A recent study using peri-coronary adipose tissue (PCAT) attenuation to identify vascular inflammation showed higher levels of inflammation in plaque rupture than in plaque erosion, which was associated with worse outcomes.
Ik-Kyung Jang, MD, PhD (Massachusetts General Hospital, Massachusetts, USA) presented study results on the novel, non-invasive PCAT attenuation marker to identify patients at higher risk for long-term outcomes at the 27th TCTAP 2022 on Apr 29.
Vascular inflammation plays a significant role in atherogenesis and the eventual development of acute coronary syndrome (ACS), making it an important predictive characteristic for long-term clinical stability.
Although several markers, including the optical coherence tomography (OCT) index, are used to identify systemic inflammation, many lack biological specificity that aids the identification of macrophages' type and status.
"In a previous study that compared vulnerability between plaque rupture and plaque erosion, we reported that OCT-measured plaque vulnerability was higher in both culprit lesions and non-culprit lesions," Jang said. "But this study was based on phenotyping coronary plaques and lacked biological information that identifies which macrophages are active."
"Detection alone fails to reveal the type and status of the macrophage, and we needed more biologic information," Jang said. "So, we turned to PCAT attenuation and coronary computed tomography angiography (CCTA)."
Investigators aimed to compare the level of vascular inflammation measured by PCAT attenuation in patients with plaque rupture or plaque erosion and confirm the hypothesis that vascular inflammation would be higher in plaque rupture.
The study enrolled 198 patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS) who had undergone preintervention CCTA- and OCT-culprit lesion imaging.
To measure PCAT attenuation, investigators used a semi-automated software called AutoPlaque ver 2.5 (Cedars-Sinai Medical Center, California, USA) to assess the culprit plaque, culprit vessel and the mean of three coronary arteries.
Findings from OCT analysis showed plaque rupture was the underlying mechanism in 54% (107) of patients and plaque erosion in 46% (91).
Key results showed PCAT attenuation, representing vascular inflammation, was higher in plaque rupture than plaque erosion at all three measured levels, including the culprit plaque (P=0.010), culprit vessel (P=0.024), and mean of three coronary arteries (P=0.030).
Stratified analysis showed the risk of plaque rupture increased by level of PCAT attenuation. The risk of plaque rupture in the lowest quartile of PCAT attenuation was 42.9%, 50% in the low-mid quartile, 52% in the mid-high quartile and 71.4% in the highest quartile (p=0.031).
Analysis also showed that PCAT attenuation was associated with lipid-rich plaque (P=0.004) and macrophages (P=0.016).
Although the trend was not statistically significant, other features such as thin-cap fibroatheroma (TCFA), micro-vessels, cholesterol crystals and layered phenotypes were also associated with high PCAT attenuation for plaque rupture.
"Univariable and multivariable analysis showed plaque rupture was significantly associated with higher PCAT attenuation, which meant more vascular inflammation at the three assessed levels," Jang said. "The results indicate that pan-coronary inflammation plays a bigger role in plaque rupture than plaque erosion."
The study was published in the Journal of American College of Cardiology (JACC): Cardiovascular Imaging last Dec 15 and co-authored by Akihiro Nakajima, MD (Harvard Medical School, Massachusetts, USA) and colleagues.
Edited by
Junghoon Lee, MD
The Catholic University of Korea, Eunpyeong St. Mary's Hospital, Korea (Republic of)
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