IC-P-018: Arterial stiffness is associated with amyloid deposition in the brain independent of blood pressure

Background: Advances in positron emission tomography imaging using amyloid specific ligands (e.g. PiB-PET) provide in vivo measurement of amyloid deposition in the brain, a hallmark of Alzheimer’s disease (AD) and dementia. Hypertension is believed to promote AD through arterial stiffening and cerebrovascular disease. We hypothesize that vascular measures are associated with amyloid in the brain. Methods: We studied 92 participants aged 83-96 in a follow-up of the Gingko Evaluation of Memory (GEM) Study with measures of: structural MRI of the brain; PiB-PET of brain amyloid deposition; resting blood pressure (BP), ankle brachial index (ABI) and mean arterial pressure (MAP); and vascular stiffness in the central (carotid-femoral ( cf PWV) and heart femoral ( hf PWV), peripheral (femoral-ankle ( fa PWV), and mixed (brachial-ankle ( ba PWV)) vascular beds, using a noninvasive and automated waveform analyzer (Colin Co., Komaki, Japan). Before study entry, all participants underwent ApoE-4 genotyping, detailed neuropsychological battery and adjudication of cognition by committee. Participants with a diagnosis of dementia were excluded from the sub-study. Results: Half (44/92) non-demented older adults in this sub-study were PiB+ for amyloid deposition in the brain. Amyloid deposition was associated with ba PWV, systolic BP and MAP. After adjustment for covariates, one standard deviation increase in ba PWV resulted in a 2-fold increase in the odds of being PiB+. ApoE-4 status was not associated with PWV. Additionally, high white matter disease burden, but not total gray matter volume, was associated with increased cf PWV (p<0.01), hf PWV (p=0.03), SBP (p=0.05) and MAP (p=0.06). Conclusions: The adverse effects of hypertension and vascular stiffness on cerebral small vessel disease is one of the most important hypotheses as to the determinants of amyloid deposition and AD. This is the first report of a possible association between vascular stiffness, BP and in vivo amyloid deposition in non-demented individuals.

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Female Gender Is Associated with Higher Susceptibility of Weight Induced Arterial Stiffening and Rise in Blood Pressure

Journal of Clinical Medicine ◽

10.3390/jcm10163479 ◽

2021 ◽

Vol 10 (16) ◽

pp. 3479

Author(s):

Junli Zuo ◽

Huijuan Chao ◽

Biwen Tang ◽

Alberto P. Avolio ◽

Markus P. Schlaich ◽

...

Keyword(s):

Blood Pressure ◽

Arterial Stiffness ◽

Systolic Pressure ◽

Female Gender ◽

Arterial Stiffening ◽

Hemodynamic Forces ◽

Traditional Risk Factors ◽

Gender Based ◽

Male Subjects ◽

The Brain

Arterial stiffness is an important predictor of cardiovascular events, independent of traditional risk factors. Stiffening of arteries, though an adaptive process to hemodynamic load, results in substantial increase in the pulsatile hemodynamic forces that detrimentally affects the microcirculation perfusing the vital organs such as the brain, heart and kidneys. Studies have proposed that arterial stiffness precedes and may contribute to the development of hypertension in individuals with obesity. Our study sought to determine the gender-based effects on arterial stiffening in obesity which may predispose to the development of hypertension. We found female sex is associated with higher susceptibility of weight-related arterial stiffening and rise in blood pressure in obesity. Women had significantly higher carotid-femoral pulse wave velocity (CF-PWV) with higher body mass index (BMI) status (normal: 7.9 ± 2 m/s; overweight: 9.1 ± 2 m/s; obese: 9 ± 2 m/s, p < 0.001), whereas it was similar in males across all BMI categories. The linear association between arterial stiffness and BMI following adjustment for age and brachial systolic and diastolic blood pressure (BP), remained significant in females (β = 0.06; 95% CI 0.01 to 0.1; p < 0.05) but not in males (β = 0.04; 95% CI −0.01 to 0.1; p > 0.05). The mean CF-PWV values increased by 0.1 m/s for every 1 kg/m2 increase in BMI in the female subjects in the age adjusted linear model, while such effect was not seen in the male subjects. In line with arterial stiffening, the overweight and obese females demonstrated significantly higher systolic brachial BP. (BP difference: ΔBP 9−11 mmHg, p < 0.01) and central systolic pressure (ΔBP 8−10 mmHg, p < 0.05) compared to their lean counterparts, unlike the male subjects. Our results suggest that female gender is associated with higher susceptibility of weight-related arterial stiffening and rise in blood pressure.

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Improvements in Blood Pressure (BP) and Markers of Arterial Stiffness with Canagliflozin (CANA) in the CANagliflozin CardioVascular Assessment Study (CANVAS) Program

Diabetes ◽

10.2337/db18-1210-p ◽

2018 ◽

Vol 67 (Supplement 1) ◽

pp. 1210-P

Author(s):

RAYMOND TOWNSEND ◽

MALA DHARMALINGAM ◽

STEFANO GENOVESE ◽

ANDREW STEELE ◽

JOSE L. ARENAS ◽

...

Keyword(s):

Blood Pressure ◽

Arterial Stiffness ◽

Assessment Study ◽

Cardiovascular Assessment

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Effect of Protein Intake During Hemodialysis on Blood Pressure and Arterial Stiffness Indices

Case Medical Research ◽

10.31525/ct1-nct03947710 ◽

2019 ◽

Author(s):

Keyword(s):

Blood Pressure ◽

Arterial Stiffness ◽

Protein Intake

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Comparison of Longitudinal Blood Pressure and Arterial Stiffness in Preeclamptic Women After Delivery

Case Medical Research ◽

10.31525/ct1-nct04142268 ◽

2019 ◽

Author(s):

Keyword(s):

Blood Pressure ◽

Arterial Stiffness

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Faculty Opinions recommendation of Blood pressure-independent reduction in proteinuria and arterial stiffness after acute endothelin-a receptor antagonism in chronic kidney disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1165248.628191 ◽

2009 ◽

Author(s):

David Pollock

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Receptor Antagonism ◽

Endothelin A Receptor ◽

Endothelin A ◽

Pressure Independent

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RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

Current Medicinal Chemistry ◽

10.2174/0929867325666180226102358 ◽

2018 ◽

Vol 25 (28) ◽

pp. 3333-3352 ◽

Cited By ~ 21

Author(s):

Natalia Pessoa Rocha ◽

Ana Cristina Simoes e Silva ◽

Thiago Ruiz Rodrigues Prestes ◽

Victor Feracin ◽

Caroline Amaral Machado ◽

...

Keyword(s):

Blood Pressure ◽

Central Nervous System ◽

Nervous System ◽

Therapeutic Potential ◽

Neuropsychiatric Disorders ◽

Extensive Literature ◽

Ang Ii ◽

Mas Receptor ◽

The Central Nervous System ◽

The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

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