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Background: There are limited data on the association between serum total bile acid level and coronary plaque characteristics. This study investigated the relationship between serum total bile acid level and the severity of coronary stenosis and coronary plaque features in an asymptomatic population using coronary computed tomography angiography (CTA). Methods: A total of 1,137 consecutive participants with no known coronary artery disease (CAD) undergoing CTA as part of a general routine health evaluation were recruited. Serum total bile acid level and clinical parameters were assayed. Coronary stenosis and high-risk plaques features (napkin-ring sign, low-attenuation plaque, spotty calcification, positive remodelling) were evaluated. Associations between serum total bile acid concentration and high-risk coronary plaques was tested through univariate and multivariate analyses.Results: A total of 101 high-risk coronary plaques subjects and 93 controls were eligible for study inclusion.The severity of coronary artery stenosis and high-risk coronary plaques increased with serum total bile acid level quartiles (all P<0.001). The independent predictor of high-risk coronary plaques in multivariate analysis was serum total bile acid level (P<0.001). Receiver operating characteristic (ROC) confirmed that serum total bile acid concentration significantly differentiated high-risk coronary plaques [the area under the curve (AUC) =0.876; P<0.001, with a sensitivity of 87.13% and a specificity of 86.02%].Conclusions: Higher serum total bile acid level was associated with the severity of coronary artery stenosis and high-risk coronary artery plaques detected by CTA in asymptomatic populations.

BackgroundIt is unclear whether high-dose atorvastatin pretreatment benefits acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI). To clarify this issue, we performed a meta-analysis of the published literature.Material/MethodsRandomized controlled trials (RCTs) assessing high-dose atorvastatin pretreatment in ACS patients undergoing PCI were enrolled. Short-term major adverse cardiac events (MACEs), changes in serum high-sensitivity C-reactive protein (hs-CRP), peak creatine kinase-myocardial band (CK-MB) level, and thrombolysis in myocardial infarction (TIMI) grade 3 flow after PCI were studied as clinical outcomes.ResultsSeventeen RCTs including 10 072 patients were retrieved. High-dose atorvastatin showed greater benefits in reducing the incidence of short-term MACEs (OR 0.72; 95% CI: 0.56 to 0.94; P=0.01) and hs-CRP level (SMD −1.59; 95% CI: −2.38 to −0.80; P<0.0001) among ACS patients after PCI. No significant difference was found between the 2 groups in terms of peak CK-MB (SMD −0.34; 95% CI: −0.79 to 0.10; P=0.13) or final TIMI flow grade 3 (OR 1.31; 95% CI: 0.73 to 2.36; P=0.36) after PCI. High-dose atorvastatin therapy also was not associated with alanine aminotransferase (ALT) elevation (OR 1.95; 95% CI: 0.95 to 4.03; P=0.07).ConclusionsThe results of this meta-analysis suggest that high-dose atorvastatin pretreatment reduces the incidence of short-term MACEs and hs-CRP level without increasing drug-induced hepatotoxicity in ACS patients after PCI.

ABSTRACT. The aim of this study was to determine whether monocyte/macrophage β2-AR could act as the therapeutic target of antisympathetic excitation-induced atherosclerotic progression. Cultivated human THP-1 cells were divided into different groups and incubated with isoprenaline, metoprolol, propranolol or β2-AR blocker for 24 h, together with oxidized low-density lipoprotein (ox-LDL). Afterwards, each group was analyzed for C-C chemokine receptor type 2 (CCR2) expression, monocyte chemotactic protein 1 (MCP-1) release into medium and cell migration ability. In the isoprenaline group, CCR2 protein level was increased, as well as the secretion of MCP-1, and cell motility was enhanced, in a concentration-dependent manner. Propranolol and ICI 118,551 significantly reversed the stimulatory effect of isoprenaline on THP-1 cells induced by ox-LDL, but only high concentrations of metoprolol interfered significantly with the action of isoprenaline (P < 0.05). Isoprenaline or a β-AR blocker could mediate through β2-AR, affecting MCP-1 secretion, CCR2 protein expression and cell migration capacity of THP-1 cells. Therefore, monocytemacrophage β2-AR may act as a target of antisympathetic excitation- Monocyte-macrophage β2-AR induced atherosclerotic progression.