ライフサイエンスコーパス: systole

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

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

3 ytosolic calcium during cardiac contraction (systole).

4 all ages, reflection times were well within systole.

5 tion moving progressively from diastole into systole.

6 ventricular wall and work production during systole.

7 and increased rates of force development in systole.

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

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

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

11 prevent leakage through the AV valves during systole.

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

13 in carotid pressure and aortic flow in early systole.

14 rmed separately at both end diastole and end systole.

15 in carotid pressure and aortic flow in early systole.

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

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

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

19 ress occurring at peak instead of isovolumic systole.

20 eptal shift, and prolonged right ventricular systole.

21 eptal shift, and prolonged right ventricular systole.

22 duced by changes in the absolute duration of systole.

23 strains was linear during the first half of systole.

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

25 are stretched rather than contracted during systole.

26 ts contract uniformly with no stretch during systole.

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

28 valve to intrabeat variation of flow during systole.

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

30 concentrations found intracellularly at peak systole.

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

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

33 89+/-3% of area reduction occurred before LV systole.

34 nt of myocardial deformation (strain) during systole.

35 ximally originating deceleration wave during systole.

36 eptal shift, and prolonged right ventricular systole.

37 uct of force and annulus displacement during systole.

38 ristics in diastole were similar to those in systole.

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

40 he dicrotic notch and retrograde flow at end systole.

41 aortic valve dynamics and blood flow during systole.

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

43 e balance between Ca entry and efflux during systole.

44 lets into the left atrium during ventricular systole.

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

46 the coronary sinus contraction during atrial systole.

47 -14 versus 19+/-11% of systole, time to peak systole 115+/-16% versus 97+/-19% (P< or =0.01), indicat

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

49 , 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

50 /- 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

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

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

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

54 01 and left ventricular internal diameter in systole = -4.0 mm vs. -0.7 mm, p < 0.001) and improvemen

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

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

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

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

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

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

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

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

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

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

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

66 <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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 brosis and cardiac function deterioration in systole and diastole.

82 educed circumferential strain rates in early systole and diastole.

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

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

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

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

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

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

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

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

91 Total electromechanical systole and left ventricular ejection time were shortene

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 (10.3 versus 6.4 mm, MR versus no-MR, at end-systole) and increased r of the anterior papillary muscl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 91.4%), in late diastole in 1 (2.9%), and in systole in 2 (5.7%).

151 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 Stimulation delivered during early systole inhibited blood pressure increases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 +/- 68 nM and 654 +/- 164 nM in diastole and systole, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

214 5+/-0.12 mm toward the mitral annulus at end systole; the posterior papillary muscle geometry was unc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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