ライフサイエンスコーパス: afterload

1 diuresis, while reducing cardiac preload and afterload.

2 in the clinical context of acute increase in afterload.

3 complete reverse remodeling after decreasing afterload.

4 nd fractional shortening and above normal LV afterload.

5 rtension is due strictly to the increased RV afterload.

6 that of wild type hearts, especially at high afterload.

7 cardiac hypertrophy in response to increased afterload.

8 onically raising the lymphatic smooth muscle afterload.

9 and relaxation delay from increased arterial afterload.

10 at greatest risk for abnormalities of FS and afterload.

11 in isolation as an index of left ventricular afterload.

12 y inflated to increase left ventricular (LV) afterload.

13 odilator that can decrease right ventricular afterload.

14 ripheral vasoconstriction is contributing to afterload.

15 tionship to a zone of high contractility for afterload.

16 dysfunction with increased left ventricular afterload.

17 function due to increased right ventricular afterload.

18 is a resultant increase in left ventricular afterload.

19 icular afterload and not to left ventricular afterload.

20 mediated primarily by an increase in cardiac afterload.

21 over time as the RV adapts to the increased afterload.

22 asingly used as an index of left ventricular afterload.

23 n (EF) decreased secondary to an increase in afterload.

24 monly falls because of a concomitant rise in afterload.

25 idered the classic index of left ventricular afterload.

26 ng stress, at least in part, by manipulating afterload.

27 m examination, despite a progressive fall in afterload.

28 ntricular performance is highly sensitive to afterload.

29 d negatively with baseline EF and changes in afterload.

30 c pulmonary artery obstruction and increased afterload.

31 nly 5 (6%), despite a concomitant rise in LV afterload.

32 ictable and constant proportion to resistive afterload.

33 a hydrogel that imposes a three-dimensional afterload.

34 es not take into consideration the effect of afterload.

35 cardiac output under changes of preload and afterload.

36 fts stiffen the aorta and likely increase LV afterload.

37 response of the right ventricle to increased afterload.

38 t ventricular function and right ventricular afterload.

39 n and strain rate were heavily influenced by afterload.

40 ion (Emax: 2.8+/-1.0 mm Hg/mL), preload, and afterload.

41 ggesting a decrease of the right ventricular afterload.

42 usside to reduce blood pressure and arterial afterload.

43 or the estimation of global left ventricular afterload.

44 cardiac myocyte sense changes in preload or afterload?

45 -4.2% in end-systolic elastance) and lowered afterload (-14.2+/-2% in systemic resistance, both P<0.0

46 (23 +/- 6 versus 17 +/- 6 mm Hg for RAP) and afterload (20 +/- 9 versus 13 +/- 6 mm Hg for TPG; 5.9 +

47 tween VCF and ESS (a preload-insensitive and afterload-adjusted index of contractility) was increased

48 Here, we investigated how afterload affects action potentials, ionic currents, int

49 How afterload affects Ca(2+) signalling was measured in card

50 relaxation, and lowered cardiac preload and afterload (all P < 0.001) without altering plasma cGMP.

51 The distribution of FS and afterload among NR survivors did not differ from that of

52 a greater inspiratory increase in markers of afterload and a decrease in stroke volume.

53 ining the effects of alterations in preload, afterload and contractile state.

54 Noninvasive measures of afterload and contractility appear useful for monitoring

55 r performance and its determinants: preload, afterload and contractility.

56 (LV) wall thickness resulting in elevated LV afterload and depressed LV function.

57 The influence of arterial afterload and diastolic dysfunction on the hemodynamic p

58 fferent components of right ventricular (RV) afterload and function remain not fully elucidated.

59 solated ejecting guinea pig hearts (constant afterload and heart rate) were studied before and after

60 eoperative PDE5i had markers of increased RV afterload and HF severity compared to unmatched controls

61 ial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function.

62 velocity <2 m/s) will have a higher arterial afterload and increased left ventricular mass index (LVM

63 groups, decreasing RV volumes, preload, and afterload and increasing RVEF in all patients, but post-

64 ewly transplanted heart because of increased afterload and is an important consideration for heart tr

65 ve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular funct

66 rophy and dysfunction secondary to increased afterload and left ventricular dilatation secondary to v

67 Nitroprusside reduces afterload and left ventricular filling pressures in pati

68 Despite similar RV afterload and mass some patients develop adaptive RVH (c

69 These changes decrease LV afterload and myocardial oxygen demand and reduce the nu

70 pressure and increases left ventricular (LV) afterload and myocardial oxygen demand.

71 related to alterations in right ventricular afterload and not intrinsic right ventricular contractil

72 oxemia is due to increased right ventricular afterload and not to left ventricular afterload.

73 ress syndrome treatment on right ventricular afterload and outcome.

74 ed intraabdominal pressure include increased afterload and preload and decreased cardiac output, wher

75 n infusion to evaluate the response to acute afterload and preload changes (interventional substudy).

76 d lower wall stress in the face of increased afterload and preload.

77 V contractility because of its dependence on afterload and preload.

78 ase progression, decreased right ventricular afterload and pulmonary vascular remodeling, and restore

79 Optimal LV function reduces RV afterload and PVR.

80 fraction and is associated with high global afterload and reduced longitudinal systolic function.

81 dividual components of left ventricular (LV) afterload and tissue Doppler echocardiography (TDE) velo

82 trics are able to estimate right ventricular afterload and track acute changes in pulmonary hemodynam

83 could be used to estimate right ventricular afterload and track acute changes in pulmonary hemodynam

84 Valvuloarterial impedance (ie, global afterload) and myocardial oxygen consumption were reduce

85 trics and phenotypes signalling an increased afterload, and an association to hypertension among othe

86 ach involves adjustments of cardiac preload, afterload, and contractility to balance oxygen delivery

87 in arterial elastance, indicating increased afterload, and elevated plasma angiotensin II.

88 uent and present with less severe AS, normal afterload, and less severe longitudinal dysfunction.

89 d the adverse hemodynamic effects, increased afterload, and LV remodeling in anti-VEGF-treated mice.

90 orse in SScPAH compared with IPAH at similar afterload, and may be because of intrinsic systolic func

91 e and reduces aortic valve gradients, global afterload, and myocardial oxygen requirements.

92 ary vascular pressures and right ventricular afterload, and progressive right ventricular hypertrophy

93 YR reduced pulmonary vascular resistance, RV afterload, and pulmonary vascular remodeling, which was

94 from an acute increase in right ventricular afterload, and was not a consequence of gas-exchange abn

95 ry vascular resistance and right ventricular afterload, and when significant enough, can result in he

96 rterial stiffness increases left ventricular afterload, any allopurinol-induced improvement in arteri

97 Significant reductions in afterload (aortic pressure, P=0.030) and myocardial oxyg

98 diac output or loading conditions, including afterload as determined by systemic vascular resistance

99 the mild COA group displayed higher arterial afterload as evidenced by a higher elastance index (3.3+

100 12.3% +/- 3.2%, p = 0.04), despite a reduced afterload as expressed by the left ventricular end-systo

101 s in blood pressure, arterial stiffness, and afterload as well, thereby improving subendocardial bloo

102 re to hemodynamic overload (both preload and afterload) as well as its intrinsic contractile function

103 S, and VCFc) were lower in SCA patients, and afterload, as measured by ESSm, was increased.

104 o determine whether higher systemic arterial afterload-as reflected in blood pressure, pulsatile and

105 RV afterload assessed by effective arterial elastance rose

106 l pressure dynamics, preload limitation, and afterload augmentation.

107 ors (PDE5i), are used off-label to reduce RV afterload before LVAD implantation, but the association

108 HR modulates Ea, and, therefore, afterload burden.

109 ed throughout most of pregnancy by a fall in afterload but decreases near term and early postpartum b

110 terial coupling was decreased with increased afterload but not affected by the induction of thoracic

111 c function of the ventricles and the optimum afterload but overestimated the flow and therefore the p

112 left ventricular (LV) preload and increases afterload, but central events do not, obstructive events

113 of elevations in right- and left-ventricular afterload, but, instead, increased O2 extraction ratio (

114 ure appears to enhance net right ventricular afterload by elevating pulsatile, relative to resistive,

115 Natriuretic peptides decrease RV afterload by promoting pulmonary vasodilation and inhibi

116 rterial elastance (Ea) and right ventricular afterload by pulmonary artery systolic pressure.

117 fficulty of reducing total right ventricular afterload by therapies that have a modest impact on mean

118 unction was assessed by 2D-strain and global afterload by valvulo-arterial impedance.

119 Right ventricular afterload can be analysed in terms of pulmonary artery i

120 2.9 +/- 2.0 vs. 10.6 +/- 1.2 ml min(-1)) or afterload (cardiac output: -5.3 +/- 2.0 vs.1.4 +/- 1.2 m

121 a consequence of a postoperative increase in afterload, caused by closure of a low resistance runoff

122 e function that is unaffected by preload and afterload changes in a physiological range and is able t

123 e function that is unaffected by preload and afterload changes within a physiological range and can b

124 COA patients had higher arterial afterload compared with controls with similar SBP.

125 3R1VSMC-/- mice developed significantly less afterload compared with HF IP3R1fl/fl mice and exhibited

126 ejection fraction display elevated arterial afterload compared with patients with HGSAS and moderate

127 ending aorta and has the potential to worsen afterload conditions and decrease coronary artery perfus

128 ted to impaired contractility and increasing afterload, consequences of a progressive reduction of ve

129 ing mechanisms beyond hypertension/increased afterload contribute to diabetic cardiomyopathy.

130 patients was related to both lower arterial afterload (decreased systemic vascular resistance) and h

131 the pulmonary artery significantly increased afterload (DeltaEa: +0.226 mm Hg/mL, P<0.001).

132 s coronary perfusion (supply) and reduces LV afterload (demand).

133 Vena contracta width appears to be less afterload-dependent than RgV.

134 Myocardial afterload depends on left ventricular (LV) cavity size,

135 l as parameters reflecting right ventricular afterload (diastolic pulmonary artery pressure; p < 0.00

136 l or compensated levels of contractility and afterload did poorly in this study.

137 ration of the Laplace relation suggests that afterload does not necessarily increase after the operat

138 of mammals protects the RV against excessive afterload during acute volume transients and its disrupt

139 At a matched increase in afterload (effective arterial elastance), L-NMMA increas

140 We invasively examined systemic arterial afterload (effective arterial elastance, Ea; total arter

141 Furthermore, all these afterload effects were significantly attenuated by inhib

142 Adjusting for preload and afterload, eFS was similar in health and severe malaria.

143 creases, the expected rise in PCWP caused by afterload elevation appears to be counterbalanced by a r

144 (left ventricular end-diastolic dimension), afterload (end-systolic wall stress) and contractility (

145 e respectively adjusted for left ventricular afterload (end-systolic wall stress) to derive an index

146 ereby double loading the LV, contributing to afterload excess and a deterioration in LV performance t

147 e new HFPEF paradigm shifts emphasis from LV afterload excess to coronary microvascular inflammation.

148 Inadequate ventricular mass with chronic afterload excess was associated with progressive contrac

149 lossal length is substantially influenced by afterload exerted by negative UAP and that genioglossal

150 ength (Lgg) is dynamically influenced by the afterload exerted by negative upper airway pressure duri

151 f PVR and left-sided filling pressures on RV afterload, explaining its strong relation with RV dysfun

152 Elevated right ventricular afterload following continuous-flow left ventricular ass

153 vement toward normal values in LV dimension, afterload, fractional shortening, and mass, but all thes

154 guat and BPA, and the relative changes in RV afterload from baseline to week 26 were more pronounced

155 Afterload from moderate aortic stenosis (AS) may contrib

156 the mammal heart is highly sensitive to the afterload imposed by a combination of the pulmonary circ

157 ved ejection fraction, increased preload and afterload imposed by obesity, hypertension and age-depen

158 the mammal heart is highly sensitive to the afterload imposed by the pulmonary circulation, and the

159 Cardiac output, stroke volume, and RV afterload improved significantly with riociguat and BPA,

160 diac performance under chronically increased afterload in female patients with PAH.

161 diac performance under chronically increased afterload in female patients with PAH.

162 Elevated hepatic afterload in Fontan, manifested by high ventricular end-

163 idase inhibitor, has been shown to reduce LV afterload in IHD and may therefore also regress LVH.

164 ciguat and BPA are effective in improving RV afterload in inoperable chronic thromboembolic pulmonary

165 e adverse effect of the sudden imposition of afterload in midsystole.

166 compliance is superior to other measures of afterload in predicting RVFnRec.

167 Surprisingly, correction of decreased afterload in septic rats, using the pure alpha-agonist p

168 alanced vasodilation, decreasing preload and afterload in states of cardiac impairment and stimulatin

169 in the stroke volume occurred with increased afterload in the failing heart.

170 Although afterload in these disorders differs, clinical differenc

171 e data suggest that SBP may underestimate LV afterload in this population.

172 Increased afterload in treated mice led to concentric LV remodelin

173 However, increased left ventricular (LV) afterload in VA-ECLS can worsen pulmonary congestion and

174 ents with HGSAS and moderate AS, measures of afterload, including Ea (4.02 +/- 0.98 versus 3.13 +/- 0

175 dobutamine and during preload reduction and afterload increase by transient balloon occlusion of the

176 e RV so much more vulnerable to failure upon afterload increase compared with the left ventricle?

177 During preload reduction and afterload increase, IVA remained constant up to a reduct

178 ne and assessed during preload reduction and afterload increase.

179 ncrease in heart work (1 microM epinephrine, afterload increased by 40%) and the involvement of key r

180 When afterload increased from 55 mmHg to 90 mmHg, stroke volu

181 ns: In the Vt range currently prescribed, RV afterload increases with increasing Vt.

182 chanism to preserve RV contractility, as the afterload increases.

183 Afterload independence was demonstrated by preload-adjus

184 eous measurement of peak power, a relatively afterload-independent index of LV contractility, in 21 p

185 stroke volumes, FS, circumferential ESS, and afterload-independent measures of LV performance (stress

186 and remodeling in a murine model of MI by an afterload-independent mechanism, in part by decreasing m

187 CCI is a simple, noninvasive, relatively afterload-independent method to stratify HF risk in popu

188 re strongly predicted by higher SV and lower afterload-independent MFS than by greater systolic press

189 cular function and its response to increased afterload, induced by temporary, unilateral clamping of

190 type calcium channel activity is critical to afterload-induced hypertrophic growth of the heart.

191 an essential role for the FoxO1-Dio2 axis in afterload-induced pathological cardiac remodeling and ac

192 Cardiac mechanical afterload induces an intrinsic autoregulatory increase i

193 Variations in the ventricular preload and afterload influence pulmonary arterial wave propagation

194 d, suggesting that heightened sensitivity to afterload is a significant contributor to LF-LGSAS patho

195 ose without patent ductus arteriosus because afterload is lower in the former group.

196 r aortic valve replacement, left ventricular afterload is often characterized by the residual valve o

197 ABSTRACT: Elevated left ventricular afterload leads to myocardial hypertrophy, diastolic dys

198 In a subset of nine patients who underwent afterload manipulation to increase diastolic blood press

199 For baseline to 1 minute, an increase in afterload (maximal pressure 95+/-9 to 126+/-7 mm Hg; P<0

200 he pulsatile component of pulmonary vascular afterload may account for anywhere between one-quarter a

201 pients, and increased right ventricular (RV) afterload may contribute.

202 based upon better understanding of arterial afterload may enable better individualization of therapy

203 lated to changes in chamber size and that LV afterload may fall when chordal preservation techniques

204 nal function is associated with increased RV afterload (mean PAP and PVRI).

205 It is not clear which RV afterload measure has the greatest impact on RV function

206 erial load and the effect of HF therapies on afterload might vary between individuals.

207 regurgitant orifice), whereas correction of afterload mismatch dominates the response in aortic regu

208 Inhibition of VEGF leads to an afterload mismatch state, increased angiotensin II, and

209 This finding later led to the concept of afterload mismatch with limited pre-load reserve.

210 and with phenylephrine infusion to increase afterload (MR jet/left atrial [LA] area 26 +/- 1% to 7 +

211 ng and cause an increase in left ventricular afterload, myocardial mass, and oxygen consumption.

212 rate (HR) reduction with ivabradine reduces afterload of patients with systolic heart failure.

213 ance (Ea) represents resistive and pulsatile afterload of the heart derived from the pressure volume

214 onstrates that increases in left ventricular afterload of the magnitude seen with the infusion of L-N

215 s of normal or compensated contractility for afterload on a modified stress-velocity relationship to

216 d investigation of the effects of increasing afterload on the normal and failing left ventricle by me

217 nt or suspected decrease in cardiac preload, afterload, or contractility.

218 changes were found in endothelial function, afterload, or metabolism.

219 S (P < .001) and increase in distribution of afterload (P < .001).

220 Both hCSC and Pim1(+) hCSC treatment reduced afterload (p = 0.02 and p = 0.004, respectively).

221 dex, a major determinant of left ventricular afterload (P<0.001).

222 of MR was associated with marked changes in afterload, particularly decreased blood pressure (p = 0.

223 ight ventricle with increased RV preload and afterload predisposes to RVD after LVAD implantation.

224 tiffness was corelated with left ventricular afterload, prehypertension, coronary artery plaques, pre

225 preload (stretch during chamber filling) and afterload (pressure the heart must work against to eject

226 r agonist isoproterenol (ISO) and by varying afterload pressures.

227 Increasing afterload prolonged relaxation more in nontransgenic tha

228 roke volume in failing hearts because of the afterload-reducing benefit (decreased transmural left ve

229 ence in the response to combined preload and afterload reduction (i.e., nitroprusside) in patients wi

230 nism is suppressed in heart failure, so that afterload reduction accounts for CGRP-enhanced function

231 Most importantly, two randomized trials of afterload reduction for preventing left ventricular dila

232 ow characterizes the response to preload and afterload reduction in mitral regurgitation (through a p

233 These data highlight the utility of afterload reduction in the diagnostic assessment of LGSA

234 erformed, with the data supporting long-term afterload reduction in this patient group.

235 Afterload reduction is a cornerstone in the management o

236 Afterload reduction is the mainstay of pharmacological t

237 jects participating in the Healing and Early Afterload Reduction Therapy (HEART) study, a double-blin

238 To test the hypothesis that afterload reduction therapy alters hemodynamic variables

239 of decreased systemic output and the use of afterload reduction to stabilize systemic vascular resis

240 ardiomyopathy and treatment with digoxin and afterload reduction was initiated.

241 between baseline SVI and change in SVI with afterload reduction was observed, suggesting that height

242 BPA provided a more substantial impact on RV afterload reduction, and RV function only improved with

243 dulate the indirect responses mediated by RV afterload reduction.

244 ch force-frequency modulation is blunted and afterload relaxation sensitivity increased in associatio

245 load after TAVR limits the procedure's acute afterload relief.

246 CVP significantly decreased, while RV afterload remained unchanged.

247 t (CO) state because of an acute increase in afterload remains controversial.

248 minated the differential force-frequency and afterload response between TnIDD22,23 and controls.

249 RATIONALE: Pathological increases in cardiac afterload result in myocyte hypertrophy with changes in

250 Despite a similar afterload, RV function is more severely affected in muta

251 Mean afterload (+/- SD) was higher for AR (58 +/- 21 g/cm(2))

252 systolic and diastolic function in vivo and afterload sensitivity of relaxation.

253 entricular mass or through modulation of the afterload, since blood pressure was not changed.

254 Acute increases in afterload slow diastolic relaxation as assessed invasive

255 regulation of pumping by lymphatic preload, afterload, spontaneous contraction rate, contractility a

256 Small animal models of afterload stress have contributed much to our present un

257 dly phenotype cardiac changes resulting from afterload stress in a small animal model.

258 lated by treatment with beta-blockers; acute afterload stress induces a deeper impairment of systolic

259 by conventional echocardiography, following afterload stress.

260 A computer-controlled afterload system either constrained the isolated heart t

261 vo canine heart preparation and computerized afterload system that mimicked the conditions of heart f

262 f LV volume and a significantly increased LV afterload (systolic pressure increase, P<0.001).

263 y be a more useful guide to left ventricular afterload than systemic vascular resistance.

264 able to work against a significantly higher afterload than that of frog hearts.

265 ar stiffening may display increased arterial afterload that is out of proportion to systolic blood pr

266 ercise leads to a steep increase in proximal afterload that is underestimated at rest and is associat

267 es cyclic changes in the heart's preload and afterload, thereby influencing the circulation.

268 s due entirely to an effect of the decreased afterload to "unload" the left ventricle.

269 hrony that was attenuated with return of the afterload to baseline levels.

270 (Zva) estimates the overall left ventricular afterload (valve and arterial component).

271 Strategies to reduce afterload, vascular stiffening, and wave reflections may

272 amics, the ventricular response to increased afterload, ventricular-vascular coupling, or the systemi

273 Doppler-derived arterial afterload was assessed using effective arterial elastanc

274 more, prolongation of pressure relaxation by afterload was markedly blunted in cMyBP-C(t/t) hearts.

275 Afterload was measured as mean pulmonary artery pressure

276 Arterial afterload was measured by effective arterial elastance (

277 (70 and 90 beats/min) pig model in which LA afterload was modified by creating LV regional ischemia

278 Change in RV afterload was primarily mediated by decreased mean pulmo

279 RV afterload was similar in SScPAH and IPAH (pulmonary vasc

280 icardial areas) at comparable LV preload and afterload was similar in the 4 basal areas (P = 0.223, M

281 RV afterload was unaffected, however, bisoprolol treatment

282 Left ventricular afterload was within normal range in the early (0.1 +/-

283 LV end-systolic stress (ESS) (a measure of afterload) was normal (Z score=0.2+/-2.3), whereas short

284 ed laboratory-based technique to increase LV afterload, was performed for 3 min at 40% maximum force

285 Mean fractional shortening (FS) and afterload were compared for survivors who did (at risk [

286 Left ventricular preload, contractility, and afterload were independently manipulated to assess the e

287 All measures of afterload were reduced with nitroprusside (P<0.001 for a

288 All invasive measures of arterial afterload were related to stroke volume index.

289 3 (P<0.02), whereas contractile responses to afterload were similar between these strains.

290 ts, indicating that the effects of increased afterload were the same before and after thoracic epidur

291 flow assessment over a range of preloads and afterloads were performed.

292 tolic blood pressure (SBP) increases cardiac afterload, whereas low diastolic blood pressure (DBP) ma

293 dditionally found to be inversely related to afterload, whereas other measures of contractility were

294 dysfunction results in increased preload and afterload, which in turn lead to pulmonary congestion.

295 H, the RV is exposed to a ~5 times increased afterload, which makes these conditions excellent models

296 more substantial effect on left ventricular afterload with a modest increase in cardiac output and w

297 pulsatility and decreasing left ventricular afterload with intra-aortic balloon pump was associated

298 herapy results in a lowering of the total LV afterload, with a decrease in LV filling pressures and p

299 ssue velocities vary inversely with arterial afterload, with late-systolic load having the greatest i

300 racterized by a disproportionate increase in afterload without profound hemodynamic compromise.