Abstract 20353: HIV and Rapid Change in Atherosclerotic Coronary Plaque Volume

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Abstract

Introduction: Patients living with HIV (PLHIV) have increased atherosclerotic coronary vascular disease (ASCVD) compared to non-HIV infected controls; a process thought to be mediated through unique inflammatory mechanisms. We hypothesized that there would novel putative inflammatory and cardiovascular proteins whose change in level would be associated with change in ASCVD plaque volume over 1-year.

Methods: 37 PLHIV underwent CT coronary angiography (CTA) to characterize volume and type of ASCVD plaque, where randomized to 40 mg of atorvastatin (n=17) vs placebo (n=20), underwent a repeat CTA 1-year later, and had frozen plasma available to be tested for 184 proteins at baseline and 1-year using the Olink CVDIII and Cardiometabolic panels (based on duel antibody epitope recognition with linked aptamer amplification for low-concentration analytical accuracy and minimal cross-reactivity to allow for repeated measures). We studied the association with change in non-calcified plaque (HU<130) typically implicated in acute coronary syndromes.

Results: Non-calcified plaque volume changed +20.4% (95% confidence interval [CI, -7.1-94.4]) with placebo and -19.4% (95%CI, -39.2 to 9.3) with atorvastatin from baseline to 1-year. R values for the change in protein levels vs. the % change in non-calcified plaque volume are shown in Figure. R values > 0.32 are associated with a P< 0.05. The 4 highest associated proteins included RARRES2, CCL16, PON3 and TFPI. In contrast to these associations with change in non-calcified plaque, change in these protein levels were weakly associated in 3 of 4 with change in LDL cholesterol (R = 0.07, 0.18, 0.06, 0.31, respectively).

Conclusions: Proteomic discovery offers insight to understand ASCVD progression and response to treatment in PLHIV. Novel biomarker discovery may enhance precision medicine strategies to estimate the efficacy of targeted therapies to reduce ASCVD progression and events.

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