The Association between Within-Visit Blood Pressure Variability and Carotid Artery Atherosclerosis in General Population

Objectives

To determine whether within-visit blood pressure (BP) variability based on three measurements over minutes is associated with increased carotid intima-media thickness (IMT) and plaque in a general population.

Methods

A cross-sectional survey was performed in 2007, and a total of 1222 Beijing community residents aged 50–79 years belonging to part of the Chinese Multi-Provincial Cohort Study (CMCS) were recruited in this study. BP was measured three times at 5-minute intervals during a single visit, and the maximum absolute difference (MAD) between any two readings of three measurements was used to indicate within-visit BP variability. Carotid IMT and plaque scanned by B-mode ultrasound were identified as the surrogate end points in the intermediate stage of atherosclerosis.

Results

After adjustment for established cardiovascular risk factors, the odds ratio (OR) (95% confidence interval (CI)) for increased carotid IMT and internal carotid plaque associated with the highest within-visit diastolic BP (DBP) variability (MAD > mean + standard deviation (SD)) compared with participants in the lowest within-visit DBP variability (MAD ≤ mean −SD) was 4.92 (1.48–16.42) and 6.07 (1.31–28.10), respectively, in the normotensives (P = 0.01; P = 0.02). The OR (95% CI) for internal carotid plaque associated with the highest within-visit systolic BP (SBP) variability (MAD >mean +SD) compared with participants in the lowest within-visit SBP variability (MAD ≤ mean −SD) was 3.54 (1.26–10.00) in the hypertensives on antihypertensive therapy (P = 0.02).

Conclusions

Within-visit DBP variability was associated with increased carotid IMT and internal carotid plaque in the normotensive population, and within-visit SBP variability was associated with internal carotid plaque in hypertensive patients undergoing antihypertensive therapy.     

Pulse transit time measured from the ECG: an unreliable marker of beat-to-beat blood pressure.

The arterial pulse-wave transit time can be measured between the ECG R-wave and the finger pulse (rPTT), and has been shown previously to have a linear correlation with blood pressure (BP). We hypothesized that the relationship between rPTT, preejection period (PEP; the R-wave/mechanical cardiac delay), and BP would vary with different vasoactive drugs. Twelve healthy men (mean age 22 yr) were studied. Beat-to-beat measurements were made of rPTT (using ECG and photoplethysmograph finger probe), intra-arterial radial pressure, PEP (using cardiac bioimpedance), and transit time minus PEP (pPTT). Four drugs (glyceryl trinitrate, angiotensin II, norepinephrine, salbutamol) were administered intravenously over 15 min, with stepped dosage increase every 5 min and a 25-min saline washout between agents. All subjects in all conditions had a negative linear correlation (R2 = 0.39) between rPTT and systolic BP (SBP), generally constant between different drugs, apart from four subjects who had a positive rPTT/SBP correlation with salbutamol. The 95% limits of agreement between measured and rPTT-predicted SBP were +/-17.0 mmHg. Beat-to-beat variability of rPTT showed better coherence with SBP variability than it did with heart rate variability (P < 0.001). PEP accounted for a substantial and variable proportion of rPTT (12-35%). Diastolic (DBP) and mean arterial BP (MAP) correlated poorly with rPTT (R2 = 0.02 and 0.08, respectively) but better with pPTT (rPTT corrected for PEP, R2 = 0.41 and 0.45, respectively). The 95% limits of agreement between measured and pPTT-predicted DBP were +/- 17.3 mmHg. In conclusion, the negative correlation between rPTT and SBP is generally constant, even with marked hemodynamic perturbations. However, the relationship is not reliable enough for rPTT to be used as a surrogate marker of SBP, although it may be useful in assessing BP variability. DBP and MAP cannot be predicted from rPTT without correction for PEP. The significant contribution of PEP to rPTT means that rPTT should not be used as a marker of purely vascular function.     

Association between light exposure at night and nighttime blood pressure in the elderly independent of nocturnal urinary melatonin excretion

Circadian misalignment between internal and environmental rhythms dysregulates blood pressure (BP) variability because of disruption of the biological clock, resulting in increased nighttime BP. Although exposure to light-at-night is associated with the circadian misalignment, it remains unclear whether exposure to light-at-night in home settings is associated with nighttime BP. In this cross-sectional analysis of 528 elderly individuals (mean age: 72.8 years), we measured bedroom light intensity at 1-min intervals on two consecutive nights along with ambulatory BP, overnight urinary melatonin excretion and actigraphy. With regard to adjusted mean comparisons using analysis of covariance, the light-at-night group (average: ≥5?lux; n?=?109) showed significantly higher nighttime systolic BP (SBP; adjusted mean: 120.8 vs. 116.5?mmHg, p?=?0.01) and diastolic BP (70.1 vs. 67.1?mmHg, p?<?0.01) compared with the Darker group (average: <5?lux; n?=?419) independently of potential confounding factors including overnight urinary melatonin excretion and actigraphic sleep quality. We observed consistent associations between light-at-night and nighttime BP in different cutoff values for light-at-night intensity (i.e. 3 and 10?lux). In conclusion, exposure to light-at-night in home settings is significantly associated with increased nighttime BP in elderly individuals independently of overnight urinary melatonin excretion. A 4.3?mmHg increase in nighttime SBP is associated with a 6.1% increase in total mortality, which corresponds to approximately 10?000 annual excess deaths in Japanese elderly population.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

Effects of one-year swimming training on blood pressure and insulin sensitivity in mild hypertensive young patients

Swimming is a lifestyle intervention recommended by many clinicians in the prevention and treatment of hypertension. Yet, not all studies have agreed that swimming training can reduce blood pressure (BP). Inclusion of normotensive subjects could be a confounder for discrepancies among studies. In this one-year longitudinal study, long-term effects of swimming training on BP were investigated in 7 mild hypertensive patients (systolic BP (SBP) > 140 mmHg) and 16 normotensive controls. At baseline, these subjects (aged 21.5 +/- 0.1 years) did not participate in any form of sport training activity for the previous 3 months before enrollment into the training program. The training distance progressed from 0 (baseline) to 7 kilometers per week. BP and the homeostasis model assessment for insulin resistance (HOMA-IR) were determined under fasted condition at baseline and 48 h after the last swimming bout. The hypertensive patients displayed significantly greater HOMA-IR than age-matched normotensive controls. When data of all subjects were pooled, plasma glucose concentration was only slightly lowered after training, but weight, height, body mass index, SBP, diastolic BP (DBP) and HOMA-IR values were not significantly altered. However, when observation was restricted to the hypertensive patients, swimming training significantly lowered SBP by approximately 17 mmHg, concurrent with 41% reduction in HOMA-IR. Intriguingly, SBP in the normotensive subjects was elevated by approximately 6 mmHg after training. CONCLUSIONS: The present study found normalization rather than universal reduction effect of swimming training on BP. Furthermore, the BP-lowering effect of training in hypertensive patients appears to be associated with improvement in insulin sensitivity.     

Hemodynamic consequences of chronic parasympathetic blockade with a peripheral muscarinic antagonist

Whereas the sympathetic nervous system has a well-established role in blood pressure (BP) regulation, it is not clear whether long-term levels of BP are affected by parasympathetic function or dysfunction. We tested the hypothesis that chronic blockade of the parasympathetic nervous system has sustained effects on BP, heart rate (HR), and BP variability (BPV). Sprague-Dawley rats were instrumented for monitoring of BP 22-h per day by telemetry and housed in metabolic cages. After the rats healed from surgery and a baseline control period, scopolamine methyl bromide (SMB), a peripheral muscarinic antagonist, was infused intravenously for 12 days. This was followed by a 10-day recovery period. SMB induced a rapid increase in mean BP from 98 +/- 2 mmHg to a peak value of 108 +/- 2 mmHg on day 2 of the SMB infusion and then stabilized at a plateau value of +3 +/- 1 mmHg above control (P < 0.05). After cessation of the infusion, the mean BP fell by 6 +/- 1 mmHg. There was an immediate elevation in HR that remained significantly above control on the last day of SMB infusion. SMB also induced a decrease in short-term (within 30-min periods) HR variability and an increase in both short-term and long-term (between 30-min periods) BPV. The data suggest that chronic peripheral muscarinic blockade leads to modest, but sustained, increases in BP, HR, and BPV, which are known risk factors for cardiovascular morbidity.     

原发性高血压患者红细胞抗高血压因子对高血压...

The effects of antihypertensive factor (AHF) from erythrocytes of essential hypertensive human subjects on the systolic blood pressure (SBP) and diastolic blood pressure (DBP) in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), Wistar-Kyoto rats (WKY) and Wistar rats were examined. Single intraperitoneal injection of AHF (1.6 mg/kg body weight) resulted in a significant decrease in SBP of SHR and RHR. At 10 min postinjection, AHF lowered the SBP in SHR by 34.0 mmHg. SBP recovered to the original level at 3 h. The maximal decrease of SBP in RHR by 92.5 mmHg was at 24h postadministration and the SBP did not recover until the 9th day. When AHF was administered via femoral vein (0.8 mg/kg body weight), the maximal decrease values of the SBP and the DBP were 42.8 and 48.2 mmHg in SHR at 12 min and 38.3 and 42.5 mmHg in RHR at 25 min postinjection respectively. The DBP in Wistar rats decreased considerably (from 96.7 +/- 12.9 to 83.3 +/- 11.7 mmHg) at 5 min postadministration of AHF, but no effect on DBP in WKY rats was observed. The depressor effect of AHF on SBP in RHR was dose-dependent. AHF could also antagonize the pressor effect of norepinephrine in Wistar rats.     

Association of 24 h–systolic blood pressure variability and cardiovascular disease in patients with obstructive sleep apnea

Background

To evaluate association of 24 h–systolic blood pressure (SBP) variability and obstructive sleep apnea (OSA) as defined by the apnea-hypopnea index ≥5/h; and association of 24 h–SBP variability and prevalent cardiovascular disease (CVD) in OSA patients.

Methods

Participants underwent polysomongraphy to evaluate the presence of OSA, and 24 h–ambulatory blood pressure monitoring was applied to evaluate 24 h–SBP variability as indexed by weighted 24 h–standard deviation (SD) of SBP. Between-group differences were evaluated in participants with and without OSA. Participants with OSA were divided into high and low 24 h–SBP variability groups and between-group differences were evaluated.

Results

Mean age of 384 participants was 50 years old and 42.2% had OSA. Mean 24 h–systolic/diastolic BP were 130/78 mmHg, with mean weighted 24 h–SD of systolic/diastolic BP were 12.9/7.3 mmHg. Compared to those without OSA, OSA participants had higher clinic-, 24 h-, daytime- and nighttime-SBP, and weighted 24 h, daytime- and nighttime-SD of SBP. Age, prevalent CVD and OSA, usage of angiotensin converting enzyme inhibitor/angiotensin receptor blocker, calcium channel blocker and diuretic were significantly associated with 24 h–SBP variability. In OSA patients, compared to those with low variability, participants with high variability had higher weighted 24 h, daytime- and nighttime-SD of SBP. After adjusted for covariates including clinic-SBP and 24 h–SBP, per 1-SD increment weighted 24 h–SD of SBP was associated with 21% increased prevalent CVD.

Conclusions

Patients with newly-diagnosed OSA have higher 24 h–SBP variability compared to those without OSA; in OSA patients, increased 24 h–SBP variability is associated with increased prevalence of CVD.

     

Blunting of circadian rhythms and increased acrophase variability in sleep-time hypertensive subjects

24 h and ultradian rhythms of blood pressure (BP) have been previously shown to be disorganized in nocturnal hypertensive subjects. The present study was undertaken to further analyze the ultradian and circadian BP rhythm structure in sleep-time hypertensive subjects with normal or elevated awake-time BP levels. Fourier analysis was used to fit 24, 12, 8, and 6 h curves to mean BP as well as heart rate (HR) time series data derived from 24 h ambulatory blood pressure monitoring. Awake and sleep periods were defined according to individual sleep diaries. Awake-time hypertension was defined as diurnal systolic (SBP) and/or diastolic BP (DBP) means ≥135/85 mmHg. Sleep-time hypertension was defined as nocturnal SBP and/or DBP means ≥120/70 mmHg. The sample included 240 awake-time normotensive subjects (180 sleep-time normotensives and 60 sleep-time hypertensives) and 138 untreated awake-time hypertensive subjects (31 sleep-time normotensives and 107 sleep-time hypertensives). The amplitude and integrity (i.e., percent rhythm) of the 24 and 12 h BP rhythms were lower in the sleep-time hypertensive subjects and higher in the awake-time hypertensive subjects. However, no differences were detected when the integrity and amplitude of the 6 and 8 h mean BP rhythms were analyzed. The sleep-time hypertensive group showed significantly higher 24 h BP rhythm acrophase variability. No differences could be found in any of the HR rhythm parameters. Altogether, the findings suggest a disorganization of the BP circadian rhythm in sleep-time hypertensives that results in reduced 24 h rhythm amplitude and integrity that could be related to cardiovascular risk.     

Intra- and extracranial artery blood velocity during a sudden blood pressure decrease in humans

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min⁻¹]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s⁻¹ (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s⁻¹ (P < 0.05) and common carotid artery blood flow (CCAbf ) decreased from 305 (23) to 233 (33) ml min⁻¹ (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s⁻¹], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min⁻¹]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes. Accepted: 8 April 1997     

Validity of auscultatory and Penaz blood pressure measurements during profound heat stress alone and with an orthostatic challenge

Despite frequent reporting of blood pressure (BP) during profound passive heat stress, both with and without a hypotensive challenge, the method by which BP is measured often varies between laboratories. It is unknown whether auscultatory and finger BP measures accurately reflect intra-arterial BP during dynamic changes in cardiac output and peripheral resistance associated with the aforementioned conditions. The purpose of this investigation was to test the hypothesis that auscultatory BP measured at the brachial artery, and finger BP measured by the Penaz method, are valid measures of intra-arterial BP during a passive heat stress and a heat-stressed orthostatic challenge, via lower body negative pressure (LBNP). Absolute (specific aim 1) and the change in (specific aim 2) systolic (SBP), diastolic (DBP), and mean BPs (MBP) were compared at normothermia, after a core temperature increase of 1.47 ± 0.09°C, and during subsequent LBNP. Heat stress did not change auscultatory SBP (6 ± 11 mmHg; P = 0.16), but Penaz SBP (-22 ± 16 mmHg; P < 0.001) and intra-arterial SBP (-11 ± 13 mmHg P = 0.017) decreased. In contrast, DBP and MBP did not differ between methods throughout heat stress. Compared with BP before LBNP, the magnitude of the reduction in BP with all three methods was similar throughout LBNP (P > 0.05). In conclusion, auscultatory SBP and Penaz SBP failed to track the decrease in intra-arterial SBP that occurred during the profound heat stress, while decreases in arterial BP during an orthostatic challenge are comparable between methodologies.     

Non-invasive measurement of blood pressures in the Yucatan micropig (Sus scrofa domestica), with and without midazolam-induced sedation

Current literature suggests that the effects of midazolam, a water-soluble benzodiazepine, on blood pressure in swine are minimal. The hypothesis of the study reported here was that a light sedative dose would induce a decrease in blood pressure in this species. Healthy female Yucatan Micropigs (n = 20), 16 to 30 (mean, 22) kg, aged four six months, were individually placed in a humane restraint sling and allowed to acclimate. Systolic (SBP), diastolic (DBP), and mean (MBP) blood pressures (mmHg) and heart rate (HR; beats per min [bpm]) were measured by use of oscillometry. The pressure cuff was placed at the base of the tail, and five sets of values were recorded at five-min intervals, beginning at 10 and ending 30 min after cuff placement. Following a three- to four-day rest period, this procedure was repeated with the addition of a dose of 0.5 mg of midazolam HCl/kg of body weight given intramuscularly at the time of cuff placement. A paired one-way Student's t-test was used to compare the means of the five measures between control and midazolam treatment. Mean (+/- SD) differences for SBP, DBP, MBP, and HR were 18.9 (+/- 3.97), 17.8 (+/- 5.27), and 18.6 (+/- 5.09) mmHg and 20.7 (+/- 3.73) bpm, respectively. All four parameters were significantly reduced in the midazolam-sedated group (P < 0.001). The maximal decrease in SBP, DBP, and MBP occurred at 15 and 20 min after dosing. Mean values based on the means of the five measures were 128 (+/- 12.6), 80 (+/- 9.4), and 99 (+/- 9.2) mmHg and 135 (+/- 17.4) bpm, and 109 (+/- 15.4), 63 (+/- 12.6), and 80 (+/- 13.6) mmHg and 115 (+/- 15.5) bpm for SBP, DBP, MBP, and HR in the control (n = 20) and midazolam (n = 20) groups, respectively. The control values can serve as normal oscillometric values for this age, sex, and breed of Micropig. We conclude that midazolam, given intramuscularly at a sedative dosage, negatively affects cardiovascular parameters measured by use of a blood pressure cuff, in sexually mature female Micropigs, compared with values in untreated pigs, which is similar to reports for humans.     

Strain differences of hypertension induced by dietary NG-nitro-L-arginine in normotensive rats.

When the potent inhibitor of nitric oxide (NO) synthesis NG-nitro-L-arginine (L-NNA) was incorporated into the diet, hypertension was induced and sustained due to the effects of the long-term inhibition of endothelium-dependent relaxing factor (EDRF)/NO. The effects of L-NNA on normotensive rats of four strains (Donryu, Sprague-Dawley (SD), Wistar, and Wistar-Kyoto (WKY)) were compared relative to control rats. L-NNA administration caused a sharp initial increase in systolic blood pressure (SBP) at 2 weeks in all animals, and this was followed by a gradual and steady increase until 4 weeks. At the end of the experiments (5 weeks), the mean SBP of Donryu and SD rats was decreased. The maximum blood pressure of Donryu and Wistar rats during the experiments exceeded 200 mmHg, but that of SD and WKY rats was below 200 mmHg. Body weight loss and death were observed only in L-NNA-fed Donryu rats. Pathological changes in the kidneys and the morbidity rates for the lesions were determined, and indicated that the Donryu L-NNA group was 100% positive. These results suggest that the Donryu strain is more sensitive to L-NNA than the other strains. That dietary L-NNA-induced hypertension in normotensive rats of the four strains provides a new artificially-induced hypertensive model in which vasoconstriction occurs mainly due to EDRF deficiency.     

Vagal cardiac function and arterial blood pressure stability

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 +/- 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 microg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 +/- 2 mmHg) was significantly augmented with atropine (+26 +/- 2 mmHg) or glycopyrrolate (+27 +/- 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (-9.2 +/- 1.2 mmHg) was significantly greater after atropine (-15 +/- 1 mmHg) or glycopyrrolate (-14 +/- 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater (P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced (P < 0.05) the low-frequency (LF; 0.04-0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated (P < 0.05) after antimuscarinic agents and was correlated (r = -0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.     

Baroreflex sensitivity as an individual characteristic feature

The reproducibility of baroreflex sensitivity (BRS in ms/mmHg; BRSf in mHz/mmHg) determined with respect to the coherence between the variability in systolic blood pressure (SBP) and inter-beat intervals (IBI) or heart rate (HR) was tested. SBP and IBI were recorded beat-to-beat for 5 min (Finapres, breathing at 0.33 Hz) in 116 subjects (aged 19-24 years) sitting at rest three times in periods of one week. BRS and BRSf was determined by a cross-spectral method in a frequency range of 0.067-0.133 Hz. Eight indices were evaluated: BRS(0.1 Hz) /BRSf(0.1 Hz) - the value at a frequency of 0.1 Hz; BRS(COHmax)/BRSf(COHmax) - the value at maximum coherence; BRS(Wcoh)/BRSf - weighted value with respect to coherence values in the whole frequency range; BRS(WPcoh)/BRS(WPcoh) - weighted value with respect to coherence for frequencies with coherence above 0.5. All indices revealed a lower intraindividual than interindividual variability (p<0.001). The individual mean values of BRS or BRSf correlated (p<0.001) with standard deviation of their individual values for all indices. Baroreflex sensitivity is an individual characteristic feature with the highest reproducibility at its low values in spite of its resting variation. Reproducibility is not influenced by modification of the spectral method used.     

Daytime blood pressure elevation after nocturnal hypoxia.

The purpose of this study was to investigate whether nocturnal hypoxia causes daytime blood pressure (BP) elevation. We hypothesized that overnight exposure to hypoxia leads the next morning to elevation in BP that outlasts the hypoxia stimulus. We studied the effect on BP of two consecutive night exposures to hypobaric hypoxia in 10 healthy normotensive subjects. During the hypoxia nights, subjects slept for 8 h in a hypobaric chamber at a simulated altitude of 4,000 m (barometric pressure = 462 mmHg). Arterial O(2) saturation and electrocardiogram were monitored throughout the night. For 30 min before the nocturnal simulated ascent and for 4 h after return to baseline altitude the next morning, BP was measured every 5 min while the subject was awake. The same measurements were made before and after 2 normoxic nights of sleep in the hypobaric chamber at ambient barometric pressure (745 mmHg). Principal components analysis was applied to evaluate patterns of BP response after the second night of hypoxia and normoxia. A distinct pattern of diastolic BP (DBP) elevation was observed after the hypoxia night in 9 of the 10 subjects but in none after the normoxia night. This pattern showed a mean increase of 4 mmHg in DBP compared with the presleep-awake baseline in the first 60 min and a return to baseline by 90 min. We conclude that nocturnal hypoxia leads to a carryover elevation of daytime DBP.     

Dynamic cardiorespiratory interaction during head-up tilt-mediated presyncope

In 28 healthy adults, we compared the dynamic interaction between respiration and cerebral autoregulation in 2 groups of subjects: those who did and did not develop presyncopal symptoms during 70 degrees passive head-up tilt (HUT), i.e., nonpresyncopal (23 subjects) and presyncopal (5 subjects). Airflow, CO2, cerebral blood flow velocity (CBF), ECG, and blood pressure (BP) were recorded. To determine whether influences of mean BP (MBP) and systolic SP (SBP) on CBF were altered in presyncopal subjects, coherencies and transfer functions between these variables and mean and peak CBF (CBFm and CBFp) were estimated. To determine the influence of end-tidal CO2 (ETco2) on CBF, the relative CO2 reactivity (%change in CBFm per mmHg change in ETco2) was calculated. We found that in presyncopal subjects before symptoms during HUT, coherence between SBP and CBFp was higher (P=0.02) and gains of transfer functions between BP (MBP and SBP) and CBFm were larger (MBP, P=0.01; SBP, P=0.01) in the respiratory frequency region. In the last 3 min before presyncope, presyncopals had a reduced relative CO2 reactivity (P=0.005), likely a consequence of the larger decrease in ETco2. We hypothesize that the CO2-mediated increase in resistance attenuates autoregulation such that the relationship between systemic and cerebral hemodynamics is enhanced. Our results suggest that an altered cardiorespiratory interaction involving cerebral hemodynamics may contribute in the cascade of events during tilt that culminate in unexplained syncope.     

Association between timing of hot water bathing before bedtime and night-/sleep-time blood pressure and dipping in the elderly: a longitudinal analysis for repeated measurements in home settings

ABSTRACT

Hot water bathing – a Japanese traditional practice – has not been evaluated for its association with night- and sleep-time blood pressure (BP) in large population. In this longitudinal analysis, bathing parameters and ambulatory BP were repeatedly measured for 2 nights in 758 Japanese elderly individuals. Participants were divided into three groups according to tertile values of time soaked in the bathtub (Duration: tertile value, 11 and 15 min), time from bathing-end to bedtime (Time before bedtime: tertile value, 42 and 106 min), and temperature of hot water in the bathtub (Water temp: tertile value, 40.3 and 41.2 °C). Participants’ mean age was 70.9 years, and mean night- and sleep-time systolic BP (SBP) and dipping were 115.1 ± 16.1, 114.2 ± 16.2 mmHg, and 14.2 ± 8.8%, respectively. Multivariable mixed-effect linear regression models adjusted for potential confounding factors suggested that nighttime SBP was significantly lower in the intermediate Time before bedtime group by 1.7 mmHg (95% CI, 0.2–3.1) and in the short group by 1.9 mmHg (95% CI, 0.1–3.7) than that in the long group. Dipping was significantly greater in the intermediate Time before bedtime group by 1.8% (95% CI, 0.7–2.9) and in the short group by 1.8% (95% CI, 0.6–3.1) than that in the long group. These associations were consistent regarding sleep-time SBP. Conversely, Water temp and Duration did not significantly associate with any ambulatory BP parameter. Remarkably, Time before bedtime significantly prolonged with increases in tertiles of Water temp (P for trend = 0.006). In conclusion, the findings of this study revealed that Japanese hot water bathing, especially the short time from bathing-end to bedtime, was associated with lower night- and sleep-time BP and greater dipping in an elderly population.     

Effects of body weight-supported treadmill training on heart rate variability and blood pressure variability in individuals with spinal cord injury.

Individuals with spinal cord injury are prone to cardiovascular dysfunction and an increased risk of cardiovascular disease. Body weight-supported treadmill training (BWSTT) may enhance ambulation in individuals with incomplete spinal cord injury; however, its effects on cardiovascular regulation have not been investigated. The purpose of this study was to examine the effects of 6-mo of BWSTT on the autonomic regulation of heart rate (HR) and blood pressure (BP) in individuals with incomplete tetraplegia. Eight individuals [age 27.6 yr (SD 5.2)] with spinal cord injury [C4-C5; American Spinal Injury Association B-C; 9.6 yr (SD 7.5) postinjury] participated. Ten-minute HR and finger arterial pressure (Finapres) recordings were collected during 1) supine rest and 2) an orthostatic stress (60 degrees head-up tilt) before and after 6 mo of BWSTT. Frequency domain measures of HR variability [low-frequency (LF) power, high-frequency (HF) power, and LF-to-HF ratio] and BP variability (systolic and diastolic LF power) were used as clinically valuable indexes of neurocardiac and neurovascular control, respectively. There was a significant reduction in HR [61.9 (SD 6.9) vs. 55.7 beats/min (SD 7.7); P=0.05] and LF-to-HF ratio [1.23 (SD 0.47) vs. 0.99 (SD 0.40); P < 0.05] after BWSTT. There was a significant reduction in LF systolic BP [183.1 (SD 46.8) vs. 158.4 mmHg2 (SD 45.2); P < 0.01] but no change in BP. There were no significant effects of training on HR variability or BP variability during 60 degrees head-up tilt. In conclusion, individuals with incomplete tetraplegia retain the ability to make positive changes in cardiovascular autonomic regulation with BWSTT without worsening orthostatic intolerance.     

Pulse arrival time is not an adequate surrogate for pulse transit time as a marker of blood pressure

Pulse transit time (PTT) is a proven, simple to measure, marker of blood pressure (BP) that could potentially permit continuous, noninvasive, and cuff-less BP monitoring (after an initial calibration). However, pulse arrival time (PAT), which is equal to the sum of PTT and the pre-ejection period, is gaining popularity for BP tracking, because it is even simpler to measure. The aim of this study was to evaluate the hypothesis that PAT is an adequate surrogate for PTT as a marker of BP. PAT and PTT were estimated through the aorta using high-fidelity invasive arterial waveforms obtained from six dogs during wide BP changes induced by multiple interventions. These time delays and their reciprocals were evaluated in terms of their ability to predict diastolic, mean, and systolic BP (DBP, MBP, and SBP) per animal. The root mean squared error (RMSE) between the BP parameter predicted via the time delay and the measured BP parameter was specifically used as the evaluation metric. Taking the reciprocals of the time delays tended to reduce the RMSE values. The DBP, MBP, and SBP RMSE values for 1/PAT were 9.8 ± 5.2, 10.4 ± 5.6, and 11.9 ± 6.1 mmHg, whereas the corresponding values for 1/PTT were 5.3 ± 1.2, 4.8 ± 1.0, and 7.5 ± 2.2 mmHg (P < 0.05). Thus tracking BP via PAT was not only markedly worse than via PTT but also unable to meet the FDA BP error limits. In contrast to previous studies, our results quantitatively indicate that PAT is not an adequate surrogate for PTT in terms of detecting challenging BP changes.