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1 nchanged from the baseline period during the hyperemic and control periods.
2 The purpose of this study was to compare the hyperemic and hemodynamic responses of intracoronary nit
3          Basal average peak velocity (bAPV), hyperemic APV (hAPV), diastolic/systolic velocity ratio
4  using a Doppler wire to measure resting and hyperemic average peak velocities in the left anterior d
5                                         Peak hyperemic BABF was not altered by dobutamine infusion co
6 ascular function, we determined the reactive hyperemic blood flow (RHBF) responses to 10 minutes of f
7            In addition, we measured rest and hyperemic blood flow in eight normotensive controls.
8 nt ratio led to substantially underestimated hyperemic blood flow measurements.
9 d greater brachial diameters and resting and hyperemic blood flow, marginally increased endothelial f
10                                 The abnormal hyperemic blood flows and flow reserve suggest an impair
11                                     However, hyperemic blood flows were significantly lower in the pa
12                             Resting and peak hyperemic brachial artery blood flow and diameter (BABF
13 nd and coronary flow measurements (basal and hyperemic by Doppler flow wire).
14 ak oxygen consumption [Vo2]) on peak Vo2 and hyperemic calf blood flow in patients with severe conges
15 ac output, arterio-venous oxygen difference, hyperemic calf blood flow, and skeletal muscle fiber mor
16                Peak exercise cardiac output, hyperemic calf blood flow, and vascular conductance were
17                                              Hyperemic CBF was less in AS compared with controls (2,1
18 pillary resistance to rise, which attenuates hyperemic CBF.
19                                      If each hyperemic component (BOLD, CBV, CBF) is demonstrated to
20                             Specific to each hyperemic component, a universal transfer function (with
21 om linear to nonlinear, associations between hyperemic components and neural activity were linear.
22                                              Hyperemic components were investigated at 11.7 T in alph
23 stenosis resistance (SR) during baseline and hyperemic conditions as well as fractional flow reserve
24 y microvascular resistances during basal and hyperemic conditions.
25 odeling now permit determination of rest and hyperemic coronary flow and pressure from CTA scans, wit
26 trongly associated with post-PCI increase in hyperemic coronary flow velocity.
27  mass (LVM), and PET to quantify resting and hyperemic (dipyridamole 0.56 mg/kg) MBF and CVR in both
28 circulatory resistance (IMR), defined as the hyperemic distal pressure multiplied by the hyperemic me
29                        However, the coronary hyperemic dose responses and systemic hemodynamic effect
30 t relationship existed between the change in hyperemic DPT (1.0+/-4.7 s/min [range, 6.8 to 9.6]) and
31                                              Hyperemic FFR flow was similar to baseline iFR flow in f
32 deflation to baseline pulse amplitude in the hyperemic finger divided by the same ratio in the contra
33        Brachial artery diameter responses to hyperemic flow (endothelium dependent), and glyceryltrin
34 aortic stiffness was associated with reduced hyperemic flow (P<0.001).
35                                         Peak hyperemic flow (PHF) and time-to-peak (TTP) were compute
36                                Although peak hyperemic flow exceeded the prestenotic value, resting f
37                               Post-treatment hyperemic flow in the patients treated with lisinopril w
38            Brachial hyperemic shear rate and hyperemic flow normalized as a function of baseline radi
39 n contrast, femoral hyperemic shear rate and hyperemic flow normalized to baseline radius were lower
40               Ascorbic acid had no effect on hyperemic flow or arterial dilation to sublingual nitrog
41                                              Hyperemic flow ratio is derived from an automatic resist
42 (5.6+/-1.6 cm/s) and significantly less than hyperemic flow velocity (21.2+/-3 cm/s; P<0.01).
43 al artery flow-mediated dilation (n=1446) or hyperemic flow velocity (n=1043).
44      We quantified the change in resting and hyperemic flow velocity after PCI in stenoses defined ph
45 ree period changes at least 4-fold less than hyperemic flow velocity after PCI.
46  a curvilinear relationship to the change in hyperemic flow velocity but was flat for resting flow ve
47 locity over the resting wave-free period and hyperemic flow velocity did not differ statistically.
48                    In these patients (n=20), hyperemic flow velocity increased significantly from 46.
49                                              Hyperemic flow velocity increases 6-fold more when steno
50                                     Pre-PCI, hyperemic flow velocity is diminished in stenoses classe
51                     The greatest increase in hyperemic flow velocity was observed when treating steno
52                         In patients with AS, hyperemic flow velocity was significantly lower as compa
53 lar resistance and a concomitant increase in hyperemic flow velocity, resulting in immediate improvem
54 =0.002) and either flow-mediated dilation or hyperemic flow velocity.
55 nosis severity was adjusted serially so that hyperemic flow was severely reduced yet always higher th
56 nterior descending (LAD) pressure divided by hyperemic flow, measured with an external ultrasonic flo
57 [-62.6 to -12.6]; P=0.005), mean decrease in hyperemic flow: 306.5 to 272.9 mL/min (difference, -33.5
58 e (resting flow=22+/-5 versus 14+/-4; P<.01; hyperemic flow=59+/-17 versus 39+/-12 mL/min; P<.05).
59 rmal rest myocardial blood flows but reduced hyperemic flows and flow reserve.
60 uman subjects but cannot be used to estimate hyperemic flows due most likely to the strong binding of
61 consumption correlated linearly with maximal hyperemic flows in the left coronary artery territories
62                                 However, the hyperemic flows were significantly lower in systemic RVs
63 in may prove more suitable for evaluation of hyperemic flows.
64  reducing the area of imaged skin containing hyperemic foci by 49.1%.
65          We show that these persistent early hyperemic foci reliably predict sites of angiogenesis an
66                                              Hyperemic foci were multifocal and heterogeneously distr
67 o reduce the area of skin that exhibit these hyperemic foci, reducing the area of imaged skin contain
68  treatment developed in sites of preexisting hyperemic foci.
69                                  We examined hyperemic forearm blood flow, an indicator of microvascu
70                                  Resting and hyperemic forearm vascular resistance and indices of the
71  were associated with increased baseline and hyperemic FVR (P<0.001).
72             We measured Pd/Pa, iFR, FFR, and hyperemic iFR.
73 ssure gradient and significantly inferior to hyperemic iFR.
74                                 The reactive hyperemic index (RHI), which measures endothelium-depend
75  resistance index, compared with established hyperemic intracoronary hemodynamic parameters, because
76                                          The hyperemic macroscopic appearance of tumors containing Sd
77                            By contrast, both hyperemic MBF (+53%, P<0.0001 versus baseline) and CFR (
78 logical study patients (n=12) showed reduced hyperemic MBF (1.25+/-0.30 versus 1.66+/-0.38 mL.min(-1)
79 owest tertile for delta HR showed a 7% lower hyperemic MBF (1.84 +/- 0.6 ml/min/g vs. 1.98 +/- 0.6 ml
80 istic curve analysis indicated that impaired hyperemic MBF (area under the curve, 0.84; 95% confidenc
81 elta MAP also showed a weak correlation with hyperemic MBF (R = 0.04, p = 0.44) and with CVR (R = 0.1
82     Overall, delta HR correlated poorly with hyperemic MBF (R = 0.10, p = 0.06) and with CVR (R = 0.1
83                          After intervention, hyperemic MBF and CFR were unchanged in groups 1, 2, and
84  significantly higher compared with that for hyperemic MBF and coronary flow reserve (0.76; P=0.32 an
85                In this pilot study, impaired hyperemic MBF and coronary flow reserve were associated
86                                  Increase in hyperemic MBF and CVR transmurally was directly related
87 e optimal cutoff values were 2.3 and 2.5 for hyperemic MBF and myocardial flow reserve, respectively.
88                               Mean values of hyperemic MBF and perfusion reserve, but not resting MBF
89                                    Moreover, hyperemic MBF and PR were correlated strongly and invers
90 ovement of diagnostic accuracy compared with hyperemic MBF assessment was determined.
91 im of this pilot study was to assess whether hyperemic MBF impairment may be related with VA inducibi
92 rdial blood flow (MBF) in a stenotic area to hyperemic MBF in a normal perfused area.
93                                 In contrast, hyperemic MBF increased when metoprolol was added to dip
94    The effect of beta 1 receptor blockade on hyperemic MBF is unknown.
95 83%, and 76%, respectively, for quantitative hyperemic MBF PET.
96 in resting MBF together with the increase in hyperemic MBF resulted in a significant increase in the
97 imed to evaluate and compare the accuracy of hyperemic MBF versus coronary flow reserve (CFR).
98                                              Hyperemic MBF was also significantly lower in subjects w
99                              The decrease in hyperemic MBF was associated with a decrease in blood ve
100                                              Hyperemic MBF was more accurate than CFR, implying that
101                   The diagnostic accuracy of hyperemic MBF was significantly higher than CFR (80% vs.
102                             Both resting and hyperemic MBF were lower in men than in women, even afte
103  MAP (i.e., greatest decline) showed similar hyperemic MBF, and an 8% lower CVR compared with those i
104 raphy was performed to quantify resting MBF, hyperemic MBF, and coronary flow reserve.
105                                              Hyperemic MBF, coronary flow reserve, and RFR were lower
106 cans on the basis of (presumably) sufficient hyperemic MBF.
107                                     However, hyperemic MBFs in the mid-to-apical LV section were lowe
108  interval [CI], 1.07-1.63; P=0.01) and lower hyperemic mean flow velocity (HR, 0.84; 95% CI, 0.71-0.9
109 tic stiffness and CVD events was mediated by hyperemic mean flow velocity.
110                           The inverse of the hyperemic mean transit time has been shown to correlate
111 onary pressure divided by the inverse of the hyperemic mean transit time provides an index of microci
112  hyperemic distal pressure multiplied by the hyperemic mean transit time.
113                                              Hyperemic microvascular resistance (expressed in mm Hg.c
114                      We investigated whether hyperemic microvascular resistance (HMR) immediately aft
115        TAVI induces an immediate decrease in hyperemic microvascular resistance and a concomitant inc
116                                              Hyperemic microvascular resistance correlated with late-
117                                              Hyperemic microvascular resistance decreased from 2.03+/
118 inistration [iFRa]), FFR, HSR, baseline, and hyperemic microvascular resistance were calculated using
119 , whereas mean values were used to calculate hyperemic microvascular resistance.
120  emission tomography to quantify resting and hyperemic myocardial blood flow (MBF) and CVR.
121 creasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64
122 low reserve (RFR) is defined as the ratio of hyperemic myocardial blood flow (MBF) in a stenotic area
123                                     Impaired hyperemic myocardial blood flow (MBF) is associated with
124                       Baseline and follow-up hyperemic myocardial blood flow did not differ (11.8% +/
125       Using model-independent deconvolution, hyperemic myocardial blood flow was evaluated, and ische
126                                              Hyperemic myocardial blood flow was lower in patients th
127                     After revascularization, hyperemic myocardial blood flow was significantly higher
128 ia PET, and MFR was calculated as a ratio of hyperemic over resting MBF.
129 mass), but there was significant increase in hyperemic peak diastolic velocity (0.71+/-0.26 vs. 1.08+
130 diated dilation was linearly proportional to hyperemic peak systolic WSS (r = 0.79, p = 0.0001).
131 line diameter (r = 0.62, p = 0.006), but the hyperemic peak WSS stimulus was also inversely related t
132 aseline perfusion values under occlusion) in hyperemic perfusion upon removal of occlusion (PEAK/OCC)
133 rteries; 95% CI, -0.2 to 2.1; P=0.116), peak hyperemic popliteal flow (0.0+/-0.4 mL/s; 95% CI, -0.8 t
134 k walking time (PWT), collateral count, peak hyperemic popliteal flow, and capillary perfusion measur
135 e then matures via development of an initial hyperemic (positive BOLD) phase that eventually masks ox
136 tance was 2.5 +/- 1.0 times higher than mean hyperemic resistance in patients.
137 ng myocardial resistance does not equal mean hyperemic resistance, thereby contravening the most basi
138 ic resting myocardial resistance equals mean hyperemic resistance.
139  antagonists potently reduced the LC-induced hyperemic response (-56%, p < 0.001 or -47%, p < 0.05).
140 is small (approximately 15%) relative to the hyperemic response (approximately 60%), (ii) this energy
141 ic effects and skewed data, we expressed the hyperemic response (called the PAT ratio) as the natural
142 dy was to determine if other pathways to the hyperemic response are present and if these neurons have
143 hemotherapy should be delayed until the peak hyperemic response has subsided.
144         Mucosal damage alone evoked a strong hyperemic response in both control and ablated rats.
145 es an equivalent but more prolonged coronary hyperemic response in normal coronary arteries.
146 l endothelial function by measuring reactive hyperemic response in the finger, was performed in 23 pa
147  acid challenge is enhanced by the sustained hyperemic response mediated through sensory afferent neu
148 cause maximal hyperemia as compared with the hyperemic response of complete coronary occlusion in 6 c
149 complete coronary occlusion yielded a better hyperemic response than either drug, indicating that max
150  was produced in dogs to reduce the reactive hyperemic response to <20%.
151 gnificant, dose-dependent attenuation of the hyperemic response to 5 nmol adenosine.
152 ffeine is believed to attenuate the coronary hyperemic response to adenosine by competitive blockade
153                                 The impaired hyperemic response to ATP persisted in older (20- to 30-
154 ation of digital pulse amplitude and digital hyperemic response to cardiovascular risk factors in the
155                                          The hyperemic response to dipyridamole and the myocardial fl
156                                   The normal hyperemic response to dipyridamole in long-term smokers
157                                          The hyperemic response to dobutamine is in excess of that pr
158                              We examined the hyperemic response to elevated luminal PCO(2) in the duo
159 ions that reduce EDNO production disturb the hyperemic response to exercise, resulting in a reduced e
160 o significant difference was observed in the hyperemic response to forearm ischemia.
161 ved significantly greater, though transient, hyperemic response to IC infusion of mannitol compared t
162 ned associations between these exposures and hyperemic response to ischemia and baseline pulse amplit
163                    Conclusions: The duodenal hyperemic response to luminal CO(2) is dependent on cyto
164                                          The hyperemic response to mucosal damage alone is not mediat
165 on size is inversely related to the cerebral hyperemic response to oxotremorine, a muscarinic agonist
166 in these groups by testing the local thermal hyperemic response to saline used as a reference compare
167 improves basal PMBF, and restores the normal hyperemic response to secretion.
168 reduction of the postocclusive peak reactive hyperemic response was also observed in control dogs (16
169              The increase in BAD during peak hyperemic response was greater after infusion of dobutam
170 owever, in animals pretreated with 8PT, this hyperemic response was severely attenuated, primarily by
171 tically involved in mediating the functional hyperemic response within rodent whisker-barrel cortex (
172                                      Digital hyperemic response, as measured by RH-PAT, is attenuated
173 sine receptor antagonist 8PT attenuated this hyperemic response, it is concluded that adenosine is in
174                      In contrast to the peak hyperemic response, the increase in BAD (%) induced by S
175 ortant components of the cortical functional hyperemic response.
176 controls, patients had a blunted and delayed hyperemic response.
177 ot produce a commensurate attenuation of the hyperemic response.
178     Acid exposure after damage sustained the hyperemic response.
179 ed rats lost gastric protection despite this hyperemic response.
180 er system in the transduction of adenosine's hyperemic response.
181 een the air pollution exposures assessed and hyperemic response.
182 p < 0.05) K+ channels primarily impaired the hyperemic response.
183                                     Reactive hyperemic responses (a measure of the severity of ischem
184 on of pyramidal cells evoked COX-2-dependent hyperemic responses in mice.
185  plasma markers of inflammation, or vascular hyperemic responses to be included in diagnostic algorit
186 aser Doppler imaging, and joint swelling and hyperemic responses to recombinant human beta-tryptase.
187 In urethane anesthetized animals, functional hyperemic responses were obtained both before and after
188 tment, particularly in those with normalized hyperemic responses.
189 onary flow reserve (CFR) of > or =2.5 (CFR = hyperemic/resting blood flow).
190               In controls and patients, MPR (hyperemic/resting perfusion) and Endo/Epi ratio were det
191 ppeared as pale necrotic areas surrounded by hyperemic rims, while chronic lesions demonstrated progr
192 nding eruption, petechiae on the palate, and hyperemic sclerae in a 44-year-old man returning from Pu
193                                     Brachial hyperemic shear rate and hyperemic flow normalized as a
194                         In contrast, femoral hyperemic shear rate and hyperemic flow normalized to ba
195                                     However, hyperemic SR, combining both pressure and flow velocity
196 ld represent physiological adaptation to the hyperemic state of adiposity in childhood.
197                       In this study, we used hyperemic stenosis resistance (HSR), a combined pressure
198 eement: -0.13 to 0.36), proportional to mean hyperemic stenosis resistance (Spearman rho =0.61; P=0.0
199  The primary end point was the difference in hyperemic stenosis resistance index between measurements
200                                         Mean hyperemic stenosis resistance was 0.37+/-0.19 Hg/cm/s fo
201  volumetric flow augmentation in response to hyperemic stimuli (i.e., abnormal coronary flow reserve)
202  nitroprusside also appears to be a suitable hyperemic stimulus for coronary physiological measuremen
203 ypercapnia of 10 mm Hg may provide a cardiac hyperemic stimulus similar to adenosine.
204 requires a pressure-monitoring guidewire and hyperemic stimulus.
205 s on 11 healthy volunteers at rest and after hyperemic stress with dipyridamole.
206                      Thus, we propose that a hyperemic switch can be exploited to visualize the cance
207    In 62 patients with RAS, TPG (resting and hyperemic systolic gradient [HSG], fractional flow reser
208 peared to produce tumors that were much more hyperemic than those formed by appropriate control cells
209 ed as the ratio of adenosine-induced maximal hyperemic to basal average peak velocity.
210       The CFR was calculated as the ratio of hyperemic to baseline coronary blood flow velocity in th
211  reserve (PR) was calculated as the ratio of hyperemic to rest MBF.
212                         CFR was the ratio of hyperemic to resting diastolic flow velocity.
213 usion reserve was calculated as the ratio of hyperemic to resting MBF.
214          MPRI was calculated as the ratio of hyperemic to resting myocardial blood flow and subdivide
215 ess apparent deviation, such as the ratio of hyperemic to resting velocity (coronary flow reserve), h
216 etrofosmin is technically feasible, although hyperemic values are significantly lower than from PET w
217                                        Total hyperemic volume in the recovery period increased by 73%
218 schemia increased by 88% (p = 0.04), whereas hyperemic volume rose by 98% (p = 0.1).
219 c resonance angiography (PMRCA), we measured hyperemic WSS and FMD in 18 healthy volunteers.
220 rterial FMD is linearly proportional to peak hyperemic WSS in normal subjects.
221 ounted for, at least partially, by a greater hyperemic WSS stimulus in small arteries.
222 F, qualitative measurements plateaued in the hyperemic zones.

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