ライフサイエンスコーパス: afterload

1 cardiac output under changes of preload and afterload.

2 rtension is due strictly to the increased RV afterload.

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

4 cardiac hypertrophy in response to increased afterload.

5 onically raising the lymphatic smooth muscle afterload.

6 and relaxation delay from increased arterial afterload.

7 at greatest risk for abnormalities of FS and afterload.

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

9 odilator that can decrease right ventricular afterload.

10 ripheral vasoconstriction is contributing to afterload.

11 tionship to a zone of high contractility for afterload.

12 dysfunction with increased left ventricular afterload.

13 function due to increased right ventricular afterload.

14 icular afterload and not to left ventricular afterload.

15 mediated primarily by an increase in cardiac afterload.

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

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

18 monly falls because of a concomitant rise in afterload.

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

20 m examination, despite a progressive fall in afterload.

21 ntricular performance is highly sensitive to afterload.

22 d negatively with baseline EF and changes in afterload.

23 response of the right ventricle to increased afterload.

24 t ventricular function and right ventricular afterload.

25 n and strain rate were heavily influenced by afterload.

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

27 ggesting a decrease of the right ventricular afterload.

28 usside to reduce blood pressure and arterial afterload.

29 or the estimation of global left ventricular afterload.

30 diuresis, while reducing cardiac preload and afterload.

31 in the clinical context of acute increase in afterload.

32 nd fractional shortening and above normal LV afterload.

33 cardiac myocyte sense changes in preload or afterload?

34 -4.2% in end-systolic elastance) and lowered afterload (-14.2+/-2% in systemic resistance, both P<0.0

35 (23 +/- 6 versus 17 +/- 6 mm Hg for RAP) and afterload (20 +/- 9 versus 13 +/- 6 mm Hg for TPG; 5.9 +

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

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

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

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

40 Noninvasive measures of afterload and contractility appear useful for monitoring

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

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

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

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

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

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

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

48 Nitroprusside reduces afterload and left ventricular filling pressures in pati

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

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

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

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

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

54 ress syndrome treatment on right ventricular afterload and outcome.

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

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

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

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

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

60 Optimal LV function reduces RV afterload and PVR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 12.3% +/- 3.2%, p = 0.04), despite a reduced afterload as expressed by the left ventricular end-systo

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

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

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

81 RV afterload assessed by effective arterial elastance rose

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

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

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

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

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

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

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

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

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

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

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

93 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Although afterload in these disorders differs, clinical differenc

126 Increased afterload in treated mice led to concentric LV remodelin

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

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

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

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

131 ne and assessed during preload reduction and afterload increase.

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

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

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

135 Afterload independence was demonstrated by preload-adjus

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Increasing afterload prolonged relaxation more in nontransgenic tha

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

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

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

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

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

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

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

180 Afterload reduction is a cornerstone in the management o

181 Afterload reduction is the mainstay of pharmacological t

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

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

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

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

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

187 dulate the indirect responses mediated by RV afterload reduction.

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

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

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

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

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

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

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

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

196 Acute increases in afterload slow diastolic relaxation as assessed invasive

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

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

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

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

201 by conventional echocardiography, following afterload stress.

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

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

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

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

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

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

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

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

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

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

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

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

214 Arterial afterload was measured by effective arterial elastance (

215 (70 and 90 beats/min) pig model in which LA afterload was modified by creating LV regional ischemia

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

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

218 RV afterload was unaffected, however, bisoprolol treatment

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

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

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

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

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

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

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

226 3 (P<0.02), whereas contractile responses to afterload were similar between these strains.

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

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

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

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

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

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