Background and Objectives：Studies on the stability of atheromatous plaques, as a determinant of the cause of complications, have been reported. Among the functional features of plaques related with vulnerability, inflammation has emerged as a leading cause of clinical presentation. The purpose of this study was to find the source of the inflammatory response in the patients with acute myocardial infarction (AMI).
Subjects and Methods：Patients with AMI, whose lesion of in either the left anterior descending artery (LAD group, n=13) or the right coronary artery (RCA group, n=11), were selected. The levels of interleukin-6 (IL-6) and P-selectin were measured in blood from the aortic root (A), great cardiac vein (G) and peripheral vein (V). The control group (n=15) included patients with either stable or variant angina.
Results：The levels of IL-6 were 4.77±6.0 (A), 11.32±7.8 (G) and 4.39±5.0 pg/mL (V) in the LAD group, and 3.64±2.1 (A), 6.05±4.9 (G) and 3.84±3.2 pg/mL (V) in the RCA group. Unrelated to the infarction related artery, the level of IL-6 in the great cardiac vein was significantly increased in patients with AMI. The percentages of platelet expressed P-selectin were 6.03±7.0 (A), 8.14±8.1 (G) and 8.83±7.9 (V) in the LAD group and 6.46±8.4 (A), 5.80±6.0 (G) and 5.91±6.9 (V) in the RCA group.
Conclusion：These findings suggest that the generalized inflammatory response is activated across the coronary vascular bed in patients with AMI, regardless of the infarction related artery site. Therefore, systemic therapy, as well as local management for vulnerable plaque, would be required.
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