Relationships between blood pressure variability and indices of large artery stiffness: does the microvasculature play a role?

2016 ◽  
Vol 40 (4) ◽  
pp. 348-350 ◽  
Author(s):  
Damiano Rizzoni ◽  
Claudia Agabiti-Rosei
2012 ◽  
Vol 6 (4) ◽  
pp. 149
Author(s):  
G. Parati ◽  
G. Bilo ◽  
G. Pucci ◽  
S. Laurent ◽  
I. Macquin-Mavier ◽  
...  

Hypertension ◽  
2012 ◽  
Vol 60 (2) ◽  
pp. 369-377 ◽  
Author(s):  
Giuseppe Schillaci ◽  
Grzegorz Bilo ◽  
Giacomo Pucci ◽  
Stéphane Laurent ◽  
Isabelle Macquin-Mavier ◽  
...  

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Lyndsey E DuBose ◽  
Seth W Holwerda ◽  
Amy K Stroud ◽  
Nealy A Wooldridge ◽  
Janie E Myers ◽  
...  

Older age is associated with elevated large elastic artery stiffness, a strong predictor of cardiovascular (CVD) risk in middle-age/older (MA/O) adults independent of blood pressure (BP). Greater 24-hour systolic BP variability (BPV) is also an independent risk factor for CVD and is linked to large artery stiffness in MA/O adults with hypertension and diabetes. However, its relation to age-related arterial stiffness in adults with low risk factor burden is unclear. We hypothesized that higher systolic BPV would be: 1) associated with advancing age, and 2) related to elevated aortic and carotid artery stiffness among healthy MA/O adults. To determine this, 98 healthy adults (ages 19-70 yrs) with measurements of systolic BPV (standard deviation of 24 hr systolic BP) via ambulatory BP monitoring, aortic stiffness (carotid-femoral pulse wave velocity, cfPWV), carotid artery stiffness (β-stiffness via carotid tonometry/B mode ultrasound) and circulating metabolic factors were included. In the entire cohort, greater systolic BPV was not associated with age, cfPWV, carotid β stiffness or circulating lipids/glucose (all P>0.05), but was correlated (age-adjusted) with 24 hr systolic BP (r= 0.41, P<0.001) and BMI (r= 0.21, P<0.05). In stepwise linear regression analyses that included age, sex, BMI, only 24 hr systolic BP was associated with systolic BPV (β= 0.14 ± 0.03, Model R 2 = 0.20, P< 0.001). Interestingly, there was no difference in 24 hr systolic BPV (11.4 ± 0.4 vs 11.4 ± 0.5 SD mmHg, P=0.99) in young (n=55; 29.0 ± 0.7 yrs) vs. MA/O (n= 43; 53.0 ± 1.2 yrs) adults despite higher cfPWV (594 ± 12 vs 913 ± 39 cm/sec, P<0.001), carotid β-stiffness (6.8 ± 0.6 vs 9.3 ±0.9 U, P=0.001) and 24 hr systolic BP (121 ± 1 vs 125 ± 2 mmHg, P<0.05). Systolic BPV was associated with BMI (r= 0.42, p< 0.01) and fasting blood glucose (r= 0.54, P= 0.001) in MA/O but not young adults. In a stepwise linear regression model among MA/O, 24 hr systolic BP (β= 0.18 ± 0.04, R 2 = 0.36, P<0.001) and fasting glucose (β= 0.10 ± 0.05, R 2 change= 0.07, P<0.001) were the only significant correlates of systolic BPV (Model R 2 = 0.43, P<0.001). In conclusion, 24 hr systolic BP and fasting blood glucose, but not age or large elastic artery stiffness, were the strongest determinants of higher systolic BPV in normotensive MA/O adults.


Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Seth Holwerda ◽  
Jess Fiedorowicz ◽  
Lyndsey DuBose ◽  
Amy Stroud ◽  
Tiwa Ajibewa ◽  
...  

Alterations in cardiac baroreflex sensitivity (BRS) and 24-hr blood pressure variability (24-hr BPV) are independent predictors of increased cardiovascular disease (CVD) risk, and occur in individuals with obesity. Obese humans are also likely to have a higher large elastic artery stiffness compared with normal-weight individuals. While an increase in stiffness of carotid and aortic arteries, the anatomical sites where baroreceptors reside, may likely be responsible in part for the decline in cardiac BRS with advancing age in adults, it remains unclear whether 1) elevated carotid and aortic stiffness are also directly associated with obesity-associated reductions in cardiac BRS in young/middle-aged individuals, and 2) if reduced BRS with obesity is associated with elevated 24hr BPV. We tested the hypothesis that lower BRS would be associated with higher carotid and aortic stiffness and 24hr BPV in young and middle-aged individuals with obesity. In a cross-sectional design, 22 normal-weight (body mass index, BMI 24.5 ± 0.6 kg/m 2 ; age 35±2 yrs; 8M/14F) and 22 obese (BMI 34.2 ± 1.1 kg/m 2 ; age 39 ± 2 yrs; 8M/14F) individuals underwent measures of spontaneous cardiac BRS (sequence technique), carotid artery β-stiffness (carotid tonometry and B-mode ultrasound of common carotid artery), aortic stiffness (carotid-femoral pulse wave velocity, CFPWV), and 24-hr-systolic BPV (24 hr ambulatory BP monitoring). A significant relation between cardiac BRS and 24-hr systolic BPV (r=-0.42, P<0.01) was corroborated by lower cardiac BRS (11.7±1.2 vs. 16.8±1.7 ms/mmHg, P<0.05) and higher 24-hr BPV (12.4±0.6 vs. 10.1±0.4 mmHg SD, P<0.05) among obese compared with normal-weight subjects. In contrast, carotid β-stiffness (7.8±0.6 vs. 6.9±0.4 U, P>0.05) and CFPWV (745±71 vs. 611±19 cm/s, P=0.07) were not significantly different between groups despite greater average 24-hr systolic BP in the obese vs. normal weight subjects (127±2 vs. 118±1 mmHg, P<0.05). These preliminary data suggest that an increase in carotid artery and aortic stiffness may not precede the decline in cardiac BRS and increase in 24hr BPV in young and middle-aged obese individuals, suggesting non-arterial stiffness related mechanisms for obesity-related reductions in cardiac BRS.


Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Virginia R Nuckols ◽  
Amy K Stroud ◽  
Debra S Brandt ◽  
Lyndsey E DuBose ◽  
Mark K Santillan ◽  
...  

Hypertension ◽  
2006 ◽  
Vol 48 (3) ◽  
pp. 404-410 ◽  
Author(s):  
Andrew D. Stewart ◽  
Benyu Jiang ◽  
Sandrine C. Millasseau ◽  
James M. Ritter ◽  
Philip J. Chowienczyk

2021 ◽  
pp. svn-2020-000718
Author(s):  
Tingting Wang ◽  
Jie Xu ◽  
Anxin Wang ◽  
Ying Liu ◽  
Xingquan Zhao ◽  
...  

Background and purposeThe association between blood pressure variability (BPV) and stroke recurrence among patients who had ischaemic stroke (IS) remains unclear. This study aimed to investigate the association between BPV and stroke recurrence in patients who had IS of large artery atherosclerosis (LAA) subtype and small artery occlusion (SAO) subtype.MethodsData from the BOSS (Blood Pressure and Clinical Outcome in Transient Ischemic Attack or Ischemic Stroke) study were examined. IS subtypes were diagnosed according to the Trial of Org 10172 in Acute Stroke Treatment criteria. BPV was performed by 24-hour ambulatory blood pressure monitoring and defined through SD of blood pressure. The primary outcome was stroke recurrence within 90 days after discharge. Multivariable Cox regression model was used to assess the association between BPV and stroke recurrence in patients who had IS of LAA subtype and SAO subtype.ResultsA total of 1390 patients who had IS from the BOSS study were included in the present study. Multivariable analysis suggests that 24-hour systolic BPV (SBPV) and night-time diastolic BPV (DBPV) were significantly associated with stroke recurrence among all patients who had IS (HR, 2.50, 95% CI 1.07 to 5.84; HR, 1.85, 95% CI 1.07 to 3.21, respectively). Night-time SBPV and night-time DBPV were significantly associated with stroke recurrence in patients with SAO subtype (HR, 2.77, 95% CI 1.07 to 7.15; HR, 3.60, 95% CI 1.39 to 9.29, respectively). However, in the adjusted model, only night-time DBPV remained significant in patients with SAO subtype (HR, 3.87, 95% CI 1.40 to 10.71). Similar results were not found in patients who had IS of LAA subtype.ConclusionsHigh night-time DBPV was associated with increased risk of stroke recurrence among patients who had IS of SAO subtype. The results of this study have implications for the secondary prevention management and future research of patients who had IS of SAO subtype. The association between BPV and stroke recurrence in patients who had IS of LAA subtype and SAO subtype should be investigated in larger, population-based studies.


2021 ◽  
Vol 8 ◽  
Author(s):  
Michelle Lin ◽  
Robyn A. Roth ◽  
Beth A. Kozel ◽  
Robert P. Mecham ◽  
Carmen M. Halabi

There is ample evidence supporting a role for angiotensin II type 2 receptor (AT2R) in counterbalancing the effects of angiotensin II (ang II) through the angiotensin II type 1 receptor by promoting vasodilation and having anti-inflammatory effects. Elastin insufficiency in both humans and mice results in large artery stiffness and systolic hypertension. Unexpectedly, mesenteric arteries from elastin insufficient (Eln+/−) mice were shown to have significant vasoconstriction to AT2R agonism in vitro suggesting that AT2R may have vasoconstrictor effects in elastin insufficiency. Given the potential promise for the use of AT2R agonists clinically, the goal of this study was to determine whether AT2R has vasoconstrictive effects in elastin insufficiency in vivo. To avoid off-target effects of agonists and antagonists, mice lacking AT2R (Agtr2−/Y) were bred to Eln+/− mice and cardiovascular parameters were assessed in wild-type (WT), Agtr2−/Y, Eln+/−, and Agtr2−/Y;Eln+/− littermates. As previously published, Agtr2−/Y mice were normotensive at baseline and had no large artery stiffness, while Eln+/− mice exhibited systolic hypertension and large artery stiffness. Loss of AT2R in Eln+/− mice did not affect large artery stiffness or arterial structure but resulted in significant reduction of both systolic and diastolic blood pressure. These data support a potential vasocontractile role for AT2R in elastin insufficiency. Careful consideration and investigation are necessary to determine the patient population that might benefit from the use of AT2R agonists.


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