Coronary artery calcification and plaque stability： an optical coherence tomography study.

Background: Coronary artery calcification (CAC), a surrogate of atherosclerosis, is related to stent underexpansion and adverse cardiac events. However, the effect of CAC on plaque stability is still controversial and the morphological significance of CAC has yet to be elucidated. Methods: A retrospective series of 419 patients with acute coronary syndrome (ACS) who underwent optical coherence tomography (OCT) were enrolled. Patients were classified into three groups based on the calcification size in culprit plaques and the features of the culprit and non-culprit plaques among these groups were compared. Logistic regression was used to analyze independent risk factors for culprit plaque rupture and the nonlinear relationship between calcification parameters and culprit plaque rupture. Furthermore, we compared the detailed calcification parameters of different kinds of plaques. Results: A total of 419 culprit plaques and 364 non-culprit plaques were identified. The incidence of calcification was 53.9 % in culprit plaques and 50.3 % in non-culprit plaques. Compared with culprit plaques without calcification, plaque rupture, macrophages and cholesterol crystals were more frequently observed in the spotty calcification group, and the lipid length was longer; the incidence of macrophages and cholesterol crystals was higher in the macrocalcification group. Calcification tended to be smaller in ruptured plaques than in non-ruptured plaques. Moreover, the arc and length of calcification were greater in culprit plaques than in non-culprit plaques. Conclusions: Vulnerable features were more frequently observed in culprit plaques with spotty calcification, whereas the presence of macrocalcification calcifications did not significantly increase plaque vulnerability. Calcification tends to be larger in culprit plaques than in non-culprit plaques.

Cholesterol crystals in non-culprit plaques of STEMI patients: A 3-vessel OCT study.

BACKGROUND: Cholesterol crystals (CCs) are regular microstructures found within the necrotic core of atherosclerotic plaques and have been hypothesized to be related to plaque destabilization. We attempted to investigate the potential association between CCs and non-culprit plaque vulnerability in patients with ST-segment elevated myocardial infarction (STEMI) and study morphological features of CCs in ruptured non-culprit plaques. METHODS: A total of 261 patients with ST-segment elevation myocardial infarction who underwent 3-vessel optical coherence tomography (OCT) imaging were included. Non-culprit plaques were divided into two groups according to the presence or absence of CCs in the plaque to compare the morphological characteristics of the plaques. The differences in parameters of the non-culprit plaque CCs were explored between ruptured plaques and unruptured plaques. RESULTS: Totally, 530 non-culprit plaques (29 ruptured plaques and 501 unruptured plaques) were identified by OCT. The incidence of CCs was 21.1%. Compared with non-culprit plaques without CCs, those with CCs had a larger lipid burden. Macrophages (p < 0.001) and spotty calcification (p = 0.002) were more frequently observed in non-culprit plaques with CCs. The frequency of CCs was significantly higher (p = 0.001) and the CCs were larger (p = 0.046) and more superficial (p = 0.005) in ruptured non-culprit plaques than in unruptured non-culprit plaques. The maximum lipid arc and fibrous cap thickness were independent predictors of plaque rupture, but the presence of CCs was not. CONCLUSIONS: Non-culprit plaques with CCs have more vulnerable features. CCs are more frequently found in ruptured non-culprit plaques and larger and more superficial CCs are associated with plaque rupture.

Effects of pitavastatin on the expression of VCAM-1 and its target gene miR-126 in cultured human umbilical vein endothelial cells.

OBJECTIVES: Reducing the expression of endothelial cell adhesion molecules is conducive to the decrease of inflammation-induced vascular complications. In this study, we observed pitavastatin on expression of vascular cell adhesion molecule-1 (VCAM-1) and its influence on VCAM-1's target gene miR-126 in endothelial cells. The purpose of this study is to explore the mechanism of pitavastatin in prevention and treatment of atherosclerosis. METHODS: HUVEC were cultured in M1640 and passages 2-5 were used in experiments. The cells were randomly divided into three groups, control, TNF-α and pitavastatin group. Cells of TNF-α group were co-incubated with different concentrations (10, 20, 30 µg/L) of TNF-α for 24 h. Cells of pitavastatin group were firstly coincubated with (0.01, 0.1, 1 µmol/L) pitavastatin, respectively, for 1 h, then coincubated with 30 µg/L TNF-α for 24 h. VCAM-1 and miR-126 mRNA were detected by RT-PCR, and Western blotting was used to detect protein expression of VCAM-1. RESULTS: Both detection methods have showed that TNF-α stimulation significantly increased the mRNA and protein expression of VCAM-1 in a dose-dependent manner, and miR-126 mRNA expression exhibited a decreasing trend. The increase of VCAM-1 mRNA and protein expression induced by TNF-α was inhibited by pitavastatin in a dose-dependent manner, too. However, there were no differences of the expression of miR-126 among three groups. CONCLUSIONS: These effects may explain the ability of pitavastatin to reduce the progression of atherosclerosis. The findings further suggest that inhibitory effect of pitavastatin on VCAM-1 is not related to miR-126 but depends on other ways.