Background:Acute coronary syndrome (ACS) is closely related to unstable plaques and secondary thrombosis. The inflammatory cells in plaques and their inflammatory products may be the cause for plaque instability and ruptures. The study aimed to disclose the changes of inflammatory factors including serum intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40), and lipoprotein-associated phospholipase A2 (Lp-PLA2) in patients with ACS and its clinical significance.Methods:A total of 120 patients with coronary heart disease (CHD) were categorized into 2 groups: 69 with ACS and 51 with stable angina pectoris (SAP); 20 patients with chest pain and normal angiography served as a control group. The 120 patients with CHD were categorized into single-vessel disease group, double-vessel disease group, and three-vessel disease group based on the number of coronary artery stenosis. The severity of coronary artery stenosis was quantified based on coronary angiography using Gensini score. They were further divided into mild CHD group with its Gensini score <26 (n = 36), moderate CHD group with its Gensini score being 26–54 (n = 48) and severe CHD group with its Gensini score >54 (n = 36). Serum levels of ICAM-1, YKL-40, and Lp-PLA2 of different groups were determined by enzyme-linked immunosorbent assay. Correlation between ICAM-1, YKL-40, Lp-PLA2, and Gensini score was analyzed.Results:The levels of serum inflammatory factors ICAM-1, YKL-40, and Lp-PLA2 were significantly higher in the ACS group than those in control group and SAP group (all P < 0.05); and compared with control group, no significant difference was observed in terms of the serum ICAM-1, YKL-40, and Lp-PLA2 levels in the SAP group (P > 0.05).The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, single-vessel disease group, double-vessel disease group, and three-vessel disease group (all P > 0.05). The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, mild CHD group (Gensini score <26), moderate CHD group (Gensini score 26–54), and severe CHD group (Gensini score >54) (all P > 0.05).Conclusions:The serum levels of ICAM-1, YKL-40, and Lp-PLA2 were correlated with different clinical types of CHD, but not well correlated the severity and extent of artery stenosis, suggesting that ICAM-1, YKL-40, and Lp-PLA2 might be involved in occurrence of instability of atherosclerotic plaque, and might reflect the severity of CHD mostly through reflecting the plaque stability.

Background:The crush and the culotte stenting were both reported to be effective for complex bifurcation lesion treatment. However, their comparative performance remains elusive.Methods:A total of 300 patients with coronary bifurcation lesions were randomly assigned to crush (n = 150) and culotte (n = 150) treatment. The primary endpoint was the occurrence of major adverse cardiac events (MACEs) at 12 months including cardiac death, myocardial infarction, stent thrombosis, and target vessel revascularization. Index lesion restenosis at 12 months was a secondary endpoint. The surface integrals of time-averaged wall shear stress at bifurcation sites were also be quantified.Results:There were no significant differences in MACE rates between the two groups at 12-month follow-up: Crush 6.7%, culotte 5.3% (P = 0.48). The rates of index lesion restenosis were 12.7% versus 6.0% (P = 0.047) in the crush and the culotte groups, respectively. At 12-month follow-up, the surface integrals of time-averaged wall shear stress at bifurcation sites in the crush group were significantly lower than the culotte group ([5.01 ± 0.95] × 10−4 Newton and [6.08 ± 1.16] × 10−4 Newton, respectively; P = 0.003).Conclusions:Both the crush and the culotte bifurcation stenting techniques showed satisfying clinical and angiographic results at 12-month follow-up. Bifurcation lesions treated with the culotte technique tended to have lower restenosis rates and more favorable flow patterns.

Inflammatory factor ICAM-1 may be an objective basis for syndrome typing of QSBS and QDBS, which provides a research direction for standardization research of CM syndrome types.