Carmen Ramos Alejos-Pita, Diego José Rodríguez Torres, Tatiana Mata Forte, Beatriz Tendero de la Asunción, Joaquín Enrique Gómez Sanz, Juan José Reyes Luján, Matteo Romano, Edurne López Soberón, Francisco Javier Membrillo de Novales, Miriam Estébanez Muñoz
In this cohort of virologically suppressed PLHIV, a non-significant inverse trend (p = 0.08) was observed between ART duration and Lp(a) levels. In the subgroup of moderate-to-high cardiovascular risk, the prevalence of coronary plaque vulnerability features was higher among those with elevated Lp(a), although the small number of imaging studies means this observation should be considered hypothesis-generating rather than indicative of an established biological association.
OBJECTIVES: Human immunodeficiency virus (HIV) infection has become a chronic condition due to antiretroviral therapy (ART), which has increased life expectancy but is also associated with a higher burden of cardiovascular disease (CVD) in people living with HIV (PLHIV). Lipoprotein(a) [Lp(a)] is an independent cardiovascular risk biomarker; however, its role in PLHIV remains unclear. This study evaluated the relationship between Lp(a) and cardiovascular risk and explored its association with subclinical coronary artery disease.
METHODS: Cross-sectional study included PLHIV aged ≥40 years on stable ART with sustained viral suppression. Individuals with prior cardiovascular events or type 1 diabetes or long-standing type 2 diabetes (≥10 years) were excluded. Lp(a) levels and clinical data were collected. Cardiovascular risk was estimated using validated clinical scores; participants with ≥10% risk underwent coronary computed tomography angiography (CTA) to assess coronary anatomy.
RESULTS: A total of 69 patients were included (81% male; mean age 54 years). The median Lp(a) level was 23.4 nmol/L (IQR: 8.2-81.6; mean: 66.7 nmol/L); 29% had ≥75 nmol/L and 23% ≥ 105 nmol/L. A non-significant inverse association was observed between Lp(a) levels and ART duration (r = -0.209; p = 0.08). Of 46 participants with a Framingham score ≥10%, 23 underwent coronary CTA. Among those with elevated Lp(a), a higher proportion had vulnerable plaques on CTA, although this was not statistically significant; because only 5 participants with elevated Lp(a) underwent CTA, this finding should be regarded as hypothesis-generating.
CONCLUSIONS: In this cohort of virologically suppressed PLHIV, a non-significant inverse trend (p = 0.08) was observed between ART duration and Lp(a) levels. In the subgroup of moderate-to-high cardiovascular risk, the prevalence of coronary plaque vulnerability features was higher among those with elevated Lp(a), although the small number of imaging studies means this observation should be considered hypothesis-generating rather than indicative of an established biological association.