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1 increase in both maximal cardiac output and stroke volume.
2 oppler left ventricular outflow minus inflow stroke volume.
3 (MR) as total left ventricular minus forward stroke volume.
4 filling pressure during exercise to maintain stroke volume.
5 flow volume from the total left ventricular stroke volume.
6 at 6 hours, corresponding with the nadir of stroke volume.
7 5.4 and 8.4 mL increases in left ventricular stroke volume.
8 ion by decreasing systemic venous return and stroke volume.
9 ocardial oxygen consumption for a particular stroke volume.
10 dance cardiogram (dZ/dt) is used to indicate stroke volume.
11 pulmonary artery pulse pressure, and reduced stroke volume.
12 lar coupling, and decreased left ventricular stroke volume.
13 and contractility influence left ventricular stroke volume.
14 iance correlated with lower left ventricular stroke volume.
15 essures, with no effect on cardiac output or stroke volume.
16 me as well as a higher ejection fraction and stroke volume.
17 aine group was due to a two-fold increase in stroke volume.
18 nd 30% reduction in hemispheric and cortical stroke volumes.
19 ion in hemispheric, cortical and subcortical stroke volumes.
21 n, HFpEF patients showed a lower increase in stroke volume (+10 +/- 16% vs. +21 +/- 12%) despite a gr
22 =0.99 by dose), associated with increases in stroke volume (15 [2] mL), fractional shortening (8% [1]
23 t ventricular mass [1.6%, P=0.008]), resting stroke volume (2.0%, P=0.002), left ventricular diastoli
24 per unit mean hemoglobin A(1c) percent) and stroke volume (-2.3 mL per unit mean hemoglobin A(1c) pe
25 dence interval [CI], -3.3 to -4.9; P<0.001), stroke volume (-2.7 ml; 95% CI, -2.2 to -3.3; P<0.001),
26 te patients with IPAH and DD decreased their stroke volume (-25% and -30%; P < 0.05) and failed to in
28 jection time 25 ms (95% CI 18-32, p<0.0001), stroke volume 3.6 mL (0.5-6.7, p=0.0217), left ventricul
29 models, older age was associated with lower stroke volume (-3.6 mL per decade; P<0.001) and higher L
32 e (77 +/- 18 ml vs. 77 +/- 17 ml; p = 0.51), stroke volume (48 +/- 9 ml vs. 46 +/- 9 ml; p = 0.83), o
33 en epoetin alfa and placebo, but declines in stroke volume (-5+/-8 versus 2+/-10 mL; P=0.09) without
34 al/noise ratio was 3-fold better for BP than stroke volume (6.8+/-3.5 versus 2.3+/-1.4; P<0.001).
35 produced a significant acute reduction in LV stroke volume (63.9 +/- 12.0 vs. 49.4 +/- 7.8 ml, P < 0.
37 rison with conventional CS site stimulation (stroke volume, 83 [79-112] mL versus 73 [62-89] mL; P=0.
38 x+LV and LV-only pacing resulted in improved stroke volume (85+/-32 mL and 86+/-33 mL versus 58+/-23
39 vq-1, that affected limb muscle survival and stroke volume after femoral artery or middle cerebral ar
40 ining venous return, central venous pressure,stroke volume and (.)Q or maintaining muscle blood flow
43 mic brain damage was measured by determining stroke volume and by stereologic quantifications of surv
45 mpensatory mechanism to maintain an adequate stroke volume and cardiac output in the face of the prog
46 r in HFpEF (p < 0.0001), and improvements in stroke volume and cardiac output were each approximately
48 n the ML than EF phase; however, heart rate, stroke volume and cardiac output were similar between ph
49 peripheral resistance were greater, whereas stroke volume and cardiac output were smaller in patient
50 pling intervals were associated with greater stroke volume and dP/dtmax despite more pronounced dyssy
51 have significantly reduced left ventricular stroke volume and ejection fraction (LVEF) and tend to d
52 ume and decreased chest compliance decreased stroke volume and increased arterial pressure variations
53 12 h after experimental stroke reduced both stroke volume and inflammatory cytokines associated with
58 In Fontan patients, the largest increases in stroke volume and stroke volume index were during zero-r
59 ationship between increased vagal tone, high stroke volumes and incident AF, and particularly so in p
61 ce to acute stroke care performance metrics, stroke volume, and bed size was not associated with down
62 as associated with worse systolic (lower EF, stroke volume, and cardiac index) and diastolic (shorter
63 ed to left ventricular end-diastolic volume, stroke volume, and cardiac output among persons without
65 was associated with an increased heart rate, stroke volume, and cardiac output, as well as increased
67 LV short-axis echocardiographic images, LV stroke volume, and dP/dtmax were obtained during all ect
68 d-diastolic volume and end-systolic volume), stroke volume, and EF were measured by 3D echocardiograp
69 r end-diastolic volume, end-systolic volume, stroke volume, and ejection fraction were determined.
72 core was linearly associated with LV volume, stroke volume, and ejection fraction: for each +1-U diff
73 t gain in ejection fraction, cardiac output, stroke volume, and fractional area change in mice treate
74 d low left ventricular diastolic volume, low stroke volume, and greater severity of mitral regurgitat
75 o impaired left ventricular filling, reduced stroke volume, and lower cardiac output without changes
77 re to enhance cardiac venous return, improve stroke volume, and reduce heart rate in these patients.
78 bell-shaped improvements in cardiac output, stroke volume, and systemic oxygen delivery (p < .05 vs.
79 end-diastolic volumes, end-systolic volumes, stroke volumes, and masses with increasing doses of life
80 e permeability assays, we observed increased stroke volumes, BBB breakdown and edema formation, reduc
81 ody surface area, a 0.43-mL/m(2) decrease in stroke volume/body surface area, and a 0.21% decrease in
84 ared with a treatment strategy of maximizing stroke volume by fluid loading, leads to less vascular e
85 calculated by dividing left ventricular (LV) stroke volume by LV myocardial volume, and long-axis str
86 he difference in automated mitral and aortic stroke volumes by real-time 3D volume color flow Doppler
87 ials evoked similar increases in heart rate, stroke volume, cardiac output and a reduction in mean ar
89 e left ventricular total isovolumic time and stroke volume, cardiac output, and cardiac index in all
90 bo 2.5 +/- 1.6 EF units; p = 0.0009), as did stroke volume, cardiac output, and diastolic strain only
91 as evidenced by decreased ejection fraction, stroke volume, cardiac output, and peak ejection rate.
92 rrelation between changes in RR interval and stroke volume, cardiac output, or cardiac index in the o
93 or stroke volume variation and the change in stroke volume/cardiac index after a fluid or positive en
94 ), pulse pressure variation (one trial), and stroke volume change with passive leg raise/fluid challe
96 Ventriculoarterial coupling implies that stroke volume changes little while preserving ventricula
99 lunted peripheral vasoconstriction and lower stroke volume contribute to compromised orthostatic tole
101 MHD, we hypothesized that a method to obtain stroke volume could be derived from extracted VMHD vecto
103 13.3 mL per decade, respectively; P < .001), stroke volume decreased (-8.8 and -8.6 mL per decade, re
104 +/- 2.2 ml min(-1) mmHg(-1); P = 0.001) and stroke volume (Delta 9.1 +/- 2.1 ml beat(-1); P < 0.001)
105 d-diastolic volume plotted against neoaortic stroke volume demonstrated a Frank-Starling-like curve t
109 circulation increases in cardiac output and stroke volume during Ex were due to the muscle pump, wit
110 maging revealed decreases in cardiac output, stroke volume, ejection fraction, and fractional shorten
111 tion of zebrafish, including the ventricular stroke volume, ejection fraction, cardiac output, heart
113 nisms, we measured simultaneous beat-to-beat stroke volume (flow) using Doppler echocardiography, and
115 e 68-79) to 80 mm Hg (75-86; p < 0.0001) and stroke volume from 50 mL (30-77) to 55 mL (39-84; p < 0.
116 Multivariate analysis was performed to fit stroke volumes from gated myocardial perfusion imaging s
117 ardiogram system could detect differences in stroke volumes from gated myocardial perfusion imaging s
118 dZ/dt was the best predictor of reduction in stroke volumes from gated myocardial perfusion imaging s
119 l/min (p = 0.003); 2) an increase in forward stroke volume (FSV) from 57 +/- 17 ml to 65 +/- 18 ml (p
120 ing improved hemodynamic indexes at all AVD (stroke volume >76 mL at all fixed intervals and 88+/-31
121 tenosis patients had smaller valve areas and stroke volumes, higher mean gradients, and comparable de
122 creased during pregnancy because of a higher stroke volume in early pregnancy and a late increase in
123 es in systolic pressure, pulse pressure, and stroke volume in patients undergoing mechanical ventilat
124 ution of the muscle and ventilatory pumps to stroke volume in patients without a subpulmonic ventricl
125 evelop a technique to noninvasively estimate stroke volume in real time during magnetic resonance ima
126 aw, a mechanism by which the heart increases stroke volume in response to an increase in venous retur
129 of cardiac contractility prompted increased stroke volume, in turn increasing cardiac output, which
130 infusion of 50 mug/kg/min, left ventricular stroke volume increased (from 43.22+/-21.5 to 51.84+/-23
131 implantation, systemic arterial pressure and stroke volume increased and pulmonary pressure decreased
132 In post hoc analysis, right ventricular stroke volume increased by 4.87 ml/m(2) (P = 0.003); rig
133 ugh multiple mechanisms including depressing stroke volume, increasing fluid loss into the intestine,
136 ts with evaluable echocardiograms (92%), LF (stroke volume index </=35 mL/m(2)) was observed in 530 (
137 flow and gradient: low flow was defined as a stroke volume index </=35 mL/m(2), low gradient as a mea
138 ction, including paradoxical low-flow (i.e., stroke volume index <35 ml/m(2)), low-gradient (LF-LG) a
139 tricular ejection fraction [LVEF] >/=50% but stroke volume index <35 ml/m(2)), low-gradient (mean gra
140 reduced aortic valve area (<1 cm(2)), normal stroke volume index (>/=35 mL/m(2)), and either high mea
142 levosimendan increased cardiac index (22%), stroke volume index (15%), and heart rate (7%) and decre
143 es mellitus (25% versus 41%, P=0.009), lower stroke volume index (36.4+/-8.4 versus 34.4+/-8.7 mL/m2,
144 ents with LF compared with those with normal stroke volume index (47% versus 34%; hazard ratio, 1.5;
145 ats per minute; P<0.001) and to reduced peak stroke volume index (47+/-10 mL/min per m(2) versus 54+/
146 confidence interval, 0.2-0.5; P=0.0001) and stroke volume index (5.2 mL.m(-2); 95% confidence interv
148 ludes important subsets of patients with low stroke volume index (low flow) and low-gradient with red
149 ce index (p < 0.001; 95% CI, 0.97-0.99), and stroke volume index (p < 0.01; 95% CI, 0.96-0.99) in pre
150 esistance index (P < .01), right ventricular stroke volume index (P </= .01), and pulmonary artery ca
151 ion (P<0.001 and P=0.0007, respectively), RV stroke volume index (P<0.0001), and left ventricular end
153 ), decreased heart rate (P(group)=0.01), and stroke volume index (P(group)=0.004) compared with TTM36
154 nafil increased cardiac index (P<0.0001) and stroke volume index (P=0.003), especially at high-intens
156 on functional class, 6-minute walk distance, stroke volume index (SVI), and right atrial pressure wer
157 Forty-one subjects (25 with low flow [LF], stroke volume index [SVI] </=35 ml/m(2), 16 with normal
159 SAS, but the patients with LGSAS had reduced stroke volume index and cardiac index (P=0.003 for both)
161 citonin, and waveform analysis of changes in stroke volume index and systemic vascular resistance ind
162 1 .9 vs. 37.7 +/- 15.4; p = .03), plus lower stroke volume index and worse cardiac function with high
163 stroke volume index, and in the study group, stroke volume index assessed prior to severe acute pancr
164 dex with a regime using individual values of stroke volume index assessed prior to severe acute pancr
165 After volume expansion, a relevant (>/= 10%) stroke volume index increase was recorded in 56% patient
168 ts with reduced aortic valve area and normal stroke volume index undergoing AVR underwent echocardiog
169 , the largest increases in stroke volume and stroke volume index were during zero-resistance cycling.
170 cular ejection fraction and left ventricular stroke volume index were most strongly predictive of sur
171 e effects of such consequent maximization of stroke volume index with a regime using individual value
174 was associated with lower ejection fraction, stroke volume index, and aortic valve mean gradient up t
175 admission, including severe tachycardia, low stroke volume index, and high inferior vena cava collaps
176 up, fluid therapy was directed by maximizing stroke volume index, and in the study group, stroke volu
177 rain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass ind
178 iac MRI measurements included cardiac index, stroke volume index, global and regional contractile fun
179 ctors, LV mass index, aortic valve area, and stroke volume index, LVEF was independently predictive o
184 etween central venous pressure and change in stroke volume index/cardiac index and the percentage of
185 seline central venous pressure and change in stroke volume index/cardiac index was 0.18 (95% CI, 0.1-
187 8%) had PLF as defined by LVEF of >/=50% but stroke volume indexed to body surface area (SVi) of </=3
189 myocardial function, as suggested by higher stroke volume indexes and left ventricular stroke work i
191 the heart (cardiac output, left ventricular stroke volume, isovolumic relaxation, E' septal annulus,
193 prevalence of LFLG (indexed left ventricular stroke volume <35 mL/m(2) and mean gradient <40 mm Hg),
197 abnormal stress changes in left ventricular stroke volume (LVSV) and aortic stiffness predict future
198 gitant orifice area [EROA], left ventricular stroke volume [LVSV]) and quality-of-life (QoL) measurem
201 ventricular stroke volume (right ventricular stroke volume minus pulmonary regurgitant volume) after
202 disease or pharmacologic reasons, changes in stroke volume must compensate, but the capacity to do so
208 s the result of an (undesirable) decrease in stroke volume or a (desirable) compensatory relief of pe
211 ulmonary arterial capacitance (PAC, ratio of stroke volume over pulmonary pulse pressure), in relatio
212 associated with lower RVEDV (p = 0.005) and stroke volume (p < 0.001), as was the presence of centri
214 ss and septal thickness (both P<0.05); lower stroke volume (P<0.0001); and lower peak lateral and sep
216 nd higher indexed left and right ventricular stroke volumes (P=0.007 and P=0.015) and ejection fracti
217 patients was associated with maintenance of stroke volume, preserved microvascular blood flow, and a
218 ]; P < 0.0001) and in improvements in median stroke volume/pulmonary pulse pressure ratio (2.6 ml/mm
219 cular resistance as co-primary endpoints and stroke volume/pulmonary pulse pressure ratio, tricuspid
220 p < 0.0001), right ventricular outflow tract stroke volume (r = 0.660; p < 0.0001), and pulmonary vas
221 d slightly lower correlations were found for stroke volume (r = 0.74), LVEF (r = 0.81), and thickness
222 , R(2)=0.43; end-systolic volume, R(2)=0.35; stroke volume, R(2)=0.30), while EF was unaffected.
224 5; 5.3] vs 3.1 [2.6; 3.9] L/min/m; p<0.001), stroke volume remained unchanged (34 [37; 47] vs 40 [31;
225 50 ml/m(2) to 36 ml/m(2), respectively) with stroke volume remaining constant (49 ml/m(2) vs. 51 ml/m
227 1.9% and 2.0% for left and right ventricular stroke volumes, respectively) than gated (coefficient of
230 tricular systolic and diastolic volumes, low stroke volume, smaller EOA, and prosthesis-patient misma
231 A showed increased LV diameters, LV volumes, stroke volume, stroke work, and septal peak systolic tis
232 e while heat stressed, a greater decrease in stroke volume (SV) for a similar decrease in ventricular
234 ise intolerance is associated with a reduced stroke volume (SV) in POTS, and that the high heart rate
235 attenuates orthostatic-induced decreases in stroke volume (SV) via altering the operating position o
236 TGA patients had lower peak VO2, Qc, and stroke volume (SV), a blunted Qc/VO2 slope, and diminish
237 diastolic volume (EDV), end systolic volume, stroke volume (SV), cardiac output (CO), LV mass, ejecti
238 ed with novel magnetic resonance measures of stroke volume (SV), cardiac output (CO), total periphera
239 lic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection fraction (EF), cardiac outp
240 Blood pressure was measured by arm cuff; stroke volume (SV), ejection fraction, and end-diastolic
242 lic volume (EDV), end-systolic volume (ESV), stroke volume(SV), and myocardial mass, were derived.
243 face area (PISA) (in vitro and patients) and stroke volume technique (patients) to assess mitral regu
245 (up to an 80 ms increase from baseline) and stroke volume (up to 9.7 mL) were recorded, associated w
246 We investigated the prognostic impact of stroke volume using the recently proposed flow-gradient
249 used to assess fluid responsiveness included stroke volume variation (nine trials), pulse pressure va
250 olute change in pulse pressure variation and stroke volume variation after increasing tidal volume fr
251 olute change in pulse pressure variation and stroke volume variation after increasing tidal volume fr
253 he standard stroke volume variation, the new stroke volume variation algorithm was able to predict fl
255 variation, pulse pressure variation, and/or stroke volume variation and the change in stroke volume/
256 te, central venous pressure, cardiac output, stroke volume variation and, with use of inspiratory hol
259 are superior to pulse pressure variation and stroke volume variation in predicting fluid responsivene
261 ng volume therapy, including cardiac output, stroke volume variation monitoring, and global end-diast
262 The changes in pulse pressure variation or stroke volume variation obtained by transiently increasi
263 Median [interquartile range, 25% to 75%] stroke volume variation values at baseline were not diff
264 cteristic curve analysis showed that the new stroke volume variation was an accurate predictor of flu
265 rterial pressure waveforms were recorded and stroke volume variation was computed from the new and fr
268 the curve = 0.892 +/-, whereas the standard stroke volume variation was not (area under the curve =
269 . 12% +/- 3%, p < .05), whereas the standard stroke volume variation was similar in the two groups (2
270 the changes in pulse pressure variation and stroke volume variation will predict fluid responsivenes
272 baseline cardiac function, as quantified by stroke volume variation, and the subsequent changes in m
273 en the baseline systolic pressure variation, stroke volume variation, and/or pulse pressure variation
275 udies that evaluated the association between stroke volume variation, pulse pressure variation, and/o
277 tween the baseline pulse pressure variation, stroke volume variation, systolic pressure variation, an
281 0.95; 95% confidence interval 0.82-0.99) and stroke volume variations (0.60; 95% confidence interval
285 ariations, systolic pressure variations, and stroke volume variations; and cardiac output were obtain
286 mL higher (95% CI: 0.0, 0.8 mL higher), the stroke volume was 0.5 mL higher (95% CI: 0.2, 0.8 mL hig
287 timing of echocardiography, although reduced stroke volume was an indicator of adverse prognosis.
288 < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all leve
289 eterization showed modest agreement, whether stroke volume was measured by oxymetry (0.69 +/- 0.16 cm
290 cTfRMAb-EPO fusion protein, the hemispheric stroke volume was reduced 81% and the neural deficit was
291 variable, pulse distension (a surrogate for stroke volume) was improved in the neurokinin-1 receptor
292 (EF, end-systolic and end-diastolic volumes, stroke volumes) was not different in 371 subjects with C
293 city, left ventricular systolic pressure and stroke volume were blunted in dysferlin-deficient mouse
294 During PEI, LV end-diastolic volume and stroke volume were increased in both groups (P < 0.001),
295 cular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compar
296 2)max, LV mass, LV end-diastolic volume, and stroke volume were significantly smaller and the LV was
297 amine deficiency, including elevated cardiac stroke volume with decreased vascular resistance, and el
298 kely than HFrEF to experience a reduction in stroke volume with nitroprusside (p < 0.0001), suggestin
299 curs in an attempt to limit the reduction in stroke volume, with uncoupling and increased wall stress
300 led to concentric LV remodeling and reduced stroke volume without impaired LV contractility determin
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