Abstract 9676: Inflammation Mediated Vitamin K Protective Effect Against Vascular Calcifications in Antiretroviral Treated People Living with HIV

Abstract

Background: People living with HIV (PLWH) experience increased inflammation, risk of cardiovascular (CV) events, and coronary artery calcium scores (CACs). In cross-sectional analyses, vitamins D and K have been associated with CACs and may have an anti-inflammatory effect. The anti-inflammatory effects of Vitamins D and K in successfully treated PLWH is less understood. Methods: We prospectively recruited 237 PLWH on antiretroviral treatment and 67 HIV- healthy controls. CACs were derived from non-contrast CT and levels of 25-hydroxyvitamin D (vitamin D) and inactive vitamin K dependent dephosphorylated-uncarboxylated matrix G1a protein (MGP, marker of vitamin K deficiency) were measured in plasma. The relationship between inflammation markers, MGP, and vitamin D on CACs were estimated using zero-inflated negative binomial regression. Adjusted models included 25(OH)D, MGP, gender, race, age, and markers of inflammation. Results: Controls had lower median age (45.8 vs. 48.8; p=0.03) and a larger proportion of females (55.2% vs. 23.6%; p<.0001). Among PLWH, <1% had detectable viral load and the median CD4 was 682.0(IQR: 473.0, 899.0). 62.17% of the sample had zero CACs and 51.32% were vitamin D deficient (<20 ng/mL). There was no difference in detectable CACs (p=0.19) or MGP (p=0.42) between PLWH and controls. In adjusted models, every one-unit increase in ( log2 )25(OH)D is associated with >200% increase in the expected CACs among PLWH. Every one-unit increase in MGP (worse K status) decreases the probability of having CACs equal to zero 21.3% (p=0.01). Evidence suggests that the effects of 25(OH)D and MGP are inflammation mediated, specifically through VCAM and TNF-α pathways. Conclusion: Vitamins K deficiency is a modifiable preventive factor against coronary calcification in PLWH. Further research should determine whether vitamin K supplementation would reduce vascular calcification and risk of CV events in PLWH and increased inflammation