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.