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Lipoprotein(a) Is Elevated and Inversely Related to Coronary Endothelial Function in People With HIV
Daniel S Kikuchi1, Yaa A Kwapong2, Michael Schär3
1Internal Medicine, Department of Medicine Johns Hopkins University School of Medicine Baltimore MD USA.
Insights
Lipoprotein(a) (Lp[a]) levels are higher in people with HIV (PWH). Elevated Lp(a) is linked to impaired coronary endothelial function (CEF) in PWH, a key factor in HIV-associated cardiovascular disease.
Area of Science:
- Cardiology
- Infectious Diseases
- Biochemistry
Background:
- HIV-associated cardiovascular disease (CVD) is a growing concern.
- Mechanisms of heightened CVD risk in people with HIV (PWH) are not fully understood.
- Lipoprotein(a) (Lp[a]) is a known CVD risk predictor in the general population.
Purpose of the Study:
- To determine if Lp[a] levels are elevated in PWH.
- To investigate the association between Lp[a] and coronary endothelial function (CEF) in PWH.
Main Methods:
- Cross-sectional study comparing 65 PWH and 52 controls.
- Cardiac MRI with isometric handgrip exercise to assess CEF.
- Lp[a] levels measured by immunoturbidimetric assay.
Main Results:
- PWH had significantly higher Lp[a] levels compared to controls (78 nmol/L vs 45.5 nmol/L).
- CEF, measured by changes in coronary cross-sectional area and blood flow, was impaired in PWH.
- In PWH, elevated Lp[a] was inversely associated with impaired coronary cross-sectional area changes (P<0.001).
Conclusions:
- Lp[a] concentrations are elevated in people with HIV.
- Elevated Lp[a] is inversely related to coronary endothelial function in PWH.
- Lp[a] may play a role in HIV-associated cardiovascular disease pathogenesis.
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.
