Fujimoto · JACC. Cardiovascular imaging 2024 · Cross-sectional observational study · n=578

Relationship Between Calcified Plaque Burden, Vascular Inflammation, and Plaque Vulnerability in Patients With Coronary Atherosclerosis.

Cited 44 times in the scientific literature.

Level 3 - non-randomized controlled study

Cross-sectional observational comparative imaging study

PubMed 39243232 · doi:10.1016/j.jcmg.2024.07.013 · record verified 2026-08-29

What was done

In an observational study of 578 patients with coronary artery disease who underwent both computed tomography angiography (CTA) and optical coherence tomography (OCT), investigators evaluated culprit lesion characteristics. Patients were divided into four groups: one group without culprit lesion calcification and three groups stratified by calcified plaque burden (CPB) tertiles (calcified plaque volume divided by vessel volume). The groups were compared for vascular inflammation via pericoronary adipose tissue (PCAT) attenuation on CTA and OCT-derived features of plaque vulnerability (lipid-rich plaque, macrophage infiltration, and microvessels).

What was found

The highest CPB tertile exhibited significantly lower culprit vessel PCAT attenuation compared to the other groups. The prevalence of vulnerable plaque features (lipid-rich plaque, macrophage presence, and microvessels) was lowest in the highest CPB tertile. In patients with calcification, higher age, statin use, and lower PCAT attenuation were independently associated with greater CPB. Exact numerical values and effect sizes were not reported in the abstract.

Why it matters

The findings support the paradigm that advanced coronary calcification represents a stabilized phase of atherosclerosis with subsided local vascular inflammation and reduced structural vulnerability, rather than active high-risk plaque.

Limits

The abstract provides no exact numerical metrics, confidence intervals, or p-values for PCAT attenuation or vulnerable feature frequencies. The cross-sectional observational design limits causal inferences regarding the timeline of inflammation resolution and plaque stabilization, and the cohort is restricted to patients selected for invasive OCT imaging.

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