Is Nocturnal Systolic Blood Pressure Rise Associated with Central Hemodynamics and Arterial Stiffness?

2012 ◽  
Vol 21 (03) ◽  
pp. 235-241
Author(s):  
Gulperi Celik ◽  
Ali Gundogdu ◽  
Rengin Elsurer Afsar ◽  
Fatih Sahin
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Pressure Rise ◽  
Central Hemodynamics ◽  
Blood Pressure Rise

Abstract P100: Enhanced External Counterpulsation Reduces Central Blood Pressure In Stable Angina Patients: A Meta Analysis

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Elizabeth Lindemann ◽  
Kevin Pham ◽  
Gautam Kedia ◽  
Ananth Prasad ◽  
Sachin A Shah
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Stable Angina ◽  
Augmentation Index ◽  
Meta Analysis ◽  
Central Hemodynamics ◽  
External Counterpulsation ◽  
Before And After ◽  
Enhanced External Counterpulsation

Introduction: Emerging evidence suggests central systolic blood pressure (cSBP) and augmentation index are superior predictors of adverse cardiovascular outcomes as compared to peripheral systolic blood pressure (pSBP). Enhanced external counterpulsation (EECP) is a non-invasive treatment modality approved for the management of refractory angina. The degree of benefit from EECP on central hemodynamics and arterial stiffness remains unknown. This meta-analysis evaluated the effect of EECP on peripheral (office) blood pressure and central hemodynamic parameters. Methods: A comprehensive literature search was conducted in Pubmed, CINAHL, and Cochrane Library databases. All prospective clinical trials assessing the impact of EECP in patients with stable angina and CAD were included. Studies were excluded for not completing a full course of EECP, having a baseline peripheral systolic blood pressure &lt100 mmHg, or not reporting adequate data for analysis. The primary endpoint was the change in cSBP before and after EECP. The change in pSBP, pDBP, cDBP, and augmentation index before and after EECP were also assessed. The weighted mean difference using the DerSimonian and Laird random-effect model was utilized for determining the change in each parameter before and after EECP. Statistical heterogeneity was evaluated using the Egger’s bias statistic. Results: Five studies containing 137 unique patients were included for the cSBP analysis. cSBP was reduced significantly by -7.56 mmHg (95% CI -11.83 to -3.28; Cochrane Q=1.81) post-EECP. In the same set of studies, pSBP was reduced significantly by -9.65 mmHg (95% CI -14.32 to -4.98) post-EECP. pDBP [-4.67 mmHg (95% CI -8.56 to -0.77)] was reduced post-EECP, while no changes were evident in cDBP. Augmentation index was reduced by -3.74% (95% CI -7.05 to -0.43) post-EECP. Two studies included a sham-EECP intervention arm and demonstrated no significant changes in cSBP [0.67 mmHg (95% CI -5.66 to 7.01)] or other parameters. Conclusion: EECP significantly reduced cSBP and pSBP by approximately 8 mmHg and 10 mmHg respectively. EECP also demonstrated a mild improvement in arterial stiffness, which translates to reduced wasted left ventricular energy and myocardial oxygen demand. In patients with stable angina and CAD, EECP exerts beneficial effects in both peripheral and central hemodynamics but whether these benefits are sustained over a longer duration need further exploration.

Chronic central potassium infusion prevents deoxycorticosterone-salt hypertension in rats

1995 ◽  
Vol 268 (2) ◽  
pp. H646-H652 ◽  
Author(s):  
S. A. Klarr ◽  
R. F. Keep ◽  
A. L. Betz
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Cerebrospinal Fluid ◽  
Systolic Blood Pressure ◽  
Potassium Concentration ◽  
Pressure Rise ◽  
Blood Pressure Rise ◽  
Lower Blood ◽  
Salt Hypertension ◽  
Blood Pressures

Although it has long been established that cerebrospinal fluid potassium concentration (CSF [K]) is very tightly regulated, it has been reported that rats made hypertensive by central infusions of aldosterone have significantly lower CSF [K] compared with normotensive controls. We investigated whether reduced CSF [K] is also present in another animal model of hypertension, the deoxycorticosterone acetate (DOCA)-salt rat, and we hypothesized that chronic intracerebroventricular (IVT) infusion of potassium with miniosmotic pumps might attenuate the rise in blood pressure observed in these rats. DOCA-salt rats without IVT infusions or with control CSF infusions (0.5 microliter/h of 2.9 mM K for 2 wk) had a significantly increased systolic blood pressure and a significantly lower CSF [K] compared with their respective sham groups. In contrast, DOCA-salt rats receiving IVT infusions with elevated [K] (10, 30, or 150 mM) had significantly lower blood pressures compared with those receiving control CSF. They also did not exhibit decreased CSF [K] compared with their respective sham groups. At 10 and 150 mM K, the blood pressure rise in DOCA-salt rats was not significantly different from shams. At 30 mM K, there was a slight, but significant, increase in blood pressure in the DOCA-salt rats compared with their shams, but this rise was still much less than in DOCA-salt rats infused with 2.9 mM K. Infusions with elevated [K] had no effect on blood pressure in the sham animals. These studies suggest that altered brain potassium homeostasis may play an important role in the development of DOCA-salt hypertension.

scholarly journals Effect of renal denervation on the arterial stiffness and central hemodynamics in patients with resistant hypertension

2016 ◽  
Vol 13 (4) ◽  
pp. 7-12
Author(s):  
G V Shchelkova ◽  
A R Zairova ◽  
N M Danilov ◽  
A N Rogoza ◽  
I E Chazova
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Ambulatory Blood Pressure ◽  
Resistant Hypertension ◽  
Renal Denervation ◽  
Antihypertensive Drugs ◽  
Applanation Tonometry ◽  
Central Hemodynamics ◽  
Tree Methods

Aim: to evaluate the effect of renal denervation (RDN) on the stiffness of the aorta and major arteries, central blood pressure and index augmentation in patients with resistant hypertension. Material and methods. We included 20 patients with systolic blood pressure 178 [170; 180] mm Hg and diastolic blood pressure 100 [94; 100] mm Hg on 5.1±0.7 antihypertensive drugs with diuretic, who underwent bilateral RDN. Blood pressure (BP) was studied before intervention, at 7 days and 6 months after RDN by tree methods: office BP, 24-hour ambulatory blood pressure (ABPM) and aortic BP with applanation tonometry a. radialis (SphygmoCor). All patients were divided into two groups by ABPM in 6 months after RDN: responders (decrease of mean ABPM≥5 mm Hg) and non-responders (decrease of mean ABPM

scholarly journals Association between Objectively Measured Physical Activity and Arterial Stiffness in Children with Congenital Heart Disease

2021 ◽  
Vol 10 (15) ◽  
pp. 3266
Author(s):  
Laura Willinger ◽  
Leon Brudy ◽  
Renate Oberhoffer-Fritz ◽  
Peter Ewert ◽  
Jan Müller
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Heart Rate ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Congenital Heart ◽  
Z Score ◽  
Objectively Measured

Background: The association between physical activity (PA) and arterial stiffness is particularly important in children with congenital heart disease (CHD) who are at risk for arterial stiffening. The aim of this study was to examine the association between objectively measured PA and arterial stiffness in children and adolescents with CHD. Methods: In 387 children and adolescents with various CHD (12.2 ± 3.3 years; 162 girls) moderate-to-vigorous PA (MVPA) was assessed with the “Garmin vivofit jr.” for 7 consecutive days. Arterial stiffness parameters including pulse wave velocity (PWV) and central systolic blood pressure (cSBP) were non-invasively assessed by oscillometric measurement via Mobil-O-Graph®. Results: MVPA was not associated with PWV (ß = −0.025, p = 0.446) and cSBP (ß = −0.020, p = 0.552) in children with CHD after adjusting for age, sex, BMI z-score, peripheral systolic blood pressure, heart rate and hypertensive agents. Children with CHD were remarkably active with 80% of the study population reaching the WHO recommendation of average 60 min of MVPA per day. Arterial stiffness did not differ between low-active and high-active CHD group after adjusting for age, sex, BMI z-score, peripheral systolic blood pressure, heart rate and hypertensive agents (PWV: F = 0.530, p = 0.467; cSBP: F = 0.843, p = 0.359). Conclusion: In this active cohort, no association between PA and arterial stiffness was found. Longer exposure to the respective risk factors of physical inactivity might be necessary to determine an impact of PA on the vascular system.

Arterial blood pressure responses to graded transient arousal from sleep in normal humans

1993 ◽  
Vol 74 (3) ◽  
pp. 1123-1130 ◽  
Author(s):  
R. J. Davies ◽  
P. J. Belt ◽  
S. J. Roberts ◽  
N. J. Ali ◽  
J. R. Stradling
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Confidence Interval ◽  
Rem Sleep ◽  
High Frequency ◽  
Pressure Rise ◽  
Nrem Sleep ◽  
Blood Pressure Rise ◽  
Obstructive Sleep

During obstructive sleep apnea, transient arousal at the resumption of breathing is coincident with a substantial rise in blood pressure. To assess the hemodynamic effect of arousal alone, 149 transient stimuli were administered to five normal subjects. Two electroencephalograms (EEG), an electrooculogram, a submental electromyogram (EMG), and beat-to-beat blood pressure (Finapres, Ohmeda) were recorded in all subjects. Stimulus length was varied to produce a range of cortical EEG arousals that were graded as follows: 0, no increase in high-frequency EEG or EMG; 1, increased high-frequency EEG and/or EMG for < 10 s; 2, increased high-frequency EEG and/or EMG for > 10 s. Overall, compared with control values, average systolic pressure rose [nonrapid-eye-movement (NREM) sleep 10.0 +/- 7.69 (SD) mmHg; rapid-eye-movement (REM) sleep 6.0 +/- 6.73 mmHg] and average diastolic pressure rose (NREM sleep 6.1 +/- 4.43 mmHg; REM sleep 3.7 +/- 3.02 mmHg) over the 10 s following the stimulus (NREM sleep, P < 0.0001; REM sleep, P < 0.002). During NREM sleep, there was a trend toward larger blood pressure rises at larger grades of arousal (systolic: r = 0.22, 95% confidence interval 0.02–0.40; diastolic: r = 0.48, 95% confidence interval 0.31–0.62). The average blood pressure rise in response to the grade 2 arousals was approximately 75% of that during obstructive sleep apnea. Arousal stimuli that did not cause EEG arousal still produced a blood pressure rise (mean systolic rise 8.6 +/- 7.0 mmHg, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract P218: The Association Of Mid-life Cumulative Exposure To Systolic Blood Pressure, Myocardial Oxygen Demand, And Hypertension With Later-life Central Arterial Stiffness And Its 5-year Change: The Atherosclerosis Risk In Communities Study - Neurocognitive Study (ARIC-NCS)

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Michelle L Meyer ◽  
Veeral Saraiya ◽  
Hirofumi Tanaka ◽  
Priya Palta ◽  
Timothy M Hughes ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Oxygen Demand ◽  
Later Life ◽  
Cumulative Exposure ◽  
Rate Pressure Product ◽  
Myocardial Oxygen Demand ◽  
Small Magnitude ◽  
Cumulative Exposures

Background: Greater central artery stiffness predicts cardiovascular disease and all-cause mortality, thus understanding arterial stiffness determinants has prevention implications. Reports of the temporal association of blood pressure with arterial stiffness are conflicting and the association with myocardial oxygen demand has not been evaluated. Objective: Characterize the association of mid- to later-life cumulative exposure to systolic blood pressure (SBP), myocardial oxygen demand, and hypertension (HTN) with arterial stiffness and its 5-year change in older adults. Methods: We included 1,975 adults (1151 women; 359 Black; visit 5 mean age 74 years) examined in visits 5 (2011-13) and 6 or 7 (2016-19) of the population-based ARIC-NCS with measures of arterial stiffness (carotid-femoral pulse wave velocity (cfPWV)). Higher cfPWV indicates greater arterial stiffness. We calculated cumulative exposures as the sum of averages from four consecutive visits from 1987-89 to 1996-98 divided by total time. Myocardial oxygen demand was calculated as the rate pressure product (RPP): (SBP x heart rate)/1,000. We derived HTN duration as the time since first HTN detection. Associations of cumulative exposures with visit 5 cfPWV and the 5-year cfPWV change were evaluated by multivariable linear regression adjusted for demographics and cardiometabolic factors. Results: Over the mean 5.7 years between visits 5 and 6 or 7, cfPWV increased by 144.9 cm/s (SD: 276.0; range -680.0, 961.5 cm/s). HTN at any visit, duration, and the time-weighted cumulative measures were associated with higher visit 5 cfPWV (Table). Prevalent HTN was inversely associated with cfPWV change. No statistically significant associations were observed for the other exposures and cfPWV change. Conclusion: Cumulative exposure to SBP, RPP, and HTN are modifiable traits associated with higher cfPWV at later-life, but not with rate of cfPWV change in older adulthood. HTN at visit 5 was associated with lower cfPWV change, albeit the change is of small magnitude.

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