In adults with treated hypertension, elevated Lp(a) concentrations and PAD were independently associated with greater central arterial stiffness, with no evidence of effect modification by PAD.
Mean carotid-femoral pulse-wave velocity increased across ascending Lp(a) tertiles in patients with treated hypertension.
After multivariable adjustment, Lp(a) in the middle tertile was associated with significantly higher cfPWV compared to the lowest tertile.
After multivariable adjustment, Lp(a) in the highest tertile was associated with even greater cfPWV compared to the lowest tertile.
Peripheral artery disease (PAD) was independently associated with higher central arterial stiffness after multivariable adjustment.
No statistically significant interaction between Lp(a) tertiles and PAD on cfPWV was observed, indicating independent rather than synergistic effects.
Robust linear regression was used to examine associations of Lp(a) tertiles and PAD with cfPWV, with adjustment for multiple covariates.
This research suggests that two cardiovascular risk factors — high levels of a blood protein called lipoprotein(a), or Lp(a), and peripheral artery disease (PAD, a condition involving narrowed arteries in the limbs) — are each independently linked to stiffer central arteries in people being treated for high blood pressure. The study measured arterial stiffness using a technique called carotid-femoral pulse-wave velocity (cfPWV), which tracks how fast a pulse travels through the main artery from the neck to the groin; higher values indicate stiffer arteries, which are associated with greater cardiovascular risk. Among 366 patients with treated hypertension, those with higher Lp(a) levels had progressively stiffer arteries, and those with PAD also had notably stiffer arteries, even after accounting for other factors that influence arterial stiffness. Importantly, the effects of Lp(a) and PAD on arterial stiffness appeared to be independent of each other — there was no evidence that having both conditions made things significantly worse than the sum of their individual effects. The increase in arterial stiffness associated with the highest Lp(a) group was about 1.29 m/s compared to those with the lowest Lp(a) levels, while PAD was associated with an increase of about 1.20 m/s — both clinically meaningful differences given that cfPWV values typically range from roughly 6 to 14 m/s in clinical populations. This research matters because it highlights Lp(a) — a largely genetically determined lipid particle that is not lowered by standard cholesterol-lowering drugs — as a potentially important contributor to arterial stiffening in hypertensive patients, separate from and in addition to the well-known effects of PAD. This suggests that measuring Lp(a) and screening for PAD may help identify hypertensive patients at higher cardiovascular risk, and that these two factors may each warrant independent clinical attention in this population.
Mwipatayi B, Dodd J, Carnagarin R, Mori T, Golledge J, Burrows S, et al.. (2026). Lipoprotein(a) and Peripheral Artery Disease as Independent Predictors of Arterial Stiffness in Patients With Hypertension: A Single-Center Cross-Sectional Study.. Journal of clinical hypertension (Greenwich, Conn.). https://doi.org/10.1111/jch.70309