What is the clinical evidence from this study?

Study design: Meta-Analysis. Population: Acute coronary syndrome (ACS) (n=826). Intervention: Culprit lesions or vessels vs. Non-culprit lesions or vessels. Primary outcome: Pericoronary adipose tissue (PCAT) attenuation (MD 4.95 HU, 95% CI 2.62-7.27, p=< 0.001).

April 8, 2026BMC Cardiovascular Disorders0 citationsOpen Access

Difference of pericoronary adipose tissue attenuation between culprit and non-culprit lesions in acute coronary syndrome: a systematic review and meta-analysis

Q: What are the key findings of this study?

Pericoronary adipose tissue attenuation was significantly higher around culprit lesions compared to non-culprit lesions in patients with acute coronary syndrome (MD 4.95 HU).

Q: What does this research mean for the field?

Pericoronary adipose tissue attenuation is significantly higher around culprit lesions compared to non-culprit lesions in patients with acute coronary syndrome. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To quantify the difference in pericoronary adipose tissue attenuation between culprit and non-culprit lesions in acute coronary syndrome.

HXH XiePeking University MHMing HaoPeking University HHHe HuangPeking University

Key Result

Pericoronary adipose tissue attenuation was significantly higher around culprit lesions compared to non-culprit lesions in patients with acute coronary syndrome (MD 4.95 HU).

Key Points

To quantify the difference in pericoronary adipose tissue attenuation between culprit and non-culprit lesions in acute coronary syndrome.
Conducted a systematic search of PubMed and Embase for relevant studies.
Included 12 studies with a total of 826 patients for meta-analysis.
Employed a random-effects model to calculate pooled mean difference in PCAT attenuation.
Performed subgroup and meta-regression analyses to assess heterogeneity.
Culprit lesions showed significantly higher PCAT attenuation than non-culprit lesions (MD 4.95 HU, p < 0.001).
Heterogeneity was substantial (I²=89%).
Perilesional PCAT measurement indicated a larger effect size (MD 7.50 HU) compared to vessel level measurement (MD 2.43 HU).
Analysis lesion unit and ACS subtype were identified as major sources of heterogeneity.

Study Design

Type

Meta-Analysis (n=826)

Structured PICO

Does pericoronary adipose tissue (PCAT) attenuation differ between culprit and non-culprit lesions in patients with acute coronary syndrome?

Population

826 patients with acute coronary syndrome (STEMI, NSTEMI, or UA) from 12 studies. Meta-analysis included 11 studies (12 cohorts) comprising 461 culprit/731 non-culprit lesions and 388 culprit/487 non-culprit vessels.

Intervention

Pericoronary adipose tissue (PCAT) attenuation measurement at culprit lesions or vessels

Comparator

Pericoronary adipose tissue (PCAT) attenuation measurement at non-culprit lesions or vessels within the same patients

Outcome

Mean difference in pericoronary adipose tissue (PCAT) attenuation between culprit and non-culprit lesions/vesselssurrogate

Pericoronary adipose tissue attenuation is significantly elevated around culprit lesions compared to non-culprit lesions in ACS, highlighting its potential as a localized imaging biomarker for plaque vulnerability.

Main Result

Effect estimate: MD 4.95 HU (95% CI 2.62-7.27)

p-value: p=< 0.001

Limitations

Restriction to major international databases and exclusion of specific local-language databases may introduce selection bias
Findings demonstrate an association but cannot establish diagnostic accuracy or a definitive cut-off value for identifying culprit lesions
Substantial statistical heterogeneity reflecting methodological disparities across studies
Predominantly retrospective design and inclusion of multiple vessel segments in some control arms introduce potential bias and preclude causal inference
Estimation of mean values from medians in two studies may introduce bias
Inconsistent reporting of time intervals between CTA and ICA across the included studies
Inconsistent reporting of ACS subtypes across studies prevented rigorous stratification

Abstract

Pericoronary adipose tissue (PCAT) attenuation, a non-invasive marker of coronary inflammation, predicts adverse cardiovascular events. However, the extent of localized inflammation at the culprit lesion site in acute coronary syndrome (ACS) has not been systematically quantified. We aimed to meta-analyze the difference in PCAT attenuation between culprit and non-culprit lesions in patients with ACS. We systematically searched PubMed and Embase for studies comparing PCAT attenuation between culprit and non-culprit lesions/vessels in ACS patients. A random-effects model was used to calculate the pooled mean difference (MD). Pre-specified subgroup and meta-regression analyses were performed to explore heterogeneity. Twelve studies with 826 patients were included. Meta-analysis was performed in 11 studies comprising 12 cohorts (461 culprit/731 non-culprit lesions and 388 culprit/487 non-culprit vessels). PCAT attenuation was significantly higher around culprit sites compared to non-culprit sites (MD 4.95 HU, 95% CI: 2.62–7.27, p < 0.001), with substantial heterogeneity (I²=89%). Subgroup analysis revealed a significantly greater effect size when PCAT was measured at the perilesional level (MD 7.50 HU) versus the vessel level (MD 2.43 HU). Meta-regression identified the analysis lesion unit (p = 0.002) and ACS subtype (p = 0.003) as major sources of heterogeneity. This meta-analysis provides consistent evidence that culprit lesions in ACS are characterized by a measurable and highly localized increase in pericoronary inflammation. A perilesional measurement approach may better capture this focal inflammatory signal, highlighting the potential of PCAT attenuation for identifying culprit lesion in ACS.

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