scholarly journals Aortic stiffness is associated with changes in retinal arteriole flow pulsatility mediated by local vasodilation in healthy young/middle-age adults

2020 ◽  
Vol 129 (1) ◽  
pp. 84-93
Author(s):  
Seth W. Holwerda ◽  
Randy H. Kardon ◽  
Ryuya Hashimoto ◽  
Jan M. Full ◽  
Julie K. Nellis ◽  
...  

By using the human retinal microvasculature as an end-organ in vivo model, we confirm that aortic stiffness and related increases in central pulse pressure are inversely correlated with retinal arteriole lumen diameter and increased microvascular resistance among heathy young/middle-age adults. Additionally, higher aortic stiffness is not associated with excessive flow pulsatility in the retinal microvasculature under tonic conditions but may be related to limited reductions in retinal arteriole flow pulsatility in response to local vasodilation.

2018 ◽  
Vol 118 (10) ◽  
pp. 2203-2211 ◽  
Author(s):  
Samuel Palmiere ◽  
Marcus Wade ◽  
Jacob P. DeBlois ◽  
Wesley K. Lefferts ◽  
Kevin S. Heffernan

2007 ◽  
Vol 1 (S1) ◽  
pp. S24
Author(s):  
F.U.S. Mattace-Raso* ◽  
W.J. Bos ◽  
T.J.M. van der Cammen ◽  
B.E. Westerhof ◽  
R. Asmar ◽  
...  

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Jose Gutierrez ◽  
Farid Khasiyev ◽  
Adam M Brickman ◽  
Jennifer L Manly ◽  
Randolph S Marshall ◽  
...  

Background: Cerebral hemodynamic dysfunction is associated with brain small artery disease and poorer cognition. With aging, systemic arteries stiffen, magnifying the spread of pulsatility to distal organs. The brain is especially susceptible to pulsatility due to low impedance to flow. Increased pulsatility causes abnormal brain arteriolar remodeling in animal models. Therefore, we hypothesize that measures of aortic stiffness relate to poorer cerebral autoregulation, an in-vivo measure of arteriolar function. Methods: We recruited participants in the Washington Heights-Inwood Community Aging Project for this study. For autoregulation, both middle cerebral arteries were insonated at a depth of 50-58 mm. End-tidal CO2 (EtCO2) was measured continuously with a facemask. After ten minutes of baseline recording, a mixture of air enriched with 5% CO2 was administered through the facemask for 2 minutes. Cerebrovascular reactivity was calculated as % change in mean CBFV (mCBFV) per 1 mm increase in mean EtCO2 during CO2 inhalation. We averaged the right and left CO2 reactivity percentage. For aortic stiffness, we acquired carotid-femoral pulse wave velocity (cfPWV) with non-invasive oscillometry using the Vicorder system (Skidmore Medical Limited, Bristol, UK). We used generalized linear model to obtain beta estimates of the association between CO2 reactivity and cfPWV. Results: We included 158 participants (mean age 77±6.4 years, 67% women, 40% non-Hispanic black, 38% non-Hispanic white, and 20% Hispanic). Hypertension was present in 54% of the participants. cfPWV was associated with poorer CO2 reactivity (B=-0.038, P=0.047), independent of age, sex, ethnicity, and hypertension. Brachial pulse pressure (B=0.007, P=0.38) and mean arterial pressure (B=-0.017, P=0.21) were not associated with CO2 reactivity, and adding brachial pulse pressure and mean arterial pressure to the adjusted model did not change the association between cfPWV and poorer CO2 reactivity. Conclusions: Aortic stiffness is associated with poorer CO2 reactivity independent of traditional measures of hypertension, a marker of cerebral autoregulation and arteriolar health. Poorer CO2 reactivity may mediate the reported effects of aortic stiffness on brain outcomes.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Connie W Tsao ◽  
Asya Lyass ◽  
Martin G Larson ◽  
Gary F Mitchell ◽  
Ramachandran S Vasan

Background: The structure and function of the aorta and left ventricle are closely coupled, but the relations of arterial stiffness, pressure pulsatility, and wave reflection to clinical heart failure (HF) are not well described. Methods: We evaluated 2904 Framingham Heart Study participants (mean age 64+11 yrs, 56% F) who were free of clinical HF and myocardial infarction (MI). Carotid-femoral pulse wave velocity (CFPWV), central pulse pressure, forward wave amplitude, and augmentation index were assessed by applanation tonometry. Cox proportional hazards models accounted for competing risk of death and adjusted for age, sex, body mass index, mean arterial pressure, total and HDL cholesterol, use of hypertensive medications, prevalent diabetes, current smoking, and prevalent cardiovascular disease. Results: On follow-up (mean 9.2 years, limits 0.04-13 years), 170 participants developed new-onset HF while 106 experienced an MI. The incidence of HF rose across CFPWV tertiles ( Figure ). Each standard deviation (SD) higher CFPWV conferred a 50% (95% CI 1.21-1.85, p=0.0002) and 30% (95% CI 1.02-1.64, p=0.037) increased risk of incident HF in age- and sex-adjusted and multivariable-adjusted analyses, respectively. CFPWV was associated with increased risk of MI (hazards ratio [HR] per SD 1.46, 95% CI 1.01-2.12, p=0.04). The inclusion of interim MI in multivariable models attenuated the association of CFPWV with HF incidence (HR per SD 1.26, 95% CI 0.99-1.60, p=0.061). Central pulse pressure, forward wave amplitude, and augmentation index were not associated with incident HF in multivariable-adjusted models. Conclusions: Higher aortic stiffness as assessed by CFPWV is associated with increased risk of incident HF, mediated in part by the increased risk of interim MI associated with vascular stiffness. These findings illustrate the importance of ventricular-vascular coupling, and underscore the need for studies to examine the benefit of therapies that modify aortic stiffness for lowering the population burden of MI and HF.


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