Higher central pulse pressure but not central artery stiffness is associated with higher retinal arteriolar flow pulsatility

Background: High large central artery (aorta, carotids) stiffness is purported to cause microvasculature remodeling and damage to high flow, low resistance organs as a result of increased transmission of excessive pressure and flow pulsatility into microvascular beds. Although our previous study showed that aortic stiffness is not a significant predictor of basal microvascular flow pulsatility in the retinal microvasculature, less is known about carotid artery stiffness or central blood pressure. Therefore, the purpose of this study was to investigate the effects of central artery stiffness, central pressure, and arterial structure on microvascular flow pulsatility of the retina. Based on our previous data, we hypothesized that there would be no association between arterial stiffness, central pressure, or arterial structure and microvascular flow pulsatility. Methods: Forty healthy individuals (age range 25-60 years) with no history of cardiovascular or related diseases underwent vascular testing and retinal imaging. Aortic stiffness was assessed as carotid-femoral pulse wave velocity (cfPWV) using tonometry and common carotid artery stiffness was assessed as β-stiffness using ultrasonography and tonometry. Hemodynamic variables included mean arterial pressure (MAP, via NIHem) and central pulse pressure (PP, via carotid tonometry). Large artery structure was assessed using carotid diameter and intima media thickness (IMT) (both via ultrasonography). Retinal arteriolar flow was measured using laser speckle flowgraphy (LSFG) which quantified flow pulsatility as overall flow amplitude (max amplitude during systole – min amplitude during diastole) and flow pulsatility index (PI, flow amplitude/mean flow). Multiple linear regression models were used to assess associations between macrovascular and retinal outcome measures. All statistical models adjusted for age, sex, and BMI. Results: There was no significant association between cfPWV and retinal flow amplitude (p=0.565) or PI (p=0.473), or between carotid β-stiffness and retinal flow amplitude (p=0.955) or PI (p=0.790). In contrast, central PP was significantly associated with both retinal flow amplitude (p=0.008) and PI (p=0.025), whereas MAP was not significantly associated with retinal flow amplitude (p=0.535) or PI (p=0.314). Carotid diameter was not significantly associated with retinal flow amplitude (p=0.889) or PI (p=0.542), and carotid IMT was not associated with retinal flow amplitude (p=0.384) or PI (p=0.514). Conclusions: Central PP may be a better predictor of pulsatile flow in the microvasculature of high flow end organs such as the retina, than central artery wall stiffness as measured by cfPWV and carotid β-stiffness. These results also indicate that interventions targeting the reduction of PP may be more beneficial to reducing microvascular pulsatility than lowering MAP or central artery stiffness. This research was supported by American Heart Association (AHA) Grant 17POST33440101 and National Heart, Lung, and Blood Institute Grant T32 HL07121 (S. W. Holwerda.) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.