Observational analysis revealed that inflammation may enhance collateral circulation in chronic total occlusion patients, indicating potential therapeutic targets.
Background The role of pericoronary adipose tissue (PCAT) inflammation in coronary collateral circulation (CCC) development remains unclear. This study compared PCAT characteristics in chronic total occlusion (CTO) patients with good versus poor collaterals. Methods Twenty left anterior descending CTO patients were stratified into poor (P-CCC, n=8) and good collateral (G-CCC, n=12) groups per Rentrop classification. CT-derived fat attenuation index (FAI), epicardial adipose tissue (EAT) volume, and histologic markers (macrophage polarization, microvascular density) were analyzed. Results Compared to the P-CCC group, the G-CCC group exhibited significantly lower FAI (−93.6±7.2 vs. −70.8±2.4 HU, p<0.05) but higher EAT volume (8491.3 [7951.6–13060.0] vs. 3452.8 [1741.7–6425.4] mm³, p<0.05). Histologically, relative to P-CCC PCAT, G-CCC PCAT showed increased M2 macrophage density (14.47±2.87 vs. 3.47±1.63, p<0.05), a higher M2/M1 ratio (4.40±2.17 vs. 0.95±0.61, p<0.05), and greater microvascular density (4.69±1.11 vs. 2.21±0.50, p<0.05). Conclusion PCAT inflammation is associated with enhanced collateral vessel formation. These findings highlight PCAT's potential as a therapeutic target for collateral promotion, warranting further investigation into its molecular mechanisms.
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