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Mechanisms

Lp(a) is elevated in people with HIV and inversely tracks with coronary endothelial function, a possible driver of HIV-associated cardiovascular risk (J Am Heart Assoc 2024)

Original title: Lipoprotein(a) Is Elevated and Inversely Related to Coronary Endothelial Function in People With HIV

J Am Heart Assoc · · 6

Kikuchi DS, Kwapong YA, Schär M, Weiss RG, Sun K, Brown TT, Piggott DA, Minhas AS, Gerstenblith G, Soleimani-Fard A, Leucker TM, Hays AG

In this cross-sectional study, 65 people with HIV (PWH) and 52 HIV-negative controls underwent cardiac magnetic resonance imaging with isometric handgrip exercise to assess coronary endothelial function (CEF), quantified as percent change in coronary cross-sectional area and coronary blood flow from rest to stress. Lp(a) was significantly higher in PWH than controls (median 78 vs. 45.5 nmol/L, P < 0.01), while both percent change in coronary cross-sectional area (0.38% vs. 7.43%, P < 0.0005) and coronary blood flow (9.1% vs. 24.1%, P < 0.05) were lower, indicating impaired CEF. In PWH, Lp(a) was inversely associated with percent change in coronary cross-sectional area (beta -6.18 plus/minus 1.01%/nmol/L, P < 0.001) even after adjusting for confounders, though not with coronary blood flow change; no such association was found in HIV-negative controls. The findings implicate elevated Lp(a) as a candidate mechanistic contributor to the endothelial dysfunction underlying HIV-associated cardiovascular risk.

Read the paper (DOI)PubMed

Original abstract

Background: HIV-associated cardiovascular disease (CVD) is increasing in prevalence. The mechanisms underlying the heightened cardiovascular risk faced by people with HIV (PWH), however, remain poorly defined. Recent studies indicate an important role of lipoprotein(a) (Lp[a]) in predicting CVD risk in the general population, but little is known regarding its role in HIV-associated CVD. Thus, we sought to evaluate whether Lp(a) is elevated in PWH and if it is associated with impaired coronary endothelial function (CEF), a known mediator of CVD in PWH.

Methods And Results: In this cross-sectional study, cardiac magnetic resonance imaging with isometric handgrip exercise, an endothelial dependent stressor, was performed to assess CEF in 65 PWH and 52 controls without HIV. Percent changes in coronary cross-sectional area and coronary blood flow from rest to stress were used to quantify CEF. Lp(a) levels were assessed by immunoturbidimetric assay at the time of magnetic resonance imaging. Lp(a) levels were higher in PWH compared with controls (78 nmol/L [39-137 nmol/L] versus 45.5 nmol/L [18-102.5 nmol/L], P<0.01). Both percent change in coronary cross-sectional area (0.38% [-6.1% to 5.4%] versus 7.43% [2.4%-11.2%], P<0.0005) and coronary blood flow (9.1% [-1.3% to 23.1%] versus 24.1% [3.3%-39.8%], P<0.05) were lower in PWH compared with controls. In PWH, Lp(a) was inversely associated with percent change in coronary cross-sectional area (β=-6.18±1.01%/nmol/L, P<0.001) but not with percent change in coronary blood flow even after adjustment for confounding risk factors. No association between Lp(a) and measures of CEF was observed in individuals without HIV.

Conclusions: Lp(a) concentrations are elevated in PWH and inversely related to CEF in PWH.

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Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.