Key result
Greater echocardiographic epicardial adipose tissue thickness is strongly linked to obstructive CAD.
Why the study?
Substantial heterogeneity exists regarding whether echocardiographic EAT thickness is assessed during systole or diastole, leaving it unclear if these measurements provide equivalent information for identifying obstructive CAD.
Does echocardiographically measured epicardial adipose tissue (EAT) thickness during systole or diastole associate with the presence of angiographically confirmed obstructive CAD?
Does echocardiographically measured epicardial adipose tissue (EAT) thickness during systole or diastole associate with the presence of angiographically confirmed obstructive CAD?
Echocardiographic measurement of epicardial adipose tissue thickness, whether in systole or diastole, is strongly associated with the presence of obstructive CAD, though the measurements may not be fully interchangeable.
Echocardiographic EAT thickness was associated with obstructive CAD; leaves open incremental value for risk stratification pending prospective validation.
Background: Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot increasingly associated with the development and progression of coronary artery disease (CAD). Transthoracic echocardiography is the most widely used modality for EAT assessment; however, substantial heterogeneity exists regarding the timing of measurement within the cardiac cycle, with EAT thickness variably assessed during systole or diastole. Whether these measurements provide equivalent information for identifying obstructive CAD remains unclear. This systematic review and meta-analysis evaluated the association between echocardiographically measured EAT thickness and angiographically confirmed obstructive CAD, with specific focus on systolic versus diastolic assessments. Methods: PubMed, Scopus, and EMBASE were systematically searched through December 2025 for observational studies comparing EAT thickness in patients with and without obstructive CAD confirmed by invasive coronary angiography. Random-effects models were used to pool standardized mean differences (SMDs) for systolic and diastolic EAT thickness. Heterogeneity was assessed using the I2 statistic, publication bias by funnel plots and Egger’s regression test, and robustness by meta-regression and leave-one-out sensitivity analyses. Results: Twenty-two studies including more than 6500 patients were analyzed. Both systolic and diastolic EAT thickness were significantly greater in patients with obstructive CAD than in non-CAD controls. Systolic EAT showed a large, pooled effect size (SMD 1.27; 95% CI 0.96–1.59; p < 0.001), while diastolic EAT demonstrated a similarly strong association (SMD 1.59; 95% CI 1.10–2.07; p < 0.001). Heterogeneity was substantial (I2 > 90%), but the direction of effect was consistent across all studies. Meta-regression analyses indicated that demographic, clinical, metabolic, geographic, and methodological characteristics, including ultrasound software/vendor category and timing of EAT measurement, did not significantly moderate the association between EAT thickness and obstructive CAD. No significant publication bias was detected, and sensitivity analyses confirmed the robustness of the results. Conclusions: Echocardiographically measured EAT thickness is strongly and consistently associated with obstructive CAD, irrespective of whether measurements are obtained during systole or diastole. Although both approaches show robust discriminatory capacity at the population level, differences in effect magnitude suggest that they may not be fully interchangeable. Moreover, in the absence of standardized and broadly applicable cut-off values, the interpretation and clinical management of EAT measurements as individual risk predictors require further investigation.
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Sonaglioni et al. (2026) studied this question. Echocardiographically measured epicardial adipose tissue thickness is strongly associated with obstructive CAD, with systolic SMD at 1.27 and diastolic SMD at 1.59.
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