UDC 616.13‑004.6‑02:577.112.85]-038:616.12‑008.331.1(048.8)

Introduction. Elevated lipoprotein(a) has emerged as an important determinant of cardiovascular risk because of its roles in atherosclerotic disease, vascular inflammation, endothelial dysfunction, arterial stiffening, and vascular calcification. Increasing evidence suggests that the clinical significance of Lp(a) extends beyond atherosclerosis, as higher concentrations have also been linked to vascular remodeling and adverse cardiovascular outcomes in patients with arterial hypertension.

Aim. To evaluate the current scientific evidence on the role of lipoprotein(a) in vascular remodeling and its effects on endothelial function, arterial stiffness, and cardiovascular risk among patients with arterial hypertension.

Materials and methods. The MEDLINE database via PubMed was searched for articles published between 2016 and 2026 using a predefined set of keywords. The search yielded 86 articles, which were initially screened and assessed based on their titles and abstracts. After evaluating relevance, we selected 56 articles for detailed assessment. Finally, 31 articles were included in the review.

Results. Elevated Lp(a) concentrations are linked to multiple mechanisms that drive vascular remodeling and cardiovascular injury. A substantial part of Lp(a)'s pathogenic activity is attributed to oxidized phospholipids, which contribute to endothelial dysfunction, vascular inflammation, extracellular matrix remodeling, fibrosis, and vascular calcification. Research indicates associations between elevated Lp(a) levels and increased pulse pressure, reduced nocturnal blood pressure decline, arterial stiffness, vascular calcification, and hypertensive target-organ damage. These findings suggest that elevated Lp(a) may influence the development of a less favorable vascular profile in arterial hypertension and contribute to cardiovascular risk beyond that explained by traditional lipid markers. The development of RNA-based therapeutic approaches, including antisense oligonucleotides and small interfering RNA agents, has enabled substantial reductions in circulating Lp(a) levels and may provide new opportunities for individualized cardiovascular risk management.

Conclusions. Elevated lipoprotein(a) levels should be regarded as an important genetically determined factor in vascular remodeling and cardiovascular risk in patients with arterial hypertension. Increased lipoprotein(a) concentrations contribute to endothelial dysfunction, vascular inflammation, arterial stiffness, vascular fibrosis, and calcification through multiple mechanisms, predominantly mediated by oxidized phospholipids.