Late-life Blood Pressure Research Articles

Association of late-life blood pressure change with cerebral small vessel disease in the MIND-China study

ObjectivesThis study aimed to investigate the associations between changes in blood pressure (BP) and cerebral small vessel disease (CSVD).MethodsThis study included 401 participants in the magnetic resonance imaging (MRI) sub-study conducted between 2018 and 2020 as a part of the Multidomain Interventions to Delay Dementia and Disability in Rural China project. MRI markers of CSVD were assessed based on international criteria. Individualized linear regression models evaluated changes in BP by estimating the trend of blood pressure changes over time and fitting a straight line from 2014 to 2018. The data were analyzed using logistic and general linear regression models.ResultThe mean age of the participants was 64.48 ± 2.69 years, with 237 (59.1%) being females. Increases in systolic BP in later life were significantly associated with larger volumes of periventricular white matter hyperintensity (WMH), greater perivascular spaces in the basal ganglia (BG-PVS) burden, and the presence of deep lacunes and cerebral microbleeds. Additionally, increases in diastolic BP in later life were significantly associated with the presence of infratentorial and deep lacunes.ConclusionsCSVDs are associated with increased exposure to elevated BP later in life.

Relationship between changes in late-life blood pressure and the risk of frailty and mortality among older population in China: a cohort study based on CLHLS.

The evidence regarding the effects of blood pressure changes on older individuals remains inconclusive, and the impact of frailty throughout the life course is not known. We investigated the associations of different change patterns of blood pressure during 3-year intervals with frailty and mortality. Participants included 7335 persons from 2008 to 2014 of the Chinese Longitudinal Healthy Longevity Survey (CLHLS). Change in blood pressure was calculated as the difference between follow-up and baseline. Frailty was evaluated using a 40-item frailty index. Mortality status was ascertained up to December 31, 2014. The mean age of participants was 82.6 ± 10.7 years. The optimal blood pressure level (SBP, 130-150 mmHg; DBP, 70-90 mmHg) was associated with the lowest risk of frailty while decreasing follow-up SBP and DBP were significantly correlated with frailty. Lower baseline blood pressure levels (SBP < 130 mmHg; DBP < 70 mmHg) were associated with decreased mortality risk when participants increased their blood pressure to optimal levels during follow-up SBP and DBP (0.78, 0.63-0.98), compared to maintaining a steady low SBP (< 130 mmHg) and DBP (< 70 mmHg). For those with DBP around 70-90 mmHg, decreasing follow-up DBP (< 70 mmHg) was associated with higher mortality (1.23, 1.07-1.42) compared to maintaining stable follow-up DBP (70-90 mmHg). These results remain significant after adjusting for frailty. Optimal blood pressure levels were associated with the lowest risk of frailty. The association between lower blood pressure and increased mortality risk persisted even after accounting for frailty. We used a nationally representative longitudinal cohort study by using 2008-2014 of the Chinese Longitudinal Healthy Longevity in China. Change in blood pressure was calculated as the difference between follow-up and baseline. We investigated the associations of different change patterns of blood pressure during 3-year intervals with frailty and mortality.

Atherosclerosis and Hippocampal Volumes in Older Adults: The Role of Age and Blood Pressure.

Lower hippocampal volume is associated with late-life cognitive decline and is an important, but nonspecific marker for clinical Alzheimer's dementia. Cerebrovascular disease may also be associated with hippocampal volume. Here we study the role of intracranial large vessel disease (atherosclerosis) in association with hippocampal volume and the potential role of age, average late-life blood pressure across all visits, and other factors (sex, apolipoprotein ε4 [APOE ε4], and diabetes). Data came from 765 community-based older people (91 years old on average at death; 72% women), from 2 ongoing clinical-pathologic cohort studies. Participants completed baseline assessment, annual standardized blood pressure measurements, vascular risk assessment for diabetes, and blood draws to determine APOE genotype, and at death, brains were removed and underwent exvivo magnetic resonance imaging and neuropathologic evaluation for atherosclerosis pathology and other cerebrovascular and neurodegenerative pathologies. Linear regression models examined the association of atherosclerosis and hippocampal to hemisphere volume ratio and whether age at death, blood pressure, and other factors modified associations. In linear regression models adjusted for demographics and neurodegenerative and other cerebrovascular pathologies, atherosclerosis severity was associated with a lower hippocampal to hemisphere volume ratio. In separate models, we found the effect of atherosclerosis on the ratio of hippocampal to hemisphere volume was attenuated among advanced age at death or having higher systolic blood pressure (interaction terms P≤0.03). We did not find confounding or interactions with sex, diabetes, or APOE ε4. Atherosclerosis severity is associated with lower hippocampal volume, independent of neurodegenerative and other cerebrovascular pathologies. Higher systolic blood pressures and advanced age attenuate associations.

Year-by-Year Blood Pressure Variability From Midlife to Death and Lifetime Dementia Risk

High visit-to-visit blood pressure variability (BPV) in late life may reflect increased dementia risk better than mean systolic blood pressure (SBP). Evidence from midlife to late life could be crucial to understanding this association. To determine whether visit-to-visit BPV at different ages was differentially associated with lifetime incident dementia risk in community-dwelling individuals. This cohort study analyzed data from the Adult Changes in Thought (ACT) study, an ongoing population-based prospective cohort study in the US. Participants were 65 years or older at enrollment, community-dwelling, and without dementia. The study focused on a subset of deceased participants with brain autopsy data and whose midlife to late-life blood pressure data were obtained from Kaiser Permanente Washington medical archives and collected as part of the postmortem brain donation program. In the ACT study, participants underwent biennial medical assessments, including cognitive screening. Data were collected from 1994 (ACT study enrollment) through November 2019 (data set freeze). Data analysis was performed between March 2020 and September 2023. Visit-by-visit BPV at ages 60, 70, 80, and 90 years, calculated using the coefficient of variation of year-by-year SBP measurements over the preceding 10 years. All-cause dementia, which was adjudicated by a multidisciplinary outcome adjudication committee. A total of 820 participants (mean [SD] age at enrollment, 77.0 [6.7] years) were analyzed and included 476 females (58.0%). A mean (SD) of 28.4 (8.4) yearly SBP measurements were available over 31.5 (9.0) years. The mean (SD) follow-up time was 32.2 (9.1) years in 27 885 person-years from midlife to death. Of the participants, 372 (45.4%) developed dementia. The number of participants who were alive without dementia and had available data for analysis ranged from 280 of those aged 90 years to 702 of those aged 70 years. Higher BPV was not associated with higher lifetime dementia risk at age 60, 70, or 80 years. At age 90 years, BPV was associated with 35% higher dementia risk (hazard ratio [HR], 1.35; 95% CI, 1.02-1.79). Meta-regression of HRs calculated separately for each age (60-90 years) indicated that associations of high BPV with higher dementia risk were present only at older ages, whereas the association of SBP with dementia gradually shifted direction linearly from being incrementally to inversely associated with older ages. In this cohort study, high BPV indicated increased lifetime dementia risk in late life but not in midlife. This result suggests that high BPV may indicate increased dementia risk in older age but might be less viable as a midlife dementia prevention target.

Hypertension Trends and White Matter Brain Injury in the Offspring Framingham Heart Study Cohort.

Hypertension is the most potent stroke risk factor and is also related to cerebral small vessel disease. We studied the relation between mid-to-late-life hypertension trends and cerebral white matter injury in community-dwelling individuals from the FHS (Framingham Heart Study). FHS Offspring cohort participants with available mid-life and late-life blood pressure measurements and brain magnetic resonance imaging were included. Multiple regression analyses were used to relate hypertension trends (normotension-normotension [reference], normotension-hypertension, and hypertension-hypertension) to white matter injury metrics on diffusion tensor imaging (free water, fractional anisotropy, and peak skeletonized mean diffusivity) and Fluid Attenuated Inversion Recovery (white matter hyperintensity volume) by different blood pressure cutoffs (130/80, 140/90, and 150/90 mm Hg). We included 1018 participants (mean age 47.3±7.4 years at mid-life and 73.2±7.3 at late-life). At the 140/90 mm Hg cutoff, the hypertension-hypertension trend was associated with higher free water (β, 0.16 [95% CI, 0.03-0.30]; P=0.021) and peak skeletonized mean diffusivity (β, 0.15 [95% CI, 0.01-0.29]; P=0.033). At a 130/80 mm Hg cutoff, the hypertension-hypertension trend had significantly higher free water (β, 0.16 [95% CI, 0.01-0.30]; P=0.035); and the normotension-hypertension (β, 0.24 [95% CI, 0.03-0.44]; P=0.027) and hypertension-hypertension (β, 0.22 [95% CI, 0.04-0.41]; P=0.022) trends had significantly increased white matter hyperintensity volume. Exploratory stratified analysis showed effect modifications by APOE ɛ4 allele and age. Mid-to-late-life hypertension exposure is significantly associated with microstructural and to a lesser extent, visible white matter injury; the effects are observed at both conventional and lower blood pressure cutoffs and are associated with longer duration of hypertension.

Relationships between Late-Life Blood Pressure and Cerebral Microinfarcts in Octogenarians: An Observational Autopsy Study.

Mid-life high blood pressure (BP) is a risk factor for cerebral microinfarcts. Less is known about the relationship between late-life BP and cerebral microinfarcts, the examination of which is the objective of the current study. This case-control study analyzed data from 551 participants (94.6% aged ≥80 years; 58.6% women) in the Adult Changes in Thought (ACT) study who had autopsy data on microinfarcts and four values of systolic and diastolic blood pressure (SBP and DBP) before death. Using the average of four values, SBP was categorized using 10 mmHg intervals; a trend was defined as a ≥10 mmHg rise or fall from the first to fourth values (average gap of 6.5 years). Multivariable-adjusted regression models were used to examine the associations of BP and microinfarcts, adjusting for age, sex, last BP-to-death time, APOE genotype, and antihypertensive medication use. Microinfarcts were present in 274 (49.7%) participants; there were multiple in 51.8% of the participants, and they were located in cortical areas in 40.5%, subcortical areas in 29.6%, and both areas in 29.9% of the participants. All SBP categories (reference of 100-119 mmHg) and both SBP trends were associated with higher odds of both the presence and number of microinfarcts. The magnitude of these associations was numerically greater for subcortical than cortical microinfarcts. Similar associations were observed with DBP. These hypothesis-generating findings provide new information about the overall relationship between BP and cerebral microinfarcts in octogenarians.

Abstract 105: Potential Effect Modifiers In The Relationship Between Late-life Systolic Blood Pressure And Alzheimer’s Neuropathology

Mixed evidence exists on the relationship between late-life blood pressure (BP) and Alzheimer’s disease (AD) pathology such as amyloid and tau deposition in the brain, possibly partly due to heterogeneous effects across population subgroups. Utilizing data from the National Alzheimer’s Coordinating Center longitudinal dataset, we investigated to what extent age (&lt;65 yrs, 65-74 yrs, &gt;74 yrs), APOE genotype, stroke history, and baseline cognitive status modified the association between systolic BP (SBP) at baseline and amyloid and tau neuropathology in 3165 older adults (mean [SD] age=74 [9.8] yrs, women 47.4% [1501 of 3165]). Amyloid pathology was assessed by Thal staging, diffuse plaque, neuritic plaque and tau pathology was assessed by Braak staging at brain autopsy. Effect modification was assessed by stratified analyses and interaction analyses in multinomial logistic regression with adjustment for age at first visit, sex, APOE genotype, education years and antihypertensive medications use. We observed that both APOE e4 carriership (interaction p-value = 0.03) and stroke history (interaction p-value = 0.03) statistically modified the association of SBP with amyloid pathology, whereas baseline cognitive status modified the association with both amyloid and tau pathology (interaction p-value &lt;0.001). The SBP-amyloid association appears to be pronounced in older age group (65-74 group: OR=1.19 [CI:1.05-1.35], &gt;74 group: OR=1.12 [CI:1.02-1.23]), APOE e4 carriers (OR=1.17[CI:1.02-1.34]), and those with stroke history (OR=1.69 [CI:1.20-2.38]) and participants with dementia at baseline (OR=1.16 [CI:1.05-1.27]), whereas SBP-tauopathy association was only found in APOE e4 carriers (OR=1.25[CI:1.05-1.48]), participants without stroke history (OR=1.12[CI:1.01-1.24]), and participants with normal cognitive function at baseline (OR=1.67[CI:1.24-2.24]). Our study suggests that the relationship between SBP and amyloid and tau pathology may vary across subgroups based on age, APOE genotype, cerebrovascular burden, and stage of cognitive impairment. The underlying mechanisms warrant further investigation to inform precision blood pressure control for the prevention of dementia.

Late-Life High Blood Pressure and Enlarged Perivascular Spaces in the Putaminal Regions of Community-Dwelling Japanese Older Persons.

Enlarged perivascular spaces (EPVS) of the brain may be involved in dementia, such as Alzheimer's disease and cerebral small vessel disease (CSVD). Hypertension has been reported to be a risk factor for dementia and CSVD, but the association between blood pressure (BP) and perivascular spaces is still unclear. The aim of this study was to determine the association between BP and EPVS volumes and to examine the interactions of relevant factors. A total of 9296 community-dwelling subjects aged ≥65years participated in a brain magnetic resonance imaging and health status screening examination. Perivascular volume was measured using a software package based on deep learning that was developed in-house. The associations between BP and EPVS volumes were examined by analysis of covariance and multiple regression analysis. Mean EPVS volumes increased significantly with rising systolic and diastolic BP levels (P for trend = .003, P for trend<.001, respectively). In addition, mean EPVS volumes increased significantly for every 1-mmHg-increment in systolic and diastolic BPs (both P values <.001). These significant associations were still observed in the sensitivity analysis after excluding subjects with dementia. The present data suggest that higher systolic and diastolic BP levels are associated with greater EPVS volumes in cognitively normal older people.

Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation at the expense of cerebral vascular damage.

Hypertension in midlife contributes to cognitive decline and is a modifiable risk factor for dementia. The relationship between late-life hypertension and dementia is less clear. We have investigated the relationship of blood pressure and hypertensive status during late life (after 65 years) to post-mortem markers of Alzheimer's disease (amyloid-β and tau loads); arteriolosclerosis and cerebral amyloid angiopathy; and to biochemical measures of ante-mortem cerebral oxygenation (the myelin-associated glycoprotein:proteolipid protein-1 ratio, which is reduced in chronically hypoperfused brain tissue, and the level of vascular endothelial growth factor-A, which is upregulated by tissue hypoxia); blood-brain barrier damage (indicated by an increase in parenchymal fibrinogen); and pericyte content (platelet-derived growth factor receptor β, which declines with pericyte loss), in Alzheimer's disease (n = 75), vascular (n = 20) and mixed dementia (n = 31) cohorts. Systolic and diastolic blood pressure measurements were obtained retrospectively from clinical records. Non-amyloid small vessel disease and cerebral amyloid angiopathy were scored semiquantitatively. Amyloid-β and tau loads were assessed by field fraction measurement in immunolabelled sections of frontal and parietal lobes. Homogenates of frozen tissue from the contralateral frontal and parietal lobes (cortex and white matter) were used to measure markers of vascular function by enzyme-linked immunosorbent assay. Diastolic (but not systolic) blood pressure was associated with the preservation of cerebral oxygenation, correlating positively with the ratio of myelin-associated glycoprotein to proteolipid protein-1 and negatively with vascular endothelial growth factor-A in both the frontal and parietal cortices. Diastolic blood pressure correlated negatively with parenchymal amyloid-β in the parietal cortex. In dementia cases, elevated late-life diastolic blood pressure was associated with more severe arteriolosclerosis and cerebral amyloid angiopathy, and diastolic blood pressure correlated positively with parenchymal fibrinogen, indicating blood-brain barrier breakdown in both regions of the cortex. Systolic blood pressure was related to lower platelet-derived growth factor receptor β in controls in the frontal cortex and in dementia cases in the superficial white matter. We found no association between blood pressure and tau. Our findings demonstrate a complex relationship between late-life blood pressure, disease pathology and vascular function in dementia. We suggest that hypertension helps to reduce cerebral ischaemia (and may slow amyloid-β accumulation) in the face of increasing cerebral vascular resistance, but exacerbates vascular pathology.

Evaluating when (and how) hypertension may be 'good for your brain'.

This scientific commentary refers to 'Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation, at the expense of cerebral vascular damage', by Tayler et al. (https://doi.org/10.1093/braincomms/fcad112).

Dementia occurring over a 32-year follow-up attributable to hypertension observed at different ages: Implications for dementia prevention.

The fraction of dementia attributable to hypertension might vary depending on the age of the population considered and the age through which dementia occurs. In the Atherosclerosis Risk in Communities study, we quantified population attributable fractions (PAF) of dementia by age 80 and 90 from hypertension assessed at ages of 45-54 (n=7572), 55-64 (n=12,033), 65-74 (n=6561), and 75-84 (n=2086). The PAF for dementia by age 80 from all non-normal blood pressure at ages 45-54 was 15.3% (95% confidence interval [CI]=6.9%-22.3%), 19.1% (95% CI=9.9%-26.9%) at ages 55-64, and 19.9% (95% CI=-4.4%-38.5%) at ages 65-74. The strongest PAFs were from stage 2 hypertension (11.9%-21.3%). For dementia by age 90, PAFs from non-normal blood pressure up through age 75 were smaller (10.9%-13.8%), and non-significant by age 75-84. Interventions targeting hypertension even in early late life might reduce a sizeable proportion of dementia. We estimated prospective population attributable risks of dementia for hypertension. 15%-20% of dementia cases by age 80 are from non-normal blood pressure (BP). Associations between hypertension and dementia persisted through age 75. Midlife to early late-life BP control might reduce a large proportion of dementia.

Associations of Midlife and Late-Life Blood Pressure Status With Late-Life Retinal OCT Measures.

To explore the relationship of long-term blood pressure (BP) patterns with late-life optical coherence tomography (OCT) structural measures reflecting optic nerve health. Participants in this community-based cohort study of black and white individuals were part of the Atherosclerosis Risk in Communities study and the nested Eye Determinants of Cognition (EyeDOC) study. Participants had BP measured six times from 1987 to 2017 and were categorized into five BP patterns: sustained normotension; midlife normotension, late-life hypertension (systolic BP [SBP] >140mmHg or diastolic BP [DBP] >90mmHg or antihypertensive medication use); sustained hypertension; midlife normotension, late-life hypotension (SBP <90mmHg or DBP <60mmHg); and midlife hypertension, late-life hypotension. Multivariable linear regression modeling was used to evaluate associations between BP patterns and late-life OCT ganglion cell complex (GCC) and peripapillary retinal nerve fiber layer (RNFL) thickness. In total, 931 eyes of 931 participants (mean age at EyeDOC visit = 80 years; 63% female; 45% black) were included. Mean GCC and RNFL thicknesses in the sustained normotension pattern were 90.8 ± 10.3 µm and 89.9 ± 11.2 µm versus 89.4 ± 11.9 µm and 90.1 ± 12.2 µm in the sustained hypertension pattern (P > 0.05). Compared to the sustained normotension pattern, no significant differences in GCC or RNFL thickness were found for any anomalous BP pattern. Assessment of long-term BP status showed no significant associations with late-life OCT structural measures. OCT imaging results in our population-based sample suggest that neither hypertension, even when present in midlife, nor late-life hypotension are significant risk factors for late-life optic nerve damage.

PREVALENCE, BURDEN, AND LOCATION OF CEREBRAL MICROINFARCTS AND THEIR ASSOCIATION WITH LATE-LIFE BLOOD PRESSURE

Abstract Little is known about the relationship of late-life blood pressure (BP) profiles (level, trend and variability) with the presence, number and regional distribution (cortical vs subcortical) of cerebral microinfarcts. We examined these associations in older adults (age ≥65) using the Adult Changes in Thought (ACT) data. 551 participants (94.6% ≥80 years, 58.6% women, 94.2% white) had complete data on microinfarcts and 4 BP measures. Late-life BP, defined by the four BP values before death (2 year-time gap between measures), was treated using 3 different approaches: (1) categories (based on mean of 4 values); (2) trend (based on the difference between values 1 and 4); and (3) variability (based on standard deviation of the mean of the changes in 4 BP values from 1 to 4). Multivariable-adjusted logistic regression models were used to examine the associations of the late-life BP with microinfarcts, adjusting for relevant covariates. Each of the 5 systolic BP categories between 120 and 169 mmHg (reference: 110–119 mmHg) had significant twice higher odds (4 times for SBP ≥170) of presence and number of microinfarcts, which was only significant for subcortical region. Similar higher odds were observed for systolic BP trend (increase/decrease/no change), which was significant for both cortical and subcortical microinfarcts. Systolic BP variability had no significant association with microinfarcts. Similar associations were observed with diastolic BP. In conclusion, the presence (especially for subcortical regions) and number of microinfarcts were more likely to be in those with higher mean BP and those whose BP changed over the study.

Modifiable risk factors for incident dementia and cognitive impairment: An umbrella review of evidence

BackgroundDementia and cognitive impairment can be attributed to genetic and modifiable factors. Considerable evidence emerged in modifiable factors and urgently requires standardized evaluation. We conducted an umbrella review to evaluate the strength and validity of the existing evidence. MethodsWe searched PubMed, Embase, CINAHL and Cochrane Database of Systematic Reviews to identify relevant systematic reviews and meta-analyses of prospective studies regarding the associations of dementia and cognitive impairment with modifiable factors. For each association, we analyzed the summary effect size, 95 % confidence interval, 95 % prediction interval, heterogeneity, small study effect and excess significance bias. Mendelian randomization studies were descriptively reviewed further exploring the causality of the associations. ResultsIn total, 12,015 articles were identified, of which 118 eligible studies yielded 243 unique associations. Convincing evidence was found for associations of dementia and cognitive impairment with early-life education, midlife to late-life plasma glucose, BMI, atrial fibrillation, benzodiazepine use, and gait speed. Suggestive to highly suggestive evidence was found for that of midlife to late-life blood pressure, homocysteine, cerebrovascular diseases, hearing impairment, respiratory illness, anemia, smoking, alcohol consumption, diet, sleep, physical activity and social engagement. Among convincing evidence, Mendelian randomization studies verified causal relationships of education and plasma glucose with Alzheimer's disease. LimitationsLow quality of the studies included. ConclusionsModifiable risk factors identified in this study, especially those with high-level evidence, should be considered in dementia prevention. Our results support a valuable rationale for future experimental designs to establish further evidence for the associations in larger populations.

Relationship of Blood Pressure and White Matter Hyperintensity Burden With Level of and Change in Cognition in Older Black Adults.

Elevations in blood pressure (BP) and associated white matter hyperintensities (WMHs) are chronic comorbid conditions among older Black adults. We investigated whether WMHs modify the association between late-life BP and cognition within older Black adults. A total of 167 Black adults (age, ~75 years; without dementia at baseline) participating in neuroimaging studies at the Rush Alzheimer's Disease Center were evaluated for BP markers of cardiovascular health, including systolic BP, diastolic BP, pulse pressure, mean arterial pressure (MAP), and hypertension, and were assessed for global and domain-specific cognition at baseline and annually for up to 8 years. WMHs adjusted for intracranial volume were quantified at baseline. Models adjusted for relevant confounders and the interaction of these variables with time revealed differential associations between BP markers and baseline cognition; however, only elevated diastolic BP predicted faster cognitive, that is, episodic memory, decline (estimate = -0.002, standard error = 0.0009, p = .002). Although WMH burden did not modify the association between diastolic BP and episodic memory decline, it did interact with diastolic BP to lower episodic memory at baseline (estimate = -0.051, standard error = 0.012, p = .0001); that is, greater WMHs combined with higher diastolic BP resulted in the lowest baseline episodic memory scores. A similar profile was noted for WMHs, MAP, and baseline episodic memory. Hypertension was neither associated with cognition nor modified by WMH burden after multiple comparisons correction. Late-life diastolic BP was associated with faster rates of episodic memory decline in older Black adults; together with higher WMH burden, it (and MAP) lowered the point at which individuals begin their course of decline toward pathological aging.

Changes in late-life systolic blood pressure and all-cause mortality among oldest-old people in China: the chinese longitudinal healthy longevity survey

BackgroundBlood pressure targets for oldest-old people have been long debated due to the concern that more stringent targets are associated with increased mortality. We aimed to investigate the association between changes of late-life systolic blood pressure (SBP), mean SBP and SBP variability (SBPV), and all-cause mortality in oldest-old.MethodsBased on the community-based Chinese Longitudinal Healthy Longevity Survey with follow-up conducted in the 3-year interval, we assembled a retrospective cohort of 6639 participants ≥ 80 years with available blood pressure measurements at baseline and second wave. The primary exposures were mean SBP and SBPV (defined as the annual difference in SBP divided by mean SBP) measured between baseline and second wave. The primary outcome was all-cause mortality assessed from the second wave.ResultsDuring 21443.1 person-years of follow-up, 4622 death was recorded. U-shaped associations of mortality with mean SBP and SBPV were identified; the value of 137 mmHg and 4.0 %/year conferred the minimum mortality risk, respectively. The associations of a larger SBPV with an increased mortality risk were observed for both rises and large falls in SBP. The hazard ratio was 1.11 (comparing lowest versus middle quintile; 95 % CI: 1.01, 1.22) with large falls in SBPV and 1.08 (comparing highest versus middle quintile; 95 % CI: 0.98, 1.18) with large rises in SBPV.ConclusionsU-shaped associations between late-life SBP and SBPV and all-cause mortality were found. Our study suggests that a stable SBP level in the middle range is related to lower mortality risk in the oldest-old.

Associations of changes in late-life blood pressure with cognitive impairment among older population in China

BackgroundThe cognitive impact of changes in late-life blood pressure is less clear. We aimed to investigate the association between late-life blood pressure changing pattern and risk of cognitive impairment.MethodsUsing data from the community-based Chinese Longitudinal Healthy Longevity Survey, change in systolic (SBP) or diastolic (DBP) blood pressure was calculated as the difference between follow-up and baseline, cognitive impairment was defined based on both the Mini-Mental State Examination and education level. The generalized additive model with penalized spline and multivariate logistic regression model were used, respectively, to examine the associations between continuous and categorized blood pressure changes with cognitive impairment at the follow-up wave.ResultsA total of 8493 Chinese elderly without cognitive impairment were included, with mean (standard deviation) age 80.6 (10.7) years. U-shaped associations between late-life blood pressure changes and risk of cognitive impairment were found, with only stable optimal blood pressure related to the lowest risk. For participants with baseline SBP around 130–150 mmHg, the adjusted odds ratio was 1.48 (1.13–1.93) for increasing follow-up SBP (> 150 mmHg), 1.28 (1.02–1.61) for decreasing follow-up SBP (< 130 mmHg), compared to stable follow-up SBP (130–150 mmHg). For participants with relative lower baseline DBP (< 80 mmHg), increasing their DBP to 80–90 mmHg during follow-up was associated with lower cognitive impairment risk (0.73 (0.58–0.93)), compared to steady low follow-up DBP (< 80 mmHg). Sex-specific analysis suggested that men were more vulnerable in term of SBP change.ConclusionsAdhering to a stable optimal level of blood pressure in late-life is related to lower risk of cognitive impairment in Chinese elderly.

Longitudinal Blood Pressure Patterns From Mid- to Late Life and Late-Life Hearing Loss in the Atherosclerosis Risk in Communities Study.

Hearing loss is prevalent and associated with adverse functional outcomes in older adults. Prevention thus has far-reaching implications, yet few modifiable risk factors have been identified. Hypertension may contribute to age-related hearing loss, but epidemiologic evidence is mixed. We studied a prospective cohort of 3343 individuals from the Atherosclerosis Risk in Communities study, aged 44-65 years at baseline with up to 30 years of follow-up. Hearing was assessed in late life (2016-2017) using a better-ear audiometric pure tone average (0.5, 1, 2, 4 kHz) and the Quick Speech-in-Noise (QuickSIN) test. Hypertension was defined as systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or antihypertensive medication use. Midlife hypertension was defined by hypertension at 2 consecutive visits between 1987-1989 and 1996-1998. Late-life hypertension was defined in 2016-2017. Late-life low blood pressure was defined as a systolic blood pressure less than 90 mmHg or diastolic blood pressure less than 60 mmHg, irrespective of antihypertensive medication use. Associations between blood pressure patterns from mid- to late life and hearing outcomes were assessed using multivariable-adjusted linear regression. Compared to persistent normotension, persistent hypertension from mid- to late life was associated with worse central auditory processing (difference in QuickSIN score = -0.66 points, 95% CI: -1.14, -0.17) but not with audiometric hearing. Participants with persistent hypertension had poorer late-life central auditory processing. These findings suggest that hypertension may be more strongly related to hearing-related changes in the brain than in the cochlea.

Contributions of Cerebral Blood Flow to Associations Between Blood Pressure Levels and Cognition: The Age, Gene/Environment Susceptibility-Reykjavik Study.

[Figure: see text].

Association of Mid- to Late-Life Blood Pressure Patterns With Risk of Subsequent Coronary Heart Disease and Death.

Background: The elevated blood pressure (BP) at midlife or late-life is associated with cardiovascular disease and death. However, there is limited research on the association between the BP patterns from middle to old age and incident coronary heart disease (CHD) and death.Methods: A cohort of the Atherosclerosis Risk in Communities (ARIC) Study enrolled 9,829 participants who attended five in-person visits from 1987 to 2013. We determined the association of mid- to late-life BP patterns with incident CHD and all-cause mortality using multivariable-adjusted Cox proportional hazards models.Results: During a median of 16.7 years of follow-up, 3,134 deaths and 1,060 CHD events occurred. Compared with participants with midlife normotension, the adjusted hazard ratio for all-cause mortality and CHD was 1.14 (95% CI, 1.04–1.25) and 1.28 (95% CI, 1.10–1.50) in those with midlife hypertension, respectively. In further analyses, compared with a pattern of sustained normotension from mid- to late-life, there was no significant difference for the risk of incident death (HR, 1.15; 95% CI, 0.96–1.37) and CHD (HR, 1.33; 95% CI, 0.99–1.80) in participants with a pattern of midlife normotension and late-life hypertension with effective BP control. A higher risks of death and CHD were found in those with pattern of mid- to late-life hypertension with effective BP control (all-cause mortality: HR, 1.24; 95% CI, 1.08–1.43; CHD: HR, 1.65; 95% CI 1.30–2.09), pattern of midlife normotension and late-life hypertension with poor BP control (all-cause mortality: HR, 1.27; 95% CI, 1.12–1.44; CHD: HR, 1.53; 95% CI, 1.23–1.92), and pattern of mid- to late-life hypertension with poor BP control (all-cause mortality: HR, 1.49; 95% CI, 1.30–1.71; CHD: HR, 1.87; 95% CI, 1.48–2.37).Conclusions: The current findings underscore that the management of elderly hypertensive patients should not merely focus on the current BP status, but the middle-aged BP status. To achieve optimal reductions in the risk of CHD and death, it may be necessary to prevent, diagnose, and manage of hypertension throughout middle age.