ライフサイエンスコーパス: systole

1 ytosolic calcium during cardiac contraction (systole).

2 ) (diastole) and 25.7% versus 5.3% (P<.001) (systole).

3 dial T1 (R = 0.73 for diastole, R = 0.72 for systole).

4 occurring from control to ring state at end-systole.

5 the coronary sinus contraction during atrial systole.

6 all ages, reflection times were well within systole.

7 tion moving progressively from diastole into systole.

8 ventricular wall and work production during systole.

9 n, and wall thickening up to 14% during peak systole.

10 and increased rates of force development in systole.

11 luated by frame-by-frame analysis throughout systole.

12 toperative MR was LV sphericity index at end-systole.

13 prevent leakage through the AV valves during systole.

14 al sides of the mitral valve (MV) during mid systole.

15 in carotid pressure and aortic flow in early systole.

16 rmed separately at both end diastole and end systole.

17 in carotid pressure and aortic flow in early systole.

18 of stress in the LVA border zone (BZ) during systole.

19 le, isovolumic systole, peak-systole and end-systole.

20 alculated from 3-D marker coordinates at end-systole.

21 ress occurring at peak instead of isovolumic systole.

22 at Ca(2+) levels in the dyadic cleft during systole.

23 duced by changes in the absolute duration of systole.

24 strains was linear during the first half of systole.

25 e balance between Ca entry and efflux during systole.

26 ivers a 65-mL pneumatic pulse during cardiac systole.

27 are stretched rather than contracted during systole.

28 ts contract uniformly with no stretch during systole.

29 valve to intrabeat variation of flow during systole.

30 hought to occur during left ventricular (LV) systole.

31 concentrations found intracellularly at peak systole.

32 ystole with minimum MA area occurring at end-systole.

33 from the center of the LVOT at time t during systole.

34 89+/-3% of area reduction occurred before LV systole.

35 ne strains throughout the leaflet surface at systole.

36 nsorimotor oscillations were stronger during systole.

37 V) to pump blood into the circulation during systole.

38 ed left ventricular diameter at diastole and systole.

39 etween Ca(2+) entry and Ca(2+) efflux during systole.

40 eptal shift, and prolonged right ventricular systole.

41 eptal shift, and prolonged right ventricular systole.

42 s and leaflets were computed at mid- and end-systole.

43 nt of myocardial deformation (strain) during systole.

44 ximally originating deceleration wave during systole.

45 eptal shift, and prolonged right ventricular systole.

46 uct of force and annulus displacement during systole.

47 ristics in diastole were similar to those in systole.

48 plasmic reticulum (SR) Ca(2+) release during systole.

49 he dicrotic notch and retrograde flow at end systole.

50 aortic valve dynamics and blood flow during systole.

51 from the Sarcoplasmic Reticulum (SR) during systole.

52 ing (re-reflected) decompression wave in mid-systole.

53 lets into the left atrium during ventricular systole.

54 -14 versus 19+/-11% of systole, time to peak systole 115+/-16% versus 97+/-19% (P< or =0.01), indicat

55 aortic valves, minimum diameter increased in systole (12.3 +/- 7.3% and 9.8 +/- 3.4%, respectively; p

56 , Duran, and Physio; ANOVA=0.005) and at end systole (14.5+/-6.2, 10.5+/-5.5, and 5.8+/-2.5 mm, respe

57 /- 2.7 to 13.7 +/- 2.4 mm, p = 0.03) and end systole (16.1 +/- 2.9 to 18.5 +/- 1.8 mm, p = 0.03), imp

58 t the endocardium than the epicardium at end systole (24+/-5% versus 16+/-3%; P<0.05, n=8), consisten

59 MVGs were reduced in FRDA during systole (3.1+/-1.2 versus 4.5+/-0.5 s(-1), P:<0.0001) an

60 very large backward compression wave during systole (38 +/- 11% vs. 21 +/- 6%; p < 0.001) and a prop

61 01 and left ventricular internal diameter in systole = -4.0 mm vs. -0.7 mm, p < 0.001) and improvemen

62 cous energy dissipation was increased during systole (5.7 uW/mL 3.0 vs 4.2 uW/mL 1.6; P = .03), incre

63 E2A increased from diastole (18 degrees ) to systole (65 degrees ; p < 0.001; E2A mobility = 45 degre

64 ), pulsatile flow (i.e., reversal of flow in systole, a marker of heightened microvascular resistance

65 In systole, AAOCA with intramural segment showed a flatteni

66 ostructural alterations in both diastole and systole after STEMI, enabling detection of MI presence a

67 jection velocity peaked in the first half of systole; after successful treatment, it peaked in the se

68 pex length increased at end-diastole and end-systole (all +1 mm, P<0.05).

69 ment, particularly intercommissural, in late-systole (all P<0.05).

70 n and compliance (LA peak v pressure) and LV systole--all vis a fronte factors.

71 occurring from control to ring state at end-systole along the annulus were calculated.

72 unique pattern, with peaks in early and late systole and a midsystolic decrease.

73 ction and saddle-shape accentuation in early systole and abnormal enlargement, particularly intercomm

74 the mitral leaflets of more than 2 mm during systole and as a maximal leaflet thickness of at least 5

75 ic pattern with two peaks at early- and late-systole and decrease in mid-systole was noticed in 57 pa

76 <0.01), mitral annular A-P dimension in both systole and diastole (24.3+/-2.5 to 19.7+/-2.4 mm; P<0.0

77 not significantly different when measured in systole and diastole (985 +/- 26 ms vs 988 +/- 29 respec

78 allows depiction of diameter changes between systole and diastole and is therefore preferable to stan

79 short and long axis area measurements during systole and diastole compared to hyperglycemic MBL-null

80 s, the complexity of calcium handling during systole and diastole has made the prediction of its rele

81 rade beat, which correlate respectively with systole and diastole of this multichambered heart.

82 rotational and torsional profiles throughout systole and diastole were compared with those by tagged

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

84 ndocardial tracings for a given ventricle at systole and diastole) were quantified and compared by us

85 /area of PM heads, and bifid PM mobility (in systole and diastole).

86 s such as pulsatility index, percent time in systole and diastole, and change in vascular blood volum

87 SCA patients had increased LV dimensions in systole and diastole, and increased indexed LV mass.

88 y, and intracellular Ca(2+) handling in both systole and diastole, as well as mean blood pressure, we

89 he assessment of global cardiac mechanics in systole and diastole.

90 tid arterial blood flow velocity during late systole and diastole.

91 gonal planes and to measure its thickness in systole and diastole.

92 associated with similar T1 and ECV values in systole and diastole.

93 oroscopy images, after balloon inflation, at systole and diastole.

94 ce was used to acquire myocardial T1 maps in systole and diastole.

95 brosis and cardiac function deterioration in systole and diastole.

96 educed circumferential strain rates in early systole and diastole.

97 sure 3-dimensional transmural strains during systole and diastolic filling, at 1 and 12 weeks postope

98 ly correlated with tagged MRI results during systole and early diastole (apical and basal rotation, r

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

100 origins of the mitral valve leaflets at end systole and end diastole.

101 es in LV volumes and sphericity index at end-systole and end-diastole.

102 Volume and mass were calculated at end-systole and end-diastole.

103 es at end-diastole, isovolumic systole, peak-systole and end-systole.

104 excitability were found to be highest during systole and following stronger neural responses to heart

105 cycle, resulting in apparent prolongation of systole and forward flow throughout diastole.

106 synchronization in diastole but much less in systole and had a lower dynamic range and higher intrasu

107 Total electromechanical systole and left ventricular ejection time were shortene

108 uires that [Ca(2+)]i be sufficiently high in systole and low in diastole.

109 s to paradoxical expansion of the annulus in systole and may often be associated with mitral valve pr

110 T, with images aquired simultaneously at end systole and middiastole.

111 iods of cardiac motion identified during end systole and middiastole.

112 entricular transverse sections which covered systole and most of diastole using twelve equally increm

113 th ventricles at twelve time points covering systole and most of diastole.

114 rtain structures in CHD are better imaged in systole and others in diastole, and therefore, the dual-

115 l strain pattern with distinct peaks pre-end-systole and post-end-systole in inferior-lateral wall wa

116 al (LA) relaxation and left ventricular (LV) systole and relaxation (vis a fronte) have been suggeste

117 more gradual developments of tension during systole and relaxation during diastole.

118 vealed that the troponin-T mutation prolongs systole and restricts diastolic dimensions of the heart,

119 Plaque stretch at systole and stretch variation during one cardiac cycle w

120 creases by approximately 30% at the start of systole and that there is no evidence of spacial heterog

121 tand the significance of an effective atrial systole and the interactions between atrial and ventricu

122 Four geometric parameters at systole and their variation during balloon deflation and

123 d deviation] in diastole, 959 msec +/- 21 in systole) and all segmental T1 values between diastole an

124 (10.3 versus 6.4 mm, MR versus no-MR, at end-systole) and increased r of the anterior papillary muscl

125 lary muscle distance (IPMD) from diastole to systole, and adversely affect mitral valve geometry and

126 olic blood pressure, right ventricle area at systole, and declined 6-minute walk distance in 410 SCD

127 severity, LV volumes at end-diastole and end-systole, and LA volumes were measured at baseline, disch

128 displaced from SERCA by high calcium during systole, and relief of functional inhibition does not re

129 hases: a) apnea, randomized jet ventilation (systole- and diastole-synchronized); b) postjet ventilat

130 V diastolic function and geometry and atrial systole are better preserved in the total AV transplanta

131 contractility and shortening of ventricular systole are characteristic of systolic heart failure and

132 ming of myocardial activation in ventricular systole are not well understood.

133 ascending aorta, based on maximum values at systole at a single location, denoted max, and a 'peak m

134 ry blood volume between end diastole and end systole at baseline.

135 lic and diastolic pressures; hence detecting systole at the first micropulse and diastole at the last

136 frank reversal of contrast-dye motion during systole) at 60 min after fibrinolytic administration was

137 amber, 2-chamber, and long axis views at mid-systole before and 3 to 10 days after surgery.

138 lengthen when LV pressure rises during early systole before onset of systolic shortening.

139 Peak myocardial stress occurs in early systole, before important contributions of reflected wav

140 d serial changes in regional geometry at end systole.Beginning as a narrow band of fully perfused hyp

141 was used to rapidly clamp LA pressure during systole below the level of the succeeding LV diastolic p

142 septal shift and prolonged right ventricular systole, both known to affect LV diastole.

143 f mitral valve prolapse predominates in late systole but may be holosystolic or purely mid-late systo

144 ess (p < 0.001 for diastole and p < 0.01 for systole), but did not differ significantly between rapid

145 These are inseparable in systole, but restricted leaflet motion has also been obs

146 mated the maximum velocity magnitude at peak systole by [Formula: see text].

147 d, independent readers on cine images in end systole by using a freely available software package.

148 Resynchronization of systole can be achieved for patients with normal QRSd an

149 e (left ventricular maximum elastance at end systole), cardiac output, circumflex artery blood flow,

150 During electrical systole, cardiomyocytes are refractory right after the o

151 ed for blood flow deceleration at the end of systole, causing AV closure, and is correlated with LV i

152 diminished accelerating wave energy in early systole compared with the reference group.

153 [Ca2+]SR dropped to 0.3 to 0.5 mmol/L during systole, consistent with a role for declining [Ca2+]SR i

154 At low arousal, systole contracted while diastole expanded time, but as

155 ent of the myosin motors during the diastole-systole cycle under sarcomere length control.

156 ring repeated stretch (diastole)-shortening (systole) cycles of the heart.

157 erance with elevated insulin levels, cardiac systole deficits, left ventricle hypertrophy, a predicto

158 ent change in leaflet width from diastole to systole (% delta W), an index of the contribution of dyn

159 Correspondingly, greater angiographic (systole-diastole) Deltaangle at the stent edge or unsten

160 Heart rate and length of systole did not differ between the two groups.

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

162 myocardial stretching and contraction during systole diminished (P=0.001).

163 S) restricts the aortic valve opening during systole due to calcification and fibrosis of either a co

164 l time (32-64 Hertz) or triggered 1:1 at end systole during a 20% C3 or C3C4 droplet infusion.

165 es of cardiac function, including sustaining systole during ejection, the heart-rate dependence of th

166 entation of sheetlets (E2A) from diastole to systole during myocardial thickening, and markers of tis

167 li presented before and during early cardiac systole elicited differential changes in neural activity

168 cts who are at-chance discriminating between systole-entrained and diastole-presented stimuli in a se

169 erved that dominance durations increased for systole-entrained stimuli, inconsistent with the Barorec

170 End-systole (ES) radial and longitudinal strain images were

171 ker coordinates at end diastole (ED) and end systole (ES) were computed.

172 from 3-dimensional marker coordinates at end-systole (ES).

173 the annulus increased only 9.2+/-6.3% at end systole (ES).

174 nent (visual awareness negativity) for high (systole/exhalation) BR activity, indicating that BR sign

175 er ACP nodules; and (5) leaflet diastole and systole flexure causing nodules to twist, fold their enc

176 ntra-aortic balloon pump (IABP) triggered at systole for 3 hours, then deactivated (n=11); (2) IABP a

177 were significantly (all P < .05) greater in systole for the right atrium (CNR, 8.9 vs 7.5; image qua

178 in the cavity area from end diastole to end systole (fractional area change [FAC]), was related to c

179 es, but a decrease in the duration of atrial systole from early to later stages.

180 decreased the peak of Ca(2+) release during systole, gradually overloading the sarcoplasmic reticulu

181 Ejection after end systole has a positive effect on ventricular performance

182 surements of Doppler parameters of the early systole have substantial intrinsic variability.

183 central aorta and augments pressure in late systole [ie, augmentation index = (augmented pressure/pu

184 91.4%), in late diastole in 1 (2.9%), and in systole in 2 (5.7%).

185 Methods DT-CMR was performed at diastole and systole in 20 CA, 11 hypertrophic cardiomyopathy, and 10

186 to 24.7+/-2.1 mm; P<0.001), and MVTa at mid systole in all 3 planes (153+/-46 to 93+/-24 mm2, P<0.01

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

188 le and LA volumes, but not LV volumes at end-systole in degenerative MR, is consistent with correctio

189 ular dynamics showed stable valvular area in systole in FED versus considerable systolic increased ar

190 eight and volume increased little throughout systole in FED versus marked increase in DMD (P<0.001).

191 distinct peaks pre-end-systole and post-end-systole in inferior-lateral wall was frequent in patient

192 Stress MBF was greater in diastole than systole in normal, remote, and stenosis-dependent segmen

193 ss MBF and MPR were greater in diastole than systole in patients with and patients without CAD.

194 crostructure and strain between diastole and systole in patients with dilated cardiomyopathy relative

195 he cardiac Ca pump, mediates abbreviation of systole in response to beta-adrenergic agonists.

196 the mitral annulus dilating rapidly in early systole in response to rising ventricular pressure.

197 Nested helical flow was seen at peak systole in the ascending aorta of 15 of 20 patients with

198 volume does not change between diastole and systole in vivo.

199 , are necessary for terminating contraction (systole) in aged animals, where their loss culminates in

200 h continuously and intermittently (every end systole) in the fundamental (2 MHz) and harmonic (transm

201 nges in MA size and shape coincident with LA systole included area reduction and shape change prior t

202 t, left ventricular maximum elastance at end systole increased and was unchanged in controls (30 +/-

203 LV internal diameter in systole increased by 40% in PTU-S and 86% in PTU-L.

204 a coronary sinus constriction during atrial systole, indicating that coronary sinus-right atrium mus

205 Stimulation delivered during early systole inhibited blood pressure increases.

206 -based active force that is developed during systole is harnessed by titin, allowing for elastic dias

207 The PSS (contraction after the end of systole) is a sensitive marker of ischemia; however, inc

208 thickened and redundant mitral valve during systole, is a relatively frequent abnormality in humans

209 conformational changes in troponin C during systole leading to sensitization of the contractile appa

210 ted border zone fiber stresses from mean end-systole levels of 28.2 kPa (control) to 23.3 kPa (treatm

211 The CDI, defined as [(lumen area at systole--lumen area at diastole)/(lumen area at diastole

212 iastole (LVIDd), and LV internal diameter in systole (LVIDs) indices were similar.

213 Left ventricular internal diameter during systole (LVIDs) was decreased in SCI females more than i

214 ased thickness of the LV cranial wall during systole (LVW(cr/s)) and the caudal wall during diastole

215 ontours were automatically propagated to end systole, mean differences were 2.0 g +/- 3.6 (P =.05) an

216 cation, including loss of correlation during systole (n = 12), shadow regions (n = 8), a short vessel

217 ents were significantly (P < .05) greater in systole (narrowest point of arch, 70 vs 53 mm(2); descen

218 function was decreased in both diastole and systole, nondipping was more prevalent, and pulse pressu

219 caused by abnormal anterior position during systole of the anterior mitral valve leaflet.

220 pulsatile flow, whereas passing WSS at peak systole of the pulsatile flow waveform does.

221 ixel transitions from blood to tissue during systole on a frame-by-frame basis.

222 ft ventricular endocardial motion throughout systole on a frame-by-frame basis.

223 The influences of left atrial (LA) and LV systole on MA size and shape, however, remain debated.

224 ance of the timing of atrial and ventricular systole on the hemodynamic response during supraventricu

225 ne, without inhibiting Ca(2+) release during systole or affecting Ca(2+) release in normal healthy he

226 resented to coincide with either the cardiac systole or diastole.

227 inus narrowed 26% from middiastole to atrial systole (P < .0001).

228 Early in systole, parts of the left ventricle are being stretched

229 m the MRI images at end-diastole, isovolumic systole, peak-systole and end-systole.

230 Thus, LA systole plays a pivotal role in MA size reduction and sh

231 ial pressure during the start of ventricular systole; point 3, peak of atrial filling (v wave); point

232 Overloading the left ventricle in systole (pressure overload) is associated with a distinc

233 between diameter and volume was good at end-systole (r = 0.91, p < 0.0001) and end-diastole (r = 0.8

234 ick filament makes the energetic cost of the systole rapidly tuned to the mechanical task, revealing

235 ed wave then returns to the central aorta in systole rather than diastole.

236 ial contractility, decreases the duration of systole relative to diastole, and enhances coronary bloo

237 s were greater to fearful faces presented at systole relative to diastole.

238 Systole remained short at faster heart rates; thus, cMyB

239 and 42+/-17%, 37+/-17%, and 21+/-10% at end systole, respectively, for Control, Duran, and Physio, r

240 +/- 68 nM and 654 +/- 164 nM in diastole and systole, respectively.

241 unable to coapt correctly during ventricular systole resulting in mitral regurgitation, and it is ass

242 tion of intramyocardial blood vessels during systole results in an abnormally large backward compress

243 itudinal strain rates were calculated during systole (S(SR)), isovolumic relaxation (IVR(SR)), and ra

244 iastole), or at the peak of the contraction (systole); sarcomere length (SL) was held constant throug

245 O) increased Ca2+ transient amplitude during systole, sarcoplasmic reticulum (SR) Ca2+ load and the o

246 ith near-simultaneous atrial and ventricular systole, short-RP tachycardia (RP<PR), and long-RP tachy

247 ased on spatially averaged local flow during systole showed substantial heritability ([Formula: see t

248 (_ES); slope of -volume relationship during systole (Sslope); end-systolic peak (peak ); and diastol

249 During systole, stimuli were detected and correctly localized l

250 High FRET states increased with Ca (systole), suggesting rigidly closed conformations for th

251 ore easily and were rated as more intense at systole than at diastole.

252 ater myocardial intensity and homogeneity in systole than diastole because of greater systolic myocar

253 uring closely coupled atrial and ventricular systole than during long-RP tachycardia (P:<0.05).

254 ing an acute relief of excess compression in systole that likely benefits subendocardial perfusion.

255 acute ischemic mitral regurgitation, at end systole, the anterolateral edge of the central scallop w

256 For 120-V shocks delivered late in systole, the depolarization sequence produced by the sho

257 5+/-0.12 mm toward the mitral annulus at end systole; the posterior papillary muscle geometry was unc

258 ally elliptic, assumes a more round shape in systole, thus increasing CSA without substantial change

259 t of contraction 53%+/-14 versus 19+/-11% of systole, time to peak systole 115+/-16% versus 97+/-19%

260 ata measured at normalized time (tN) and end systole (tmax) to predict intercept: Vo(SB) = [EN(tN) x

261 entration ([Ca(2+) ]i ) must increase during systole to activate contraction and then fall, during di

262 ed onto the MA plane at end diastole and end systole to assess PM dynamics.

263 d-systolic pressure and volume, and ratio of systole to diastole can all be precisely manipulated to

264 t-specific dynamic compression mainly in the systole under resting conditions.

265 Baroreceptor discharge at ventricular systole underpins afferent signalling of cardiovascular

266 Crypts tended to narrow in systole, varying slightly in size, shape- and number, wi

267 stole (via Na+-Ca2+ exchange) rather than in systole (via the L-type Ca2+ current).

268 val: 130 to 141 ms) and the mean duration of systole was 328 ms (99% confidence interval: 310 to 347

269 These presystolic changes vanished when LA systole was absent (LV pacing).

270 Sphericity change from diastole to systole was also significantly reduced in MR patients.

271 correspondence between end diastole and end systole was computed with a novel algorithm.

272 ecrease in tethering length from diastole to systole was eliminated (P < 0.01).

273 a relative counterclockwise rotation during systole was followed by a relative clockwise rotation of

274 In the FG041 group, LV area in systole was less (P<0.05), the dP/dt(max) after isoprote

275 The total electromechanical systole was measured from the onset of the electrocardio

276 The smallest A(LVOT) during systole was measured using anatomically oriented two-dim

277 early- and late-systole and decrease in mid-systole was noticed in 57 patients.

278 eral shortening of the IPMD from diastole to systole was severely reduced in patients with moderate/s

279 d in the in vitro model, ESA was more rapid, systole was shortened, EDV was decreased, and PSV was in

280 LV volumes at end-systole was significantly reduced in functional MR but n

281 tretch experienced by the MV leaflet at peak systole was substantially reduced when referred to the c

282 The changes in total [Ca2+] during systole were obtained using measurements of the intracel

283 The diagnostic accuracies at diastole and systole were similar (area under the ROC curve = 0.79 an

284 free wall curvature (C(FW)) measured at end systole were used to derive the curvature ratio (C(IVS)/

285 ula: see text]-ATP peaks was best during end-systole when blood contamination of ATP and Pi signals w

286 e-driven misidentification of weapons during systole, when baroreceptor afferent firing is maximal, r

287 ating whether pulses occurred during cardiac systole, when baroreceptors signal to the brain that the

288 At the peak of systole, when bound to the extensively activated cTF, NT

289 In contrast, during systole, when developed intraventricular pressure disten

290 ere presented to human volunteers at cardiac systole, when ejection of blood from the heart causes ar

291 ts, stimulus presentation was time-locked to systole, when the heart contracts and baroreceptors fire

292 (approximately 53%) increase in force during systole, which may help to partly compensate for diastol

293 ole in limiting full aortic expansion during systole, which modulates left ventricular performance an

294 he aortic valve plane toward the apex during systole, which results in improper inclusion of aortic c

295 er, all MA area reduction occurred during LV systole with minimum MA area occurring at end-systole.

296 about the dynamic SAM-septal relation during systole, with A(LVOT) ranging from 0.6 to 5.2 cm(2) (mea

297 eft ventricular volume reduction (VR) at end systole, with EDV kept constant.

298 acing was not different between diastole and systole within 1%; this was true also over a wide range

299 yocardial stress typically occurred in early systole (within the first 100 milliseconds of ejection),

300 Integrating over systole yielded total TKEsys and by normalizing for stro