxation, and diastole.

26 action, ejection, isovolumic relaxation, and diastole.

27 blood flow velocity during late systole and diastole.

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

29 outside the circuit were rarely activated in diastole.

30 worsening chamber function, particularly in diastole.

31 segment of the circuits was activated during diastole.

32 ation of systole and forward flow throughout diastole.

33 s of the reentrant circuits activated during diastole.

34 ch increases cardiac minute work and shorten diastole.

35 al to the circuit were also activated during diastole.

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

37 s then stimulated to contract during cardiac diastole.

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

39 thickness is much less than that measured in diastole.

40 ere constructed from the MRI images at early diastole.

41 mass were calculated at end-systole and end-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 rough its removal of cytosolic Ca(2+) during diastole.

48 ventricular systole, both known to affect LV diastole.

49 ents in generating subcellular strain during diastole.

50 ptor afferent firing is maximal, relative to diastole.

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

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

53 0.425 [0.072]; P<0.001) because of shortened diastole.

54 those without LBBB during early but not late diastole.

55 to acquire myocardial T1 maps in systole and diastole.

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

57 arful faces presented at systole relative to diastole.

58 xcursion of the leaflets from the annulus in diastole.

59 coincide with either the cardiac systole or diastole.

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

61 ardiac function deterioration in systole and diastole.

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

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

64 mferential strain rates in early systole and diastole.

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

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

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

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

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

70 -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).

71 , 29 cm2, respectively; P<0.005), RV area in diastole (21, 27, 27 cm2, respectively; P<0.005), and pu

72 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.

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

74 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Diastole developed progressively from 5% of VF cycles at

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

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

145 75% of diastole (dPR25-75), and midpoint of diastole (dPRmid), along with Matlab calculated iFR (iFR

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 to wave reflection moving progressively from diastole into systole.

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

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

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

175 Diastole is the summation of processes by which the hear

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

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

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

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

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

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

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

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

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

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

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

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

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

189 ansplantation recipient (all required atrial diastole pacing).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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