ライフサイエンスコーパス: heart rate

1 ess, time to hatch, length, deformities, and heart rate).

2 nicity, worse glycemic control, and elevated heart rate.

3 an intrinsic respiratory modulated pacing of heart rate.

4 th a decrease in mean cardiac output or mean heart rate.

5 ariety of wearable technology devices report heart rate.

6 ated respiration rates, close to the resting heart rate.

7 ne, and (2) process intensity data to derive heart rate.

8 homeostatic mechanism for rapid switches in heart rate.

9 mid-to-anterior cingulate cortex, influence heart rate.

10 e duration of analysed ECG fragments and the heart rate.

11 to modulation and/or synchronization of the heart rate.

12 [7.3-9.3] hours at 68+/-10% of their maximum heart rate.

13 rtical regions involved in the regulation of heart rate.

14 no significant changes in blood pressure or heart rate.

15 n important role in the autonomic control of heart rate.

16 stronger for individuals with a more stable heart rate.

17 autonomic activation and acute increases in heart rate.

18 significantly lower peak whole-body exercise heart rates.

19 ic metabolic rates are likely powered by low heart rates.

20 r (+ 0.85%), mobility and stability (+ 22%), heart rate (- 1.1%) and lean muscle mass (+ 1.4%)] and c

21 [SD, 8] years; 74 [46%] women; mean baseline heart rate, 100/min [SD, 18/min]), 145 (91%) completed t

22 .4 versus 22.7+/-4.0 mL/kg/min; P<0.001) and heart rate (122+/-20 versus 155+/-14 bpm; P<0.001) were

23 ic response to regadenoson (mean increase in heart rate 13.1+/-5.4 bpm vs. 28.5+/-8.9 bpm in those wi

24 me (- 7.7%), processing efficiency (+ 1.8%), heart rate (- 2.4%) and lean muscle mass (+ 1.5%).

25 the heart rate in ECG strips obtained at low heart rates (25-60 bpm) and processed by the feature det

26 9 vs. 1.70 +/- 0.23 cm s(-1) ) and decreased heart rate (321 +/- 23 vs. 304 +/- 22 bpm, both P < 0.05

27 ; subsequent intervention led to higher mean heart rate (56 +/- 2 beats/min vs. 50.1 +/- 0.4 beats/mi

28 where they are involved in the regulation of heart rate(6), pulmonary artery tone(5,7), sleep/wake cy

29 alivary cortisol (6.8 nmol/l, P < 0.001) and heart rate (7.2 beats/min, P = 0.035) increased signific

30 s/min (-3.7 to 0.1 beats/min) (p = 0.06) for heart rate; 96.8 mL/min/m (71.1-122.5 mL/min/m) (p < 0.0

31 between groups) despite lower peak mean+/-SD heart rates (98.6+/-19.4 versus 112.0+/-20.3 beats per m

32 fferences for 16 outcomes, including resting heart rate (a mean of 76.9/min [SD, 12.1/min] with digox

33 l network, was trained on anonymized data of heart rate, activity level, and ECGs from 7500 AliveCor

34 cal auditory processing and vagal control of heart rate and (2) to verify a possible association betw

35 ory increases in sympathetic nerve activity, heart rate and arterial blood pressure induced by reduct

36 ggressive medical therapy to achieve optimal heart rate and blood pressure control.

37 sinus initiates autonomic reflexes to change heart rate and blood pressure for cardiovascular homeost

38 Heart rate and blood pressure oscillate in phase with re

39 thetic vasomotor neuron activity, generating heart rate and blood pressure oscillations in phase with

40 ing that both cardiovascular physiology (eg, heart rate and blood pressure) and pathophysiology (eg,

41 dications cause modest elevations in resting heart rate and blood pressure.

42 arkers were systolic blood pressure, resting heart rate and body mass index.

43 tions ranging from appetite and digestion to heart rate and breathing.

44 the ATP demand required to support increased heart rate and cardiac output.

45 PCR that plays important roles in regulating heart rate and CNS functions.

46 tein Gs by beta(1)-ARs, leading to increased heart rate and contractility.

47 s for this circuitry in the daily control of heart rate and corticosterone secretion, collectively es

48 nts with Covid-19 developed pQTc; age, basal heart rate and dual antiviral therapy were found as inde

49 atrial fibrillation, basal QTc values, basal heart rate and dual antiviral therapy, age(OR 1.06, 95%

50 Heart rate and heart rate variability (HRV) are mainly d

51 utomatically selected based on the patient's heart rate and heart rate variability, derived from the

52 g SE, mice developed an increased interictal heart rate and heart rhythm abnormalities (i.e. sinus pa

53 S6 and HCN4); showed that ivabradine reduces heart rate and increases HRV in zebrafish embryos, as it

54 iac electrical activity, including decreased heart rate and irregular, arrhythmic RR (interbeat) inte

55 lunting of the positive relationship between heart rate and left ventricular (LV) contractility known

56 Glucocorticoids increased the heart rate and muscle contractions.

57 of ozanimod-related symptomatic reduction in heart rate and no second-degree or third-degree cases of

58 er maximum heart rate, and larger changes in heart rate and rating of perceived exertion during the t

59 nduced PB the dynamics and coherence between heart rate and respiration and their relationship to und

60 The phase coherence between instantaneous heart rate and respiration is shown to increase signific

61 Maps of the spatial distribution of heart rate and respiratory rate information were develop

62 confirmed the role of established genes for heart rate and rhythm (RGS6 and HCN4); showed that ivabr

63 oupling at respiratory rates slower than the heart rate and shown that respiratory oscillations lead

64 Results showed that synchrony in both heart rate and skin conductance level emerged during fac

65 Heart rate and skin conductance were recorded continuous

66 continuous monitoring of photoplethysmogram, heart rate, and activities of athletes.

67 ntly affect coagulation time, bleeding time, heart rate, and blood pressure.

68 re, physical activity, indirect calorimetry, heart rate, and brain activity.

69 ion is hyper-additive for blood pressure and heart rate, and hypo-additive for peripheral haemodynami

70 oncentration and weight loss, higher maximum heart rate, and larger changes in heart rate and rating

71 We assessed waveform intervals, heart rate, and rhythm, including the signature LQTS rhy

72 Intraarterial blood pressure, heart rate, and simultaneous brachial artery diameter an

73 as three to five heartbeats depending on the heart rate, and was repeated 15 minutes following the ad

74 reased arrhythmic risk, and Tpe changes with heart rate are even stronger predictors.

75 ng pathways responsible for raising exercise heart rate are impaired in HFpEF is unknown.

76 er BI, a history of malignancy, and elevated heart rate are not included in most VTE risk assessment

77 d RMH paced; the latter had the same average heart rate as the monotonically paced animals.

78 s per heartbeat in patients with a CIED with heart rates as high as 102 beats per minute.

79 s per heartbeat in patients with a CIED with heart rates as high as 102 beats per minute.

80 rioventricular (AV) block without changes in heart rate, as measured by ECG and ex vivo optical mappi

81 formance was negatively correlated with mean heart rate, as well as single-item cognitive load measur

82 ted in a dose-dependent higher HRV and lower heart rate at 5 days post-fertilization.

83 le rats exposed to DE demonstrated increased heart rate at the start of LVP assessments, heart rate,

84 isting methods, for continuous monitoring of heart rate at the wrist.

85 However, these animals displayed lower heart rates at different levels of cerebral perfusion, s

86 ng the levels of salivary cortisol, IOP, and heart rate before, immediately after, and 40 minutes aft

87 established biophysical measurements such as heart rate, blood oxygenation, and body temperature.

88 xpenditure, lipid utilization, SNS activity, heart rate, blood pressure or lean body mass.

89 perative physiological parameters, including heart rate, blood pressure, oxygen saturation, and venti

90 Compared to heart rate, body temperature and blood pressure, respira

91 rhythmia or paced monotonically at a matched heart rate; cardiac function was measured using non-inva

92 systemic fetal hypoxia, or changes in fetal heart rate, carotid blood flow or carotid oxygen deliver

93 s of neural activation and physiology (i.e., heart rate change) in detecting affective valence induct

94 The PQ interval also responded to the heart rate changes with a delay which was highly sex dep

95 increased sensitivity of the QT interval to heart rate changes.

96 min, thus opening the possibility to monitor heart rate continuously in a clinical environment.

97 ere bacteremia (daily), body temperature and heart rate (continuously monitored by telemetry), and su

98 e is little evidence to support selection of heart rate control therapy in patients with permanent at

99 Logistic regression identified EMW, heart rate-corrected QT interval (QTc), female sex, and

100 drome (LQTS) is characterized by a prolonged heart rate-corrected QT interval (QTc).

101 ile range [IQR], 7.7-23; range, 0-59, median heart rate-corrected QT interval [QTc] at diagnosis 557

102 EMW outperformed heart rate-corrected QT interval as a predictor of sympt

103 On the Isle of May in Scotland, we collected heart rate data as a proxy for energy expenditure in 52

104 with a fitness trainer and provides her with heart rate data from his smartwatch.

105 l, these findings support the acquisition of heart rate deceleration concurrently with fMRI to provid

106 cited change in breathing rate (DeltaBR) and heart rate (DeltaHR), respectively.

107 r pressure slopes) and anesthetic (change in heart rate [DeltaHR], average heart rate [HR], reflexes,

108 h renal function or resting and postexercise heart rate demonstrated a positive association of lympho

109 We studied PQ heart rate dependency in 599 healthy subjects (aged 33.5

110 (ECG) PQ interval is known to be moderately heart rate dependent, but no physiologic details of this

111 roups, Tpe intervals were not systematically heart rate dependent.

112 simulations predicted a further reduction in heart rate during amiodarone administration, indicating

113 se appear to have ample cardiac reserves, as heart rate during hypoxic flights was not higher than in

114 trol network, and increased EMG activity and heart rate during spider conditions in PP in comparison

115 ing lunges followed by a gradual decrease of heart rate during the prolonged glide as engulfed water

116 Heart rates during dives were typically 4 to 8 beats min

117 CG)-depth recorder tag to measure blue whale heart rates during foraging dives as deep as 184 m and a

118 trasound), end-tidal CO(2) (capnography) and heart rate (ECG) were performed for 5 min at rest (normo

119 , beat-to-beat BP (photoplethysmography) and heart rate (electrocardiogram) responses during the LBNP

120 hich the camera could not produce a reliable heart rate estimate lasted under 3 min, thus opening the

121 The mean absolute error between the heart rate estimates from the camera and the average fro

122 higher levels of perceived effort when their heart-rate feedback was faster compared with when they c

123 pants did not report lower effort when their heart-rate feedback was slower, which is reassuring, giv

124 stimuli were correlated with the mean of the heart rate ([Formula: see text]) and heart rate variabil

125 icipants false acoustic feedback about their heart-rate frequency during an effortful cycling task.

126 signals and a novel algorithm to extract the heart rate from these signals.

127 their wrists showed higher and more variable heart rates, greater electrodermal activity, and even hi

128 CM should be suspected in patients with mean heart rate >100 beats/min, atrial fibrillation, and/or p

129 ns and wireless autonomic monitors to record heart rate, heart rate variability, and movement in infa

130 hods of quantifying stress (cortisol levels, heart rate/heart rate variability) require specialist eq

131 changes in bee survival, flower visitation, heart rate, hemocyte levels, and expression of genes rel

132 these patients were older, had higher basal heart rates, higher rates of paroxysmal atrial fibrillat

133 lf circumference (CC, central hypovolaemia), heart rate (HR) and digital heart-level mean arterial bl

134 ode (SAN) dysfunction (SND) manifests as low heart rate (HR) and is often accompanied by atrial tachy

135 1), SNA response to evoked PVCs (p = 0.005), heart rate (HR) at rest (p = 0.003), and exercise (p < 0

136 ctions of affective valence with measures of heart rate (HR) deceleration to predict predefined norma

137 eter, crown-rump length (CRL), and embryonal heart rate (HR) dimensions to identify early pregnancy l

138 To limit autonomic neural influences on heart rate (HR) during isoproterenol, dexmedetomidine an

139 ermal activity (EDA), temperature (TEMP) and heart rate (HR) from 66 people with epilepsy (9.9 +/- 5.

140 y a rise in mean arterial pressure (MAP) and heart rate (HR) in response to exercise and is necessary

141 Heart rate (HR) is extremely valuable in the study of co

142 mulation also evokes blood pressure (BP) and heart rate (HR) responses in rats.

143 Cardiorespiratory parameters and heart rate (HR) variability (HRV) (rMSSD, SD1, HF [ms(2)

144 distressing films as a trauma analogue while heart rate (HR) was measured.

145 RV indices, BRS, office beat-to-beat BP, and heart rate (HR) were measured for 10 minutes at rest.

146 determining BP, that is, stroke volume (SV), heart rate (HR), and total peripheral resistance (TPR),

147 Heart rate (HR), heart rate variability (HRV) [rMSSD, SD

148 ency distal body temperature (DBT), sleeping heart rate (HR), sleeping heart rate variability (HRV),

149 to the exercise intensity quantified by the heart rate (HR).

150 output (CO) while causing reflex sinus rate (heart rate [HR]) increase.

151 tic (change in heart rate [DeltaHR], average heart rate [HR], reflexes, induction/recovery times) par

152 rofiles both without and with correction for heart rate hysteresis.

153 resting mean arterial pressure and increased heart rate in all but 2 controls.

154 el-Ziv '76 and Titchener T-complexity on the heart rate in ECG strips obtained at low heart rates (25

155 xhibit significant associations with resting heart rate in human populations.

156 and sympathetic neural circuits that control heart rate in mice.

157 isms responsible for exertional increases in heart rate, in patients with HFpEF and senior controls.

158 uscarinic M2 receptors resulted in transient heart rate increases following dosing.

159 ss on social preferences, but stress-related heart-rate increases predicted outgroup-hostile behavior

160 Materials and Methods A heart rate-independent, free-breathing 3D T2 mapping tec

161 and mediate increases in blood pressure and heart rate induced by falls in brain perfusion.

162 Acute neurogenic control of heart rate is achieved locally through direct neuro-card

163 rt failure, where respiratory entrainment of heart rate is diminished and respiratory entrainment of

164 gal stimulation [ECVS]), analyzing 15 s mean heart rate, longest RR, pauses, and atrioventricular blo

165 Even newly released drugs such as heart-rate lowering agent ivabradine block the rapid del

166 crease of 4.2% [95% CI = 0.8-7.6; P = .03]), heart rate (mean increase 11.6% [95% CI = 8.4-14.8; P <

167 en found in health and wellness trackers for heart rate measurements, have been used to estimate HRV

168 The purpose was to determine the validity of heart rate measures in three commercially available spor

169 es, epidural analgesia, non-reassuring fetal heart rate, meconium in the amniotic fluid, shoulder dys

170 A progressive decline in maximum heart rate (mHR) is a fundamental aspect of aging in hum

171 we recorded a 2.5-fold increase above diving heart rate minima during the powered ascent phase of fee

172 e 17 secondary end points (including resting heart rate, modified European Heart Rhythm Association [

173 HRV was measured using a Polar RS800CX heart rate monitor.

174 terms of quality of care, intrapartum fetal heart rate monitoring decreased by 13.4% (-15.4 to -11.3

175 grated in photoplethysmography for real-time heart-rate monitoring, suggesting its potential for prac

176 vity (SNA) and baroreflex control of SNA and heart rate more dramatically in obese male rats; in obes

177 PHSG versus HG fetuses had decreased fetal heart rate-movement coupling (P < 0.05), which may indic

178 at 26 of them (81%) had alterations in their heart rate, number of daily steps or time asleep.

179 of IOP, salivary cortisol, STAI scores, and heart rate occurred after inducing psychologic stress wi

180 group differences in effects of nicotine on heart rate or blood pressure, confirmed comparable dosin

181 There was no significant change in heart rate or left ventricular diastolic pressure.

182 could be accentuated without an increase in heart rate or left ventricular filling pressures.

183 ta3 AR agonists did not significantly change heart rates or blood pressures.

184 r BMI (OR, 1.03 [95% CI 1.102-1.05]), higher heart rate (OR, 1.01 [95% CI 1.00-1.01]), higher respira

185 (OR 1.06, 95% C.I. 1.00-1.13, p<0.05), basal heart rate(OR 1.07, 95% C.I. 1.02-1.13, p<0.01) and dual

186 did not significantly alter blood pressure, heart rate, or plasma cortisol concentrations (all Pover

187 Concomitantly, we observed an increase in heart rate (p < 0.0001) and an increase of cardiac outpu

188 ignificant changes in temperature (P = .31), heart rate (P = .92), diastolic pressure (P = .31), or s

189 P < 0.001) compared to Amb, without changing heart rate (P = 0.6) or vascular-sympathetic baroreflex

190 Elderly had significantly lower heart rates (p < 0.05), cardiac index (p < 0.05), mean a

191 ls and leukocyte count and directly to basal heart rates(p<0.01).At multivariate stepwise analysis in

192 reshold (H = 82 +/- 4 vs. C = 85 +/- 3% peak heart rate, P = 0.86) after which levels of both molecul

193 eveloped for all 102 ECG variables including heart rate; P, R, and T axis; R-T axis deviation; PR int

194 ere 25 to 37 bpm, near the estimated maximum heart rate possible.

195 from other foreign societies, as indexed by heart rate, pupillometry and electrodermal activity.

196 Abnormal QT interval responses to heart rate (QT dynamics) is an independent risk predicto

197 Heart rate recordings were acquired in supine position i

198 and the averaged baseline measures of HRV to heart rate recovery (HRR) following maximal exercise.

199 k between human genetic variants influencing heart rate recovery after exercise and a variant RE with

200 to MED13L harboring variants associated with heart rate recovery after exercise.

201 remodelled targets mainly contributed to the heart rate reduction.

202 in the sinoatrial node (SAN) is involved in heart rate regulation by the autonomic nervous system.

203 occurrence of extreme elevations in resting heart rate relative to the individual baseline.

204 se of a sympathetic surge or by changing the heart rate, reproducing the different genotype-dependent

205 d into AT (n = 14, 40 min of cycling, 50-75% heart rate reserve), RT (n = 14, 6 resistance exercises,

206 ivities and exercise-real-time recordings of heart rate, respiration rate, energy intensity and other

207 uivalency to existing clinical standards for heart rate, respiration rate, temperature and blood oxyg

208 eart defects (CHD), changes in blood volume, heart rate, respiration, and edema during pregnancy may

209 Heart rate, respiratory rate and temperature were measur

210 hysiologic states, including blood pressure, heart rate, respiratory rate, and oxygen saturation, sho

211 lpha, beta, and theta rhythms, instantaneous heart rates, respiratory rates, and sweat pH, uric acid,

212 here were no significant differences in peak heart rate response during static handgrip between group

213 to examine whether using FFR data to tailor heart rate response in patients with HFrEF with cardiac

214 We also report that the heart rate response to optogenetic versus electrical sti

215 nce of CDR leads to inappropriately enhanced heart rate responses of the SAN to vagal nerve activity

216 pecific Cx43 knock-out mice the magnitude of heart rate responses to acute increases in intracranial

217 bly, we also found that insects show similar heart rate responses to body position as vertebrates, an

218 sue saturation index, calf circumference and heart rate responses to SAHC, thereby promoting g-tolera

219 ion is hyper-additive for blood pressure and heart rate (responses during co-activation of the two re

220 d neurocirculatory (MSNA, blood pressure and heart rate) responses to chemoreflex inhibition elicited

221 eflex autonomic pathways regulating exercise heart rate responsiveness are intact in HFpEF.

222 ce HRV (hcn4 and si:dkey-65j6.2 [KIAA1755]); heart rate (rgs6 and hcn4); and the risk of sinoatrial p

223 f diastolic blood pressure (DBP) and resting heart rate (RHR) in patients with hemodynamically signif

224 ed if reinstatement of respiratory-modulated heart rate (RMH) would improve cardiac performance in he

225 oup did not show significant changes in IOP, heart rate, salivary cortisol levels, and STAI scores.

226 Heart rate sensing smart bras are manufactured for femal

227 FFR-guided heart rate settings had no adverse effect on LV structur

228 nction, active smoking, or a higher baseline heart rate showed less improvement.

229 subjects led to increased blood pressure and heart rate, similar to traditional cigarettes.

230 external measurements (e.g., motion capture, heart rate, skin conductance, respiration, eye tracking,

231 Reflex vagal activity causes abrupt heart rate slowing with concomitant caudal shifts of the

232 nstantaneous variability of the beat-to-beat heart rate): spontaneous swallowing 12.02 +/- 1.07 ms vs

233 otoxicity was also assessed by measuring the heart rate, stroke volume, and cardiac output, as cardia

234 Changes in hemodynamic parameters (heart rate, stroke volume, blood pressure, and periphera

235 s dynamics similar to that of pupil size and heart rate, suggesting that task-related activity is rel

236 heart rate at the start of LVP assessments, heart rate, systolic pressure, and double product fell b

237 psible inferior vena cavae (IVC), and higher heart rates than survivors.

238 m wave condition-occurring near normal human heart rates-that minimizes pulsatile energy transmission

239 trial: P < 0.01, interaction: p = 0.01) and heart rate (time: P < 0.01, trial: P < 0.01, interaction

240 ympathetic nerve stimulation (SNS) increased heart rate to a lesser degree in DBH-Sap hearts compared

241 of the heart rate ([Formula: see text]) and heart rate variability ([Formula: see text]).

242 Fetal heart rate variability (FHRV) emerges from influences of

243 activity [normalized high frequency power of heart rate variability (HFn)] were evaluated using GLM a

244 Heart rate (HR), heart rate variability (HRV) [rMSSD, SD1, HF (ms(2))] an

245 complexity analysis, derived from non-linear heart rate variability (HRV) analysis, has been proposed

246 Heart rate variability (HRV) and CAEP were evaluated bef

247 Heart rate variability (HRV) and pulse rate variability

248 Heart rate and heart rate variability (HRV) are mainly determined by th

249 of cardiac autonomic modulation assessed by heart rate variability (HRV) during 14-month expeditions

250 MAE) on inhibitory control and resting-state heart rate variability (HRV) in children with Attention-

251 ts of effortful swallowing maneuver (ESM) on heart rate variability (HRV) in subjects with neurogenic

252 rdiac autonomic function was evaluated using heart rate variability (HRV) indices, cardiovascular aut

253 Heart rate variability (HRV) is a valid and non-invasive

254 extract features from ECGs including simple heart rate variability (HRV) metrics, commonly used sign

255 re (DBT), sleeping heart rate (HR), sleeping heart rate variability (HRV), and sleep timing, could be

256 the relationship of a single day measure of heart rate variability (HRV), and the averaged baseline

257 entified eight loci that are associated with heart rate variability (HRV), but candidate genes in the

258 a technique to test whether intrinsic fetal heart rate variability (iFHRV) exists and we show the ut

259 We tested whether intrinsic heart rate variability (iHRV), devoid of any external in

260 Heart rate variability (time and frequency domain) and a

261 Heart rate variability and plasma catecholamine levels w

262 ress event (sham clipping) and compared with heart rate variability and salivary cortisol.

263 For the entire sample, SBR correlated with heart rate variability and salivary cortisol.

264 Basal cardiovascular activity, including heart rate variability and sympathovagal balance, which

265 There was no difference in heart rate variability between the 1-year and 2-year pos

266 Time- and frequency-domain heart rate variability demonstrated significant decrease

267 90 minutes after stress, and high-frequency heart rate variability during stress were also assessed.

268 ess-induced interleukin-6 and high-frequency heart rate variability explained 15.5% and 32.5% of the

269 tic age acceleration was not associated with heart rate variability in either preterm or term born in

270 mponents showed that HIV+ men had: (1) lower heart rate variability irrespective of VL status, and (2

271 A contributor to heart rate variability is respiratory sinus arrhythmia o

272 However, the long-phase heart rate variability parameter, very-low-frequency pow

273 Neither analyzed heart rate variability parameters nor plasma catecholami

274 susceptibility to arrhythmias, whereas lower heart rate variability signals a component of autonomic

275 fluctuations in distal body temperature and heart rate variability that consistently anticipate the

276 igher interleukin-6 and lower high-frequency heart rate variability with stress.

277 ctivation of sgACC/25 reduces vagal tone and heart rate variability, alters cortisol dynamics during

278 Natural pacing of the heart results in heart rate variability, an indicator of good health and

279 ess autonomic monitors to record heart rate, heart rate variability, and movement in infants and pare

280 lected based on the patient's heart rate and heart rate variability, derived from the patient's ECG.

281 e levels of interleukin-6 and high-frequency heart rate variability, higher rmPFC stress reactivity w

282 cardiac phase, nor individual differences in heart rate variability.

283 lipids, fecal SCFAs, blood pressure, or 24-h heart rate variability.

284 utonomic balance was assessed by determining heart rate variability.

285 lations typically seen in blood pressure and heart rate variability.

286 Second, participant's heart-rate variability (HRV) - a marker of parasympathet

287 tegrative physiological parameter of resting heart-rate variability (HRV); low resting HRV indicating

288 g measure of QT-interval variance indexed to heart rate variance.

289 At peak stress, the mean increase in heart rate was 23.9+/-11.4 beats per minute and the mean

290 stand of the STS test, compared to baseline, heart rate was 50% higher on the day of exit from bedres

291 The increase in heart rate was greater in symptomatic patients (27.4+/-1

292 However, the heart rate was increased in the presence of disopyramide

293 irls: -0.00; 95% CI: -0.07, 0.07 mmol/L) and heart rate was reduced by 3.4 bpm (95% CI: 0.2, 6.6 bpm)

294 activity responses, mean blood pressure and heart rate were higher during moderate hypovolemia after

295 Headache and increased heart rate were increased on levosimendan, although it w

296 ed CR (O(2) -CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood

297 nd as low as 2 bpm, while after-dive surface heart rates were 25 to 37 bpm, near the estimated maximu

298 In IUGR and IUGR-AR lambs heart rates were greater, which was independent of cardi

299 ncrease systemic arterial blood pressure and heart rate with the purpose of maintaining brain blood f

300 whereas WT mice exhibited a mild decrease in heart rate without irregular RR intervals.