Key result
Higher pericoronary adipose tissue density linked to ~95% higher mortality per 10 HU in HIV.
Why the study?
The effects of statin therapy on pericoronary adipose tissue and its relationship with plaque progression and outcomes in people with HIV remain poorly understood.
Does pitavastatin mitigate the increase in pericoronary adipose tissue density and adverse plaque progression in people with HIV?
RCT (n=753)
Randomized
Does pitavastatin mitigate the increase in pericoronary adipose tissue density and adverse plaque progression in people with HIV?
In people with HIV, pericoronary adipose tissue density increases over time as a marker of perivascular inflammation and mortality risk, but pitavastatin mitigates this progression in those with high baseline coronary artery disease burden.
Answers are grounded in this paper and cite their sources.
PCAT density tracking may refine CV risk monitoring in PWH; leaves open whether statin modulation alters plaque progression or events.
BACKGROUND: The effects of statin therapy on pericoronary adipose tissue (PCAT) and its relationship with plaque progression and outcomes in people with HIV (PWH) remain poorly understood. OBJECTIVES: The aim of this study was to evaluate PCAT density changes over time; statin effects on PCAT; and associations among PCAT changes, coronary plaque, and clinical outcomes. METHODS: In the REPRIEVE (Randomized Trial to Prevent Vascular Events in HIV) mechanistic computed tomographic (CT) substudy (n = 753, mean age: 51 ± 6 years, 17% women), PCAT density was measured from noncontrast CT images at baseline and 2 years, while coronary plaque volumes (total, calcified, and noncalcified) were assessed from contrast-enhanced CT angiograms. Analyses were stratified by coronary artery disease burden (segment involvement score 0, 1-3, or ≥4) and adjusted for technical parameters, atherosclerotic cardiovascular disease risk, body mass index, inflammatory biomarkers, and statin allocation. Associations among PCAT, plaque changes, and events (all-cause mortality, major adverse cardiovascular events [MACE], and MACE or death) were evaluated. RESULTS: ; P = 0.031). Over a median of 6.3 years, 4.2% of patients died. Baseline PCAT density was independently associated with all-cause mortality (HR per +10 HU: 1.95; 95% CI: 1.03-3.69; P = 0.040), but not MACE. CONCLUSIONS: PCAT density increases over time in PWH, but pitavastatin mitigates this in those with high coronary artery disease burden. PCAT density is associated with vulnerable plaque morphology and all-cause mortality, supporting its potential as a prognostic imaging biomarker in PWH. (Randomized Trial to Prevent Vascular Events in HIV [REPRIEVE]; NCT02344290).
No takes yet. Share an insight, caveat, or question.
Foldyna et al. (2025) conducted an RCT in HIV (n=753). Pitavastatin vs. Control was evaluated on All-cause mortality (risk per +10 HU increase in baseline PCAT density) (HR 1.95, 95% CI 1.03-3.69, p=0.040). Baseline pericoronary adipose tissue density was independently associated with all-cause mortality in people with HIV.
Synapse has enriched 10 related papers. Consider them for comparative context: