Background And Aims: Bile acids, the key products for elimination of cholesterol, play an important role in coronary artery disease (CAD). However, few studies focused on the roles of more accessible serum total bile acids (TBA) in the prediction of adverse cardiovascular events for coronary chronic artery occlusion (CTO). The aim of this study was to explore the potential relationship between serum TBA and long-term prognosis in patients with CTO undergoing percutaneous coronary intervention (PCI).
Methods: Baseline TBA was determined in 613 patients with CTO after PCI in the present study. All patients were divided into 3 groups according to the median (3.5 mol/l) and the normal upper limit of the TBA (10 mol/l). The primary endpoint was all-cause mortality, and the secondary endpoint was major adverse cardiovascular events (MACE).
Results: Average age in this study was 65.44 ± 9.94 years old. The median of TBA was 3.5 (2.1-6.1) mol/l. Over a median follow-up of 33.5 months, compared to those with below 3.5 mol/l TBA, 3.5 ~ 10 mol/l TBA was associated with significantly reduced risk for the MACE (hazard ratio (HR): 0.59, 95% confidence interval (CI): 0.40 to 0.88; = 0.009) even after adjustment for baseline variables. However, TBA did not predict all-cause mortality and cardiovascular death. Spline analyses showed an L-shaped relationship of the serum TBA with the incidence of MACE.
Conclusions: Moderate fasting serum TBA level has a predictive value for MACE even after adjusting for lifestyle and clinical risk factors in CTO patients undergoing PCI.
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http://dx.doi.org/10.1155/2022/1434111 | DOI Listing |
Dig Dis Sci
December 2024
Huadu District People's Hospital of Guangzhou, Huadu District, No. 48 Xinhua Road, Guangzhou, 510800, China.
Background: NXT629, a PPAR-alpha antagonist, exerts widespread effects in many diseases; however, its function and relevant mechanism in cholesterol gallstones (CG) remain largely unknown.
Methods: Male C57BL/6 J mice were fed a regular diet or lithogenic diet (LD), followed by treatment with intraperitoneal injection of NXT629. H&E staining was performed to analyze hepatic pathological changes, and Oil red O staining was conducted to detect lipid accumulation.
Objective: Aim: to find out the gender characteristics of oxidative mechanisms of liver damage in rats with ethanol hepatitis (EH).
Patients And Methods: Materials and Methods: The study was performed on 48 white male and female rats: 1 - control, 2 - acute EH (12,5 ml/kg of a 40% ethanol solution prepared on 5% solution of glucose for 7 days).The diene and triene conjugates (DC, TC), Schiff's bases (SB), TBA-active products (TBA-ap), activity of superoxide dismutase (SOD) and catalase (CAT) were determined in the blood serum.
Zhongguo Zhong Yao Za Zhi
November 2024
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China.
A liquid chromatography-tandem mass spectrometry method was established and validated for determining the concentrations of costunolide(CO), piperine(PI), agarotetrol(AG), glycyrrhizic acid(GL), vanillic acid(VA), and glycyrrhetinic acid(GA) in rat plasma. This method was then applied to the toxicokinetic study of these six compounds in rats with chronic cerebral ischemia(CCI) following multiple oral doses of Zhachong Shisanwei Pills. Finally, the effects of continuous multiple-dose administration of Zhachong Shisanwei Pills on the liver of CCI rats were investigated.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Wuxi Maternity and Child Health Care Hospital, Affiliated Women's Hospital of Jiangnan University, Jiangnan University, Wuxi 214002, China. Electronic address:
Biosci Biotechnol Biochem
December 2024
Central Laboratory, Department of Pharmacy, Wuhan Fourth Hospital, Wuhan, China.
Lipopolysaccharide (LPS) causes inflammatory cholestasis in sepsis. We investigated the role of PDZK1 in the repression of ABC transporters in LPS-induced cholestasis. Lentiviral gene transfer of PDZK1 to rats was conducted to explore its influence on cholestasis induced by LPS.
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