Key result
Dual elevation of Lp(a) and homocysteine links to ~1.6 m/s higher cfPWV in treated hypertension.
Why the study?
The independent and combined associations of lipoprotein(a) and homocysteine with arterial stiffness in treated hypertension remained uncertain.
Do elevated Lipoprotein(a) and homocysteine levels increase central arterial stiffness in adults with treated hypertension?
Cross-Sectional (n=366)
No
Do elevated Lipoprotein(a) and homocysteine levels increase central arterial stiffness in adults with treated hypertension?
Mean Difference: 1.56 (95% CI 1–2.13)
p-value: p=<0.001
In adults with treated hypertension, higher Lp(a) and homocysteine levels are independently and additively associated with greater central arterial stiffness.
May support risk stratification in treated hypertension; leaves open whether lowering Lp(a) and homocysteine reduces stiffness.
Background/Objectives: Carotid–femoral pulse-wave velocity (cfPWV) is the reference-standard non-invasive measure of central arterial stiffness and a validated marker of cardiovascular risk in hypertension. While lipoprotein(a) [Lp(a)] and homocysteine have each been implicated in vascular injury, their independent and combined associations with arterial stiffness in treated hypertension remain uncertain. In this study, we examined the associations of Lp(a), homocysteine, and peripheral artery disease (PAD) with cfPWV and assessed whether concomitant elevation of Lp(a) and homocysteine was associated with excess arterial stiffness. Methods: We conducted a single-centre, cross-sectional study of 366 consecutive adults with treated hypertension attending a tertiary hypertension centre and associated vascular service between February 2016 and October 2019. cfPWV was measured non-invasively through applanation tonometry using the SphygmoCor XCEL system. Multivariable robust linear regression was used to assess associations with cfPWV after adjustment for age, sex, body mass index, mean 24 h systolic blood pressure (BP), diabetes mellitus, chronic kidney disease, smoking status, low-density lipoprotein cholesterol, and PAD. Joint associations and interactions on multiplicative and additive scales were also evaluated. Results: Of 366 participants, 99 (27.0%) had high arterial stiffness, defined as cfPWV ≥ 10 m/s. After full adjustment, cfPWV increased by 0.13 m/s per 0.1 g/L increase in Lp(a) (95% CI, 0.08 to 0.18; p < 0.001) and by 0.26 m/s per 5 μmol/L increase in homocysteine (95% CI, 0.02 to 0.49; p = 0.03). Participants with concomitantly elevated Lp(a) and homocysteine had the highest adjusted cfPWV, with a mean difference of 1.56 m/s versus the low-Lp(a)/low-homocysteine group (95% CI, 1.00 to 2.13; p < 0.001). No meaningful multiplicative or additive interaction was observed. Conclusions: In adults with treated hypertension, higher Lp(a), higher homocysteine, and PAD were independently associated with greater central arterial stiffness. Concomitant elevation of Lp(a) and homocysteine identified participants with the highest cfPWV without evidence of synergistic interaction, supporting a complementary vascular-risk model.
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Mwipatayi et al. (2026) conducted a cross-sectional in Treated hypertension (n=366). Concomitant elevation of lipoprotein(a) and homocysteine vs. Low lipoprotein(a) and low homocysteine was evaluated on Carotid-femoral pulse-wave velocity (cfPWV) (MD 1.56 m/s, 95% CI 1.00 to 2.13, p=<0.001). Concomitant elevation of lipoprotein(a) and homocysteine in adults with treated hypertension was associated with significantly higher central arterial stiffness, with a mean difference in cfPWV of 1.56 m/s.
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