When to expect cognitive disorders in hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Khomazyuk ◽  
V.U Krotova

Abstract   In large-scale clinical studies, age, arterial hypertension (AH), multi-focal atherosclerosis, and cognitive disorders (CD) are interrelated, affecting the level of disability, quality of life, and social adaptation of patients with cardiovascular diseases. Aim of the study To determine the prognostic criteria for cognitive disorders in patients with hypertension. Methods To achieve the aim of the study, the examinations were performed in 182 outpatients with AH II stage, 34–68 years, in 164 of them were CD according to neuropsychological tests of MMSE and MoCA, mostly of mild and moderate degree. The relationship between clinical data, cognitive function characteristics and daily monitoring data of hypertension were evaluated. The data obtained were analyzed using medical methods statistics. Results Among factors such as age (>60 years), gender (male / female), disease duration (>10 years), waist circumference, overweight or obesity, hypercholesterolemia, no influence on the development of CD was detected (p>0.05)). Risk factors for the development of CD in hypertension were an burdensome history of CD in closest relatives (2.79 (95% CI 1.15–6.77) relative to practically healthy individuals and 2.41 (1.01–5.88)), high vegetative index (rs +0,15; p<0,05). The correlation between CD and high rates of blood pressure variability according to daily monitoring of blood pressure in patients with hypertension, even under conditions of blood pressure control, is confirmed by the results of correlation and one-factor logit analysis. Thus, elevated levels of systolic blood pressure variability in the day and at night increased the chances of developing CD in patients with hypertension by 2.11 times, (rs = +0.57 and rs = +0.61; p<0.001). It was found that the likelihood of developing cognitive impairment exceeds 50% (high risk) if the level of systolic blood pressure variability is above 12 mm Hg in the day (area under ROC curve AUC = 0.891; 95% CI 0.883–0.940. (AUC = 0.891; 95% CI 0.883–0.940; ST = 82.5% and SP = 92.9%) and at night over 10 mm Hg (AUC = 0.922; 95% CI 0.861–0.963; ST = 82.5% and SP = 85.7%) according to daily blood pressure monitoring. Conclusion The prognosis for the development of cognitive impairment in arterial hypertension is influenced by: evidence of family CD history, autonomic nervous system index and variability of day and night blood pressure characteristics, according to ambulatory daily monitoring data. Funding Acknowledgement Type of funding source: None

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Viktoriia Krotova ◽  
Tatyana Khomazyuk

To study the relationship between quality of life (LQ) and cognitive impairment, as well as to identify risk factors for their development in patients with arterial hypertension (AH). Examined 509 outpatients with controlled AH stage II with SCORE risk of CVD <5 %. Non-dementia cognitive impairment were found 24,32±0,11 points on МCA scale in 164 (32.2 %). Patients also demonstrated a significant (p <0.001) decrease in the LQ indicators on all SF-36 scales compared to healthy ones by an average of 24.5-66.0 points. According to the results of correlation analysisthe most significant was the direct relationship between cognitive impairment on МCA scale and assessment of physical health (rs=+0,65; p<0,001), mental health (rs=+0,60; p<0,001), life activity limitations (rs=+0,33; p<0,001) and social activity (rs=+0,35; p<0,001), indicating an association between deterioration in LQ components and cognitive impairment.It turned out that the risk factors for developing cognitive impairment with AH were a history of cognitive impairment in close relatives (2.79 (95 % CI 1.15-6.77) compared with healthy people and 2.41 (95 % CI 1.01-5.88) - AH patients without cognitive impairment), a high vegetative index (rs +0.15; p <0.05) according to daily monitoring of BP and elevated levels of systolic BP variability in day and at night, that increased the chances of developing cognitive impairment in AH patients by 2.11 times, (rs = + 0.57 and rs = + 0.61; p<0.001). It was found that the likelihood of developing cognitive impairment exceeds 50 % (high risk) if the level of systolic BP variability is above 12 mm Hg in day (area under ROC curve AUC = 0.891; 95 % CI 0.883-0.940. (AUC = 0.891; 95 % CI 0.883-0.940; ST = 82.5 % and SP = 92.9 %) and at night – over 10 mm Hg (AUC = 0.922; 95 % CI 0.861-0.963; ST = 82.5 % and SP = 85.7 %) according to daily BP monitoring. In patients with AH for more than 10 years with dissatisfaction of life quality, even with controlled blood pressure, the presence of cognitive impairment needs to be clarified in immediate families, and pay attention to the high autonomic index and variability of systolic blood pressure monitored day and night, due to the high risk of development and progression of cognitive impairment, which worsens the prognosis of cardiovascular events.


2020 ◽  
Vol 77 (4) ◽  
pp. 1655-1669
Author(s):  
Isabel J. Sible ◽  
Daniel A. Nation ◽  

Background: Elevated blood pressure is linked to cognitive impairment and Alzheimer’s disease (AD) biomarker abnormality. However, blood pressure levels vary over time. Less is known about the role of long-term blood pressure variability in cognitive impairment and AD pathophysiology. Objective: Determine whether long-term blood pressure variability is elevated across the clinical and biomarker spectrum of AD. Methods: Alzheimer’s Disease Neuroimaging Initiative participants (cognitively normal, mild cognitive impairment, AD [n = 1,421]) underwent baseline exam, including blood pressure measurement at 0, 6, and 12 months. A subset (n = 318) underwent baseline lumbar puncture to determine cerebrospinal fluid amyloid-β and phosphorylated tau levels. Clinical groups and biomarker-confirmed AD groups were compared on blood pressure variability over 12 months. Results: Systolic blood pressure variability was elevated in clinically diagnosed AD dementia (VIM: F2,1195 = 6.657, p = 0.001, η2 = 0.01) compared to cognitively normal participants (p = 0.001), and in mild cognitive impairment relative to cognitively normal participants (p = 0.01). Findings were maintained in biomarker-confirmed AD (VIM: F2,850 = 5.216, p = 0.006, η2 = 0.01), such that systolic blood pressure variability was elevated in biomarker-confirmed dementia due to AD relative to cognitively normal participants (p = 0.005) and in biomarker-confirmed mild cognitive impairment due to AD compared to cognitively normal participants (p = 0.04). Conclusion: Long-term systolic blood pressure variability is elevated in cognitive impairment due to AD. Blood pressure variability may represent an understudied aspect of vascular dysfunction in AD with potential clinical implications.


Author(s):  
Xiaoyong Xu ◽  
Xianghong Meng ◽  
Shin-ichi Oka

Abstract Objective Our work aimed to investigate the association between vigorous physical activity and visit-to-visit systolic blood pressure variability (BPV). Methods We conducted a post hoc analysis of SPRINT (Systolic Blood Pressure Intervention Trial), a well-characterized cohort of participants randomized to intensive (&lt;120 mmHg) or standard (&lt;140 mmHg) SBP targets. We assessed whether patients with hypertension who habitually engage in vigorous physical activity would have lower visit-to-visit systolic BPV compared with those who do not engage in vigorous physical activity. Visit-to-visit systolic BPV was calculated by standard deviation (SD), average real variability (ARV), and standard deviation independent of the mean (SDIM) using measurements taken during the 1-, 2-, 3-, 6-, 9- and 12-month study visits. A medical history questionnaire assessed vigorous physical activity, which was divided into three categories according to the frequency of vigorous physical activity. Results A total of 7571 participants were eligible for analysis (34.8% female, mean age 67.9±9.3 years). During a follow-up of 1-year, vigorous physical activity could significantly reduce SD, ARV, and SDIM across increasing frequency of vigorous physical activity. There were negative linear trends between frequency of vigorous physical activity and visit-to-visit systolic BPV. Conclusions Long-term engagement in vigorous physical activity was associated with lower visit-to-visit systolic BPV.


PLoS ONE ◽  
2019 ◽  
Vol 14 (10) ◽  
pp. e0224538
Author(s):  
Katy J. L. Bell ◽  
Lamiae Azizi ◽  
Peter M. Nilsson ◽  
Andrew Hayen ◽  
Les Irwig ◽  
...  

2005 ◽  
Vol 288 (2) ◽  
pp. H710-H715 ◽  
Author(s):  
Mikko P. Tulppo ◽  
Heikki V. Huikuri ◽  
Elli Tutungi ◽  
Derek S. Kimmerly ◽  
Adrian W. Gelb ◽  
...  

The amplitude of low-frequency (LF) oscillations of heart rate (HR) usually reflects the magnitude of sympathetic activity, but during some conditions, e.g., physical exercise, high sympathetic activity results in a paradoxical decrease of LF oscillations of HR. We tested the hypothesis that this phenomenon may result from a feedback inhibition of sympathetic outflow caused by circulating norepinephrine (NE). A physiological dose of NE (100 ng·kg−1·min−1) was infused into eight healthy subjects, and infusion was continued after α-adrenergic blockade [with phentolamine (Phe)]. Muscle sympathetic nervous activity (MSNA) from the peroneal nerve, LF (0.04–0.15 Hz) and high frequency (HF; 0.15–0.40 Hz) spectral components of HR variability, and systolic blood pressure variability were analyzed at baseline, during NE infusion, and during NE infusion after Phe administration. The NE infusion increased the mean blood pressure and decreased the average HR ( P < 0.01 for both). MSNA (10 ± 2 vs. 2 ± 1 bursts/min, P < 0.01), LF oscillations of HR (43 ± 13 vs. 35 ± 13 normalized units, P < 0.05), and systolic blood pressure (3.1 ± 2.3 vs. 2.0 ± 1.1 mmHg2, P < 0.05) decreased significantly during the NE infusion. During the NE infusion after PHE, average HR and mean blood pressure returned to baseline levels. However, MSNA (4 ± 2 bursts/min), LF power of HR (33 ± 9 normalized units), and systolic blood pressure variability (1.7 ± 1.1 mmHg2) remained significantly ( P < 0.05 for all) below baseline values. Baroreflex gain did not change significantly during the interventions. Elevated levels of circulating NE cause a feedback inhibition on sympathetic outflow in healthy subjects. These inhibitory effects do not seem to be mediated by pressor effects on the baroreflex loop but perhaps by a presynaptic autoregulatory feedback mechanism or some other mechanism that is not prevented by a nonselective α-adrenergic blockade.


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