Abstract

Introduction: Inflammation of the perivascular adipose tissue (PAT) has been associated with coronary artery disease (CAD); however, lymphocyte B in PAT has not been previously investigated, neither the presence of inflammation in acute CAD. Hypothesis: The number of macrophages, T and B lymphocytes in PAT are greater in CAD than in controls. Methods: We collected whole hearts and abdominal subcutaneous adipose tissue (SAT) from individuals ≥ 30 years-old. Coronary artery atherosclerosis were evaluated using morphometric methods to determine the level of obstruction and the presence of unstable plaques (e.g. ulceration, hemorrhage, or thrombotic occlusion). Samples of PAT next to the atheromatous plaque and SAT were stained using immunochemistry: macrophages (CD68), T lymphocytes (CD3) and B lymphocytes (CD20) and quantified in 20 random fields. The number of inflammatory cells was compared among controls, chronic CAD, and acute CAD in PAT and in SAT. Results: We evaluated 49 participants (controls n=12; chronic CAD n=27, and acute CAD n=10). Compared to controls, the number of B lymphocytes was greater in participants with CAD in PAT [acute CAD: 7.7 (IQR 3.8-17.3); chronic CAD: 5.8 (IQR 1.9-9.6); controls: 1.9 (IQR 0-4.8); p=0.01]. In SAT, macrophages was greater in CAD groups [chronic CAD: 175 (IQR 94-326); and acute CAD: 138 (IQR 15-277)] than in controls [65 (ITQ 28-110); p=0.02]; and also for T lymphocytes [chronic CAD: 45 (IQR 25-75); acute CAD: 40 (IQR 25-56)]; controls [13 (IQR 8-38) p=0.03]. In paired analysis, we found more macrophages in the PAT than in the SAT in all groups [controls:PAT-288 (IQR 98-597); SAT-65 (IQR 28-110) p=0.02]; [chronic CAD: PAT-505 (IQR 434-987); SAT-175 (IQR 94-326) p<0.0001]; [acute CAD: PAT-496 (IQR 200-743); SAT-104 (IQR 15-277) p=0.007]. B lymphocytes in CAD were larger in the PAT than in the SAT, respectively [chronic: 5,8 (IQR 1,9-9,6) vs. 1,9 (IQR 1,9-7,2) p=0.04]; [acute: 7,7 (IQR 1,9-17,3) vs. 1,0 (IQR 0-2,9) p=0.03]. Conclusions: We found an association between inflammation in the PAT and CAD mediated by humoral response. Besides, we detected inflammation in SAT in CAD groups mediated through T lymphocytes and macrophages, suggesting a systemic response in individuals with CAD that is more intense in PAT than in SAT.

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