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Summary Objective Epidemiological data suggest that moderate habitual coffee consumption associates with lower cardiovascular disease (CVD) risk; however scarce data exist regarding the association of coffee with subclinical vascular disease (SVD). We aimed at investigating the above association with habitual instant coffee consumption - a widely consumed coffee in Greece–in high CVD risk but free of established CVD adults. Research methods & procedures In a cross-sectional design study we measured: (i) two 24 h dietary recalls to assess coffee consumption, (ii) arterial stiffness, by carotid to femoral pulse wave velocity - (PWV) and carotid compliance, arterial remodeling by carotid intima-media thickness (IMT), pressure wave reflection by augmentation index (AIx) and atheromatosis by carotid plaques. Results In 1041 participants (55.6% females, 53.6 ± 14.0 years), 30% habitually consumed instant coffee (0.53 ± 1.15 cups/day). Consumption of instant coffee was inversely associated with systolic blood pressure (β = −1.19, p = 0.007), AIx (β = −0.71, p = 0.043), PWV (β = −0.22, p = 0.000) and IMT (β = −0.01, p = 0.025), but these associations lost their significance after multiple adjustments for confounders. Instant coffee consumption was positively associated with carotid compliance independent from all possible confounders (β = 0.005, p = 0.003). Conclusion Habitual moderate instant coffee consumption is inversely associated with arterial stiffening and potential with arterial remodeling. These favorable vascular associations offer a potential pathophysiological link between habitual coffee consumption and lower incidence of CVD. Future studies are needed to examine the long-term effects of habitual instant coffee consumption on vascular structure and function.

Aim To characterize different patterns of variability of three repeated within-visit blood pressure (BP) readings and to determine the prevalence of specific variation trends in systolic (SBP), diastolic (DBP) blood pressure and pulse pressure (PP). Methods Data from 53 737 subjects from the National Health and Nutrition Examination Survey were analyzed. In each subject, three consecutive BP measurements were performed with a minimum time-interval of at least 30 s. We propose three patterns of within-visit BP variability (separately for SBP, DBP and PP): (1) increasing trend (BP3 > BP2 > BP1); (2) decreasing trend (BP1 > BP2 > BP3) and (3) no trend (BP3 ≈ BP2 ≈ BP1). A threshold of minimum change (ΔP > 3 mmHg) between BP1-BP2 and BP2-BP3 was also applied as a prerequisite for the definition of these trends. Results An increasing trend was observed among three consecutive measurements of SBP, DBP and PP in 7.4, 10.4 and 10.2%, respectively. When a minimum threshold of 3 mmHg was set the respective increasing trends were observed in 1.8, 2.9 and 4.4%, respectively. There was a higher prevalence of decreasing trend within three consecutive SBP, DBP and PP readings: 17, 13.1 and 16.2%, respectively, whereas using a threshold of ΔP >3 mmHg the respective prevalence was 6.3, 4.1 and 7.7%. A maximum absolute difference >10 mmHg within triplicate of SBP/DBP/PP readings was observed in 12.9, 13 and 29.4%, respectively. In the era of personalized medicine, these patterns are well worth further investigation concerning their pathophysiologic and clinical relevance.

Late-night overeating (LNO) is associated with several cardiovascular disease (CVD) risk factors. Limited data exist regarding the association between late-night (LN) systematic food consumption, LNO, and LN poor food quality with subclinical vascular damage (SVD) which precedes the onset of CVD. This study aimed to investigate the above associations with SVD in a large sample of adults, free of established CVD, with one or more CVD risk factors. In total, 901 adults (45.2% males) underwent anthropometric, dietary (through two 24 h dietary recalls) and vascular assessment. LN systematic eating was defined as consumption of food after 19:00 h in both dietary recalls and LNO was defined as systematic consumption of >40% of daily total energy intake (dTEI) after 19:00 h. Systematic LN food consumption was inversely associated with diastolic blood pressure (DBP) (−1.44 95% C.I. (−2.76, −0.12)) after adjusting for age, sex, hypertension, diabetes, dyslipidemia, smoking, BMI and dTEI. LNO was positively associated with existence of carotid plaques (1.70 95% C.I. (1.07, 2.68)), while LN increased consumption of red meat, refined grains and wine and low consumption of whole wheat grains was positively associated with Aix (Augmentation Index) (0.84 95% C.I. (0.09, 1.59)), after adjusting for all the mentioned confounders. Systematic LN eating is associated with lower DBP while systematic LNO and consumption of poor-quality food late at night, is associated with SVD. Further research is needed to define more accurately the impact of LN eating habits on vascular health.

Objective:Accurate and easy to use methods for dietary Na intake estimation in population level are lacking. We aimed at (i) estimating the mean Na intake in the group level using a variety of dietary methods (DM) and urinary methods (UM) and correlating them with 24-h urine collection (24UCol) and (ii) improving the accuracy of the existing DM.Design:The most common DM (three 24-h dietary recalls (24DR) and FFQ) and UM (24UCol and spot urine collection using common equations) were applied. To improve the existing: (i) 24DR, discretionary Na was quantified using salt-related questions or adding extra 15 % in total Na intake and (ii) FFQ, food items rich in Na and salt-related questions were added in the standard questionnaire (NaFFQ).Setting:National and Kapodistrian University of Athens, Greece.Participants:Totally, 122 high cardiovascular risk subjects (56·0 ± 12·6 years; 55·7 % males).Results:Mean 24 h Na excretion (24UNa) was 2810 ± 1304 mg/d. Spot urine methods overestimated the 24UNa (bias range: −1781 to −492 mg) and were moderately correlated to 24UCol (r = 0·469–0·596, P ≤ 0·01). DM underestimated the 24UNa (bias range: 877 to 1212 mg) and were weakly correlated with 24UCol. The improved DM underestimated the 24UNa (bias range: 877 to 923 mg). The NaFFQ presented the smallest bias (−290 ± 1336 mg) and the strongest correlation with 24UCol (r = 0·497, P ≤ 0·01), but wide limits of agreement in Bland–Altman plots (−2909 mg; 2329 mg), like all the other methods did.Conclusions:The existing methods exhibit poor accuracy. Further improvement of the newly developed NaFFQ could be promising for more accurate estimation of mean dietary Na intake in epidemiological studies. Additional validation studies are needed.

Objective:Unhealthy diet is a modifiable risk factor leading to subclinical arterial damage (SAD), high BP and CVD. It was aimed to investigate the possible associations of dietary patterns (DPs) with SAD in adults having multiple CVD risk factors.Design:Dietary intake was evaluated through two 24-h dietary recalls and principal component analysis was used to identify DPs. Oscillometry, applanation tonometry with pulse wave analysis and carotid ultrasound were used to assess peripheral and aortic BP, arterial stiffness and pressure wave reflections.Setting:Laiko University Hospital, Athens, Greece.Participants:A total of 470 individuals (53·1 ± 14·2 years) with CVD risk factors were enrolled.Results:A pattern characterised by increased consumption of whole-grain cereals, white meat and reduced consumption of sugar was positively associated with common carotid compliance (β = 0·01, 95 % CI 0·00, 0·01), whereas a pattern high in refined cereals, red and processed meat was positively associated with brachial but not aortic systolic pressure (β = 1·76, 95 % CI 0·11, 3·42) and mean arterial pressure (MAP) (β = 1·18, 95 % CI 0·02, −2·38). Low consumption of low-fat dairy products, high consumption of full-fat cheese and butter was positively associated with MAP (β = 0·97, 95 % CI 0·01, 1·95). Increased consumption of vegetables, fruits, fresh juices, fish and seafood was inversely associated with augmentation index (AIx) (β = -1·01, 95 % CI -1·93, −0·09).Conclusion:Consumption of whole grains, white meat, fruits/vegetables, fish/seafood and avoidance of sugar was associated with improved SAD. Preference in refined grains, red/processed meat, high-fat cheese/butter and low intake of low-fat dairy products were associated with BP elevation. Future studies are needed to confirm the present findings.

Aortic stiffness assessed by carotid-femoral pulse wave velocity (PWV) is an important predictor to gauge the overall risk of hypertensive patients; nonetheless, it is underutilized in everyday practice. We propose a simple scoring system based on clinical variables that can identify patients with a priority for measurement of PWV, that is, those with elevated PWV (≥10 m/s) and, consequently, at higher risk for events.Patient data from three outpatient clinics (n = 3943) were used to form a derivation, internal and external validation cohort. For derivation, independent predictors of high PWV from a binary logistic regression model were split in subcategories and implemented in a simple clinical prediction scoring system with the acronym SAGE (office systolic blood pressure, age, glycemia and eGFR categories).Its performance was validated at the internal and external validation cohorts with c-statistics being 0.83 (95% CI 0.81-0.86) and 0.77 (95% CI 0.73-0.80), respectively. A cut-off of eight points to identify patients with high PWV in the internal/external validation cohorts yielded a positive-predictive value, negative-predictive value, sensitivity and specificity of 52/36%, 88/81%, 56/70% and 88/65%, respectively.The SAGE score that takes into account easily measured clinical variables (office SBP, age, fasting glucose and eGFR categories) can be used to accurately predict elevated levels of PWV and prioritize its measurement in specific hypertensive patients. Its use will result in greater acknowledgement of the role of aortic stiffness and aid physicians in implementing it in clinical practice.

The last decade, a growing number of evidence support J-shape or inverse - instead of positive linear -- associations between dietary sodium intake and cardiovascular morbidity/mortality. A careful evaluation of these studies leads to the following observations: less accurate methods for dietary sodium assessment are usually used; most studies included high-risk participants, enhancing the possibility of a 'reverse causality' phenomenon. However, these limitations do not explain all the findings. Few carefully designed randomized clinical trials comparing different levels of sodium intake that address the issue of the optimal and safe range exist; therefore, current guidelines recommend a higher cut-off instead of a safe range of intake. Given the demonstrated harmful effects of very low sodium diets leading to subclinical vascular damage in animal studies, the 'J-shape hypothesis' cannot yet be either neglected or verified. There is a great need of well-designed general population-based prospective randomized clinical trials to address the issue.

Background and aims The association between dietary sugars and vascular damage has been scarcely examined out of the context of established cardiovascular disease. We aimed to investigate the association between different types of sugars with subclinical atheromatosis and arteriosclerosis, in individuals free of cardiovascular disease being, however, at moderate-to-high cardiovascular risk. Methods and results Two 24-h dietary recalls were conducted to estimate sugars intake. Subclinical atheromatosis was assessed by B-mode ultrasonography and arteriosclerosis (arterial stiffness) via tonometry (carotid-to-femoral pulse wave velocity). Multiple logistic regression analysis was performed to determine the relationship of quartiles of total sugars, monosaccharides and disaccharides with atheromatosis and arteriosclerosis, adjusting for potential confounders [Odds Ratio (95%Confidence Interval)]. In 901 participants (52.4 ± 13.8 years, 45.2% males), total sugars intake was not associated with any type of subclinical vascular damage. Subjects at 4th quartile of lactose intake (15.3 ± 5.5 g/day) had lower probability to present atheromatosis compared to those at 1st quartile (0.00 ± 0.01 g/day) even in the fully adjusted model [0.586 (0.353–0.974)]. Subjects at 3rd quartile of total disaccharides intake and particularly sucrose (15.1 ± 2.2 g/day) had higher probability to present arteriosclerosis compared to those at 1st quartile (3.0 ± 1.9 g/day) even after adjustment for all potential confounders [2.213 (1.110–4.409)]. Conclusions Overall, the present data suggest a distinct role of each type of sugars on vascular damage. These observations highlight the need for further studies investigating not only foods rich in sugars, but sugars as separate components of food as they probably contribute via different ways on the development of arterial pathologies.

Masked hypertension (MH) and masked uncontrolled hypertension (MUH) remain largely underdiagnosed with no efficient detection algorithm. We recently proposed a novel classification of office systolic hypertension phenotypes defined on the basis of both brachial and aortic systolic blood pressure (bSBP/aSBP) and showed that type III ("isolated high office aSBP" phenotype: normal office bSBP but high office aSBP) has higher hypertension-mediated organ damage (HMOD). We tested whether MH/MUH (1) can be detected with the "isolated high office aSBP" phenotype and (2) if it is associated with elevated office aSBP with respect to normotension. We classified two separate and quite different cohorts (n = 391 and 956, respectively) on the basis of both bSBP and aSBP into four different phenotypes. Participants were classified as sustained hypertensives, masked hypertensives/masked uncontrolled hypertensives (MHs/MUHs), white coat hypertensives, and normotensives according to their office and out-of-office BP readings. The majority (more than 60% in cohort A and more than 50% in cohort B) of type III individuals were MHs/MUHs. Almost 35% of MHs/MUHs had optimal office bSBP rather than high normal bSBP. In both cohorts, the detection of more than 40% of MH/MUH was feasible with the type III phenotype. MHs/MUHs had higher office aSBP than individuals with sustained normotension (p < 0.05). In conclusion, in the absence of an efficient screening test, the diagnosis of MH/MUH can be assisted by the detection of the "isolated high office aSBP" phenotype, which can be measured in a single office visit. MHs/MUHs have increased aSBP relative to normotensives, further explaining the increased mortality of MH/MUH.

Background and aims Increased alcohol consumption has been associated with CVD risk. Subclinical arterial damage (SAD) precedes the onset of cardiovascular disease (CVD), and allows early identification and study of the pathophysiology of CVD. Reliable, noninvasive vascular biomarkers are available for the early detection of SAD and reclassification of CVD risk. To investigate the association of alcohol consumption with multiple SAD biomarkers and central hemodynamics in a large sample of Greek adults with CVD risk factors. Methods and results This cross-sectional study was conducted with 938 participants (43.5% men) and collected data on SAD biomarkers, central hemodynamics, and dietary intake. Multiple linear regression analysis was performed according to sex after adjusting for several confounders. In men, alcohol consumption of 20–30 g/d was positively associated with mean, diastolic, and peripheral systolic blood pressure (BP). The consumption of >30 g/d was positively associated with the augmentation index. In women, no statistically significant associations were found between alcohol consumption and BP or SAD indices. No statistically significant associations were found between alcohol consumption and arterial compliance or distensibility in both sexes. Conclusion In men even a small deviation from the current recommendation for alcohol consumption is associated with both higher BP indices and pressure wave reflections. The absence of association in women might be due to very low alcohol intake, even in the high consumption group. More studies are needed to verify our findings and establish the above associations in each sex.

The difference in pulse pressure (PP) between peripheral arteries and the aorta, called pulse pressure amplification (PPamp), is a well-described physiological phenomenon independently associated with cardiovascular events. Recent studies suggest that it exhibits circadian variability. Our aim was to detect the factors associated with the circadian variability of PPamp. In 497 consecutive subjects (aged 54 years, 56.7% male, 79.7% hypertensives), we assessed the circadian pattern of peripheral and central arterial hemodynamics by 24-hour evaluation of brachial and aortic blood pressure (BP), augmentation index (AI), and pulse wave velocity (PWV) using a validated oscillometric device (Mobil-O-Graph). All parameters exhibited a circadian variation. Sleep dipping (decrease) pattern was observed for PPamp, brachial and aortic systolic BP, mean BP, and PWV, whereas a rising pattern (higher sleep than wake values) was observed for brachial PP, aortic PP, and AI. The factors independently associated with the less sleep dipping in PPamp were older age, lower height, the use of antihypertensive medication, and sleep decrease in arterial stiffness (PWV), whereas female gender, the presence of hypertension, sleep increase of pressure wave reflections (AI), sleep decrease in heart rate, and mean BP were associated with a greater sleep-dipping in PPamp. These data provide further pathophysiological understanding of the mechanisms leading to PPamp dipping. Several implications regarding the clinical use of the aortic and brachial BP, especially during sleep time, are raised that should be addressed in future research.

Background People living with HIV (PLWH) are at high cardiovascular disease (CVD) risk. Traditional CVD risk scores do not accurately reflect their CVD risk. Noninvasive subclinical vascular damage (SVD) biomarkers are valid surrogates of CVD and able to stratify CVD risk. Setting We tested whether 4 widely applied CVD risk scores [Framingham (FRS), Atherosclerotic CVD, Data Collection on Adverse Effects of Anti-HIV Drugs Study (D:A:D), and Greek-specific European Society of Cardiology (ESC) risk scores] are associated with or detect the presence, incidence, and progression of arteriosclerosis, atheromatosis, and arterial hypertrophy in PLWH and uninfected individuals. Methods We prospectively examined (at baseline and 3-year follow-up) 10 different arterial sites applying 5 different noninvasive vascular biomarkers and measured all 4 CVD risk scores at baseline. Results In both PLWH (n = 138) and uninfected (n = 664) individuals, the CVD risk scores (except the ESC) performed differently but reasonably well in identifying the presence of SVD, but all scores failed to predict the incidence/progression of overall SVD. The most clinically useful biomarkers (carotid plaque/atheromatosis) revealed that in PLWH, only the FRS was able to stratify the progression (11% of the low-risk, 33.3% of the medium-risk, and 0% of the high-risk group). Conclusions This extensive vascular phenotyping study demonstrated the clear need to incorporate vascular imaging in CVD risk stratification, in addition to designing more accurate HIV-specific CVD risk models. The use of FRS would further enable treatment optimization and CVD prevention strategies in PLWH at medium CVD risk because one-third of carotid atheromatosis progresses within 3 years.

Pulse wave velocity (PWV), a measure of arterial stiffness, and intima‐media thickening (IMT), a measure of early atherosclerosis, are intermediate markers of cardiovascular disease which are predictive of cardiovascular events. Traditionally, both were thought to result from accumulative exposure to traditional cardiovascular risk factors. However, their association with risk factors in young adults in low‐income settings is unknown. We sought to investigate the association between PWV and IMT with traditional cardiovascular risk factors in the Andhra Pradesh Children and Parents Study cohort from Southern India. Male and female adults (N = 1440) aged between 20 and 24 years underwent measures of PWV and IMT. Exposure variables included smoking, body mass index (BMI), mean arterial pressure (MAP), glucose, homeostatic model assessment of insulin resistance (HOMA‐IR), total cholesterol, high‐density lipoprotein cholesterol (HDL‐cholesterol), and triglycerides. Association between outcome and exposure variables was assessed using linear regression analysis. Average values for PWV and IMT were 5.9 ± 0.6 m/s and 0.5 ± 0.1 mm. In univariable analysis, PWV associated with MAP, BMI, smoking, total cholesterol, glucose, and HOMA‐IR and IMT associated with MAP, BMI, tobacco use, and HDL‐cholesterol. In multivariable analysis, PWV remained strongly positively associated with MAP increasing by 0.5 m/s (P

Adipose tissue production of adipokines and cytokines, neurohumoral pathways and metabolic functions contribute to mechanisms that cause hypertension. Obesity-related hypertension may be the result of a combination or overlap of a number of these factors. The diabetic patient should have orthostatic blood pressure measured, as the coexistence of diabetic neuropathy may exaggerate orthostatic hypotension. Diagnosis of hypertension should be done with the correct cuff size because of the increased circumference of the obese subject's arm. Obesity increases blood volume and cardiac output, leading to excess venous return to heart. Obesity-induced hypertension may also in part explain the development of left ventricle hypertrophy. Diabetes mellitus and hypertension are independent factors for chronic kidney disease. Lifestyle interventions constitute behavioural modifications and hypocaloric diets. Behavioural therapy is based on self-monitoring of food intake, increased physical activity, stimulus control, problem solving and relapse prevention.

Background Surrogates of aortic wave reflection and arterial stiffness, such as augmentation index (AIx), augmentation pressure, pulse wave velocity (PWV) and pulse pressure amplification (PPampl) are independent predictors of cardiovascular risk. A novel ambulatory, brachial cuff-based oscillometric device has been recently developed and validated, yielding 24-h assessment of the aforementioned parameters (Mobilo-O-Graph). Aim of this study was to investigate the feasibility and reproducibility of wave reflection and arterial stiffness estimation by pulse wave analysis using this device. Methods Thirty treated or untreated hypertensives (mean age: 53.6±11.6years, 17 men) had test–retest 24-h monitoring one week apart using the test device. Results Mean numbers of valid aortic readings per subject, between test and retest, were comparable. Approximately 12 aortic readings per subject (17%) were not feasible or valid. No differences were observed for any 24-h parameter between the two assessments. Bland–Altman plots showed no systemic difference, while the limits of agreement for each parameter indicated high reproducibility (AIx: −7.2 to 8.2%, AP: −3.7 to 4.1mm Hg, PWV: −0.39 to 0.41m/s, PPampl: −0.08 to 0.06). This was further verified by intraclass correlation coefficients which were >0.8 for each parameter. Conclusions Non-invasive 24-h estimation of wave reflection and arterial stiffness indices, derived by the test device, appear to be highly reproducible. Future studies should investigate whether these measurements have additive prognostic value for cardiovascular risk stratification, beyond common brachial blood pressure measurements or single estimations of wave reflection and PWV at office settings.

Both brachial blood pressure (BP) level and its variability (BPV) significantly associate with left ventricular (LV) structure and function. Recent studies indicate that aortic BP is superior to brachial BP in the association with LV abnormalities. However, it remains unknown whether aortic BPV better associate with LV structural and functional abnormalities. We therefore aimed to investigate and compare aortic versus brachial BPV, in terms of the identification of LV abnormalities. Two hundred and three participants who underwent echocardiography were included in this study. Twenty-four-hour aortic and brachial ambulatory BP was measured simultaneously by a validated BP monitor (Mobil-O-Graph, Stolberg, Germany) and BPV was calculated with validated formulae. LV mass and LV diastolic dysfunction (LVDD) were evaluated by echocardiography. The prevalence of LV hypertrophy (LVH) and LVDD increased significantly with BPV indices (P⩽0.04) in trend tests. After adjustment to potential confounders, only aortic average real variability (ARV), but not brachial ARV or weighted s.d. (wSD, neither aortic nor brachial) significantly associated with LV mass index (P=0.02). Similar results were observed in logistic regression. After adjustment, only aortic ARV significantly associated with LVH (odds ratio (OR) and 95% confidence interval (CI): 2.28 (1.08, 4.82)). As for LVDD, neither the brachial nor the aortic 24-hour wSD, but the aortic and brachial ARV, associated with LVDD significantly, with OR=2.28 (95% CI: (1.03, 5.02)) and OR=2.36 (95% CI: (1.10, 5.05)), respectively. In summary, aortic BPV, especially aortic ARV, seems to be superior to brachial BPV in the association of LV structural and functional abnormalities.

Aortic blood pressure (BP) and 24-h ambulatory BP are both better associated with target organ damage than office brachial BP. However, it remains unclear whether a combination of these two techniques would be the optimal methodology to evaluate patients' BP in terms of left ventricular diastolic dysfunction (LVDD) prevention. In 230 participants, office brachial and aortic BPs were measured by a validated BP monitor and a tonometry-based device, respectively. 24-h ambulatory brachial and aortic BPs were measured by a validated ambulatory BP monitor (Mobil-O-Graph, Germany). Systematic assessment of patients' LVDD was performed. After adjustment for age, gender, hypertension and antihypertensive treatment, septum and lateral E/Ea were significantly associated with office aortic systolic BP (SBP) and pulse pressure (PP) and 24-h brachial and aortic SBP and PP (P ⩽ 0.04), but not with office brachial BP (P ⩾ 0.09). Similarly, 1 standard deviation in SBP was significantly associated with 97.8 ± 20.9, 86.4 ± 22.9, 74.1 ± 23.3 and 51.3 ± 22.6 in septum E/Ea and 68.6 ± 2 0.1, 54.2 ± 21.9, 37.9 ± 22.4 and 23.1 ± 21.4 in lateral E/Ea, for office and 24-h aortic and brachial SBP, respectively. In qualitative analysis, except for office brachial BP, office aortic and 24-h brachial and aortic BPs were all significantly associated with LVDD (P ⩽ 0.03), with the highest odds ratio in 24-h aortic SBP. Furthermore, aortic BP, no matter in the office or 24-h ambulatory setting, showed the largest area under receiver operating characteristic curves (P ⩽ 0.02). In conclusion, 24-h aortic BP is superior to other BPs in the association with LVDD.

Background: Arterial stiffness measured under static conditions reclassifies significantly cardiovascular (CV) risk and associates with organ damage, including narrower retinal arterioles. However, arterial stiffness exhibits diurnal variation, thus single static stiffness recordings do not correspond to the “usual” 24 hr, awake and asleep average arterial stiffness. We aimed to test the hypothesis that ambulatory 24 hr, awake and asleep aortic (a) pulse wave velocity (PWV) associate with retinal vessel calibers, independently of confounders and of static arterial stiffness, in hypertensive individuals free from diabetes and CV disease. Methods: Digital retinal images were obtained (181 individuals, age: 53.9 ± 10.7 years, 55.2% men) and retinal vessel calibers were measured with validated software to determine central retinal arteriolar and venular equivalents (CRAE and CRVE, respectively); ambulatory (24 hr, awake, asleep) and static office aPWV were estimated by Mobilo-O-Graph; and static office carotid-femoral (cf) PWV by SphygmoCor. Results: Regression analysis performed in 320 gradable retinal images showed that, after adjustment for confounders: (i) ambulatory aPWV was significantly associated with narrower retinal arterioles but not with venules; (ii) asleep aPWV had stronger associations with CRAE than awake aPWV; (iii) both ambulatory aPWV and cfPWV were associated mutually independently with narrower retinal arterioles; aPWV introduction in the model of cfPWV, improved model’s R2 (p = 0.012). Similar discriminatory ability of 24 hr aPWV and of cfPWV to detect the presence of retinal arteriolar narrowing was found. Conclusion: Ambulatory aPWV, estimated by an operator-independent method, provides additional information to cfPWV regarding the associations of arterial stiffness with the retinal microcirculation.