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Background and aims: Arterial stiffness (AS), quantified by pulse wave velocity (PWV), arises due to impaired arterial elastic tissue and smooth muscle dysfunction. We aimed to examine the longitudinal association of genetic, lipid and inflammation biomarkers with PWV and how these associations may change with aging. Materials and methods: We utilized genotype and four time-point biomarker data from the SardiNIA cohort [n = 6,301; mean baseline age 43.3 (SD 17.3); 58% females]. To investigate the association of PWV with genetic variants, lipid, and inflammation biomarkers, we employed linear mixed modeling, using age as the time scale. Biomarkers exhibiting significant longitudinal associations were categorized into tertiles and individuals within the second tertile or those with heterozygous alleles were excluded, leaving a cohort of 2,000 individuals. This cohort was further divided into four risk groups: low genetic and low biomarker (L-L), low genetic and high biomarker (L-H), high genetic and low biomarker (H-L), and high genetic and high biomarker risk (H-H). Subsequent analyses focused on these risk groups to assess their association to PWV with time. Results: Using the complete dataset, we found a significant longitudinal association of total cholesterol (TC), triglycerides (TG), fibrinogen (FGN), and total white blood cell count (TWBC) with PWV, all with p < 3.33 × 10-3. After grouping, individuals with homogeneous risk alleles of SNP rs3742207 and high baseline TG levels (H-H group) exhibited a 1.39-fold higher PWV (m/s) (95% CI, 1.17-1.64, p=1.21 × 10-4) compared to the L-L group. Similarly, individuals in the H-H group of rs3742207-TWBC combination showed 1.75 times higher PWV (95% CI, 1.48-0.2.07, p=1.01 × 10-10) compared to the L-L group. Similar patterns were observed for groups based on SNP rs7152623-TWBC risk. Furthermore, these associations became more pronounced with increasing age (p < 3.33 × 10-3). Conclusion: The longitudinal association of TG and TWBC biomarkers with PWV varied by SNPs rs3742207 and rs7152623 genotype. Further studies are warranted to investigate the function of genetics, lipids, and inflammation biomarkers on PWV change. [ABSTRACT FROM AUTHOR]

Carotid-femoral pulse wave velocity (PWV), an index of arterial stiffness and a proxy of arterial aging, has been reported to be an independent determinant of cardiovascular health. Whether the effects of antihypertensive treatment vary in the presence of accelerated arterial aging (stiffer artery, ie, PWV >10 m/s) has not been established. We tested this hypothesis in a longitudinal study in a large community-dwelling population. Longitudinal population study with repeated measures. Study population consisted of a cohort of 6011 volunteers (2546 men and 3465 women, age range 14-101 years; 15,011 observations over a median follow-up of 6.8 years) participating in the SardiNIA Study. Repeated measures of PWV, blood pressure (BP), and metabolic risk factors and the antihypertensive medication trajectories of BP and PWV over time were assessed via mixed effects models. Antihypertensive treatment significantly affected the trajectory of BP in both participants with (−0.47 ± 0.20 mmHg/y, P =.02) and participants without stiffer arteries (−0.47 ± 0.07 mmHg/y, P =.001). They also affected the trajectory of PWV in participants with stiffer artery, independent of the BP values. Antihypertensive treatment is effective in reducing both BP and PWV in older individuals with stiffer arteries. [ABSTRACT FROM AUTHOR]

Background There is no definite consensus on the CV burden associated to Masked hypertension (MH) or White Coat Hypertension (WCH) — conditions that can be detected by out-of-office blood pressure measurements (24 hour Ambulatory Blood Pressure Monitoring, 24 h ABPM). Methods We investigated the association of WCH and MH with arterial aging, indexed by a range of parameters of large artery structure and function in 2962 subjects, taking no antihypertensive medications, who are participating in a large community-based population of both men and women over a broad age range (14–102 years). Results The overall prevalence of WCH was 9.5% and was 5.0% for MH, with 54.9% of subjects classified as true normotensive and 30.6% as true hypertensive. Both WCH and MH were associated with a stiffer aorta, a less distensible and thicker common carotid artery, and greater central BP than true normotensive subjects. Notably, the profile of arterial alterations in WCH and MH did not significantly differ from what was observed in true hypertensive subjects. The arterial changes accompanying WCH and MH differed in men and women, with women showing a greater tendency towards concentric remodeling, greater parietal wall stress, and PWV than men. Conclusion Both WCH, and MH are associated with early arterial aging, and therefore, neither can be regarded as innocent conditions. Future studies are required to establish whether measurement of arterial aging parameters in subjects with WCH or MH will identify subjects at higher risk of CV events and cognitive impairment, who may require more clinical attention and pharmacological intervention. [ABSTRACT FROM AUTHOR]