2023 China Guidelines for Lipid Management / 老年心脏病学杂志（英文版）

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death among urban and rural residents in China, and elevated low-density lipoprotein cholesterol (LDL-C) is a risk factor for ASCVD. Considering the increasing burden of ASCVD, lipid management is of the utmost importance. In recent years, research on blood lipids has made breakthroughs around the world, hence a revision of China guidelines for lipid management is imperative, especially since the target lipid levels in the general population vary in respect to the risk of ASCVD. The level of LDL-C, which can be regarded as appropriate in a population without frisk factors, can be considered abnormal in people at high risk of developing ASCVD. As a result, the "Guidelines for the prevention and treatment of dyslipidemia" were adapted into the "China Guidelines for Lipid Management" (henceforth referred to as the new guidelines) by an Experts' committee after careful deliberation. The new guidelines still recommend LDL-C as the primary target for lipid control, with CVD risk stratification to determine its target value. These guidelines recommend that moderate intensity statin therapy in adjunct with a heart-healthy lifestyle, be used as an initial line of treatment, followed by cholesterol absorption inhibitors or/and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, as necessary. The new guidelines provide guidance for lipid management across various age groups, from children to the elderly. The aim of these guidelines is to comprehensively improve the management of lipids and promote the prevention and treatment of ASCVD by guiding clinical practice.

Therapeutic effect of vitamin D combined benazepril on reducing urine microalbumin in hypertensive patients / 心血管康复医学杂志

Objective :To study safety and effectiveness of vitamin D combined benazepril on patients with essential hyper-tension (EH) and positive urine microalbumin (UMA).Methods :A total of 92 EH patients with positive UMA were ran-domly divided into benazepril group (n＝44 , received benazepril 5md/d ,placebo 1 capsule/d) and combined treatment group (n＝48 , received vitamin D3 400mg/d and benazepril 5mg/d) ,both groups were treated for 12 weeks.Levels of mean arterial pressure (MAP) ,serum creatinine (SCr) and UMA were measured and compared between two groups before and after treatment .Results :Compared with before treatment ,there were significant reductions in levels of MAP and UMA in two groups after treatment , P＝0.001 all ;compared with benazepril group ,there were significant reductions in levels of MAP [ (108.45 ± 15.09) mmHg vs.(101.1 ± 15.02) mmHg] and UMA [ (52.35 ± 17.45) mg/L vs.(43.75 ± 13.29) mg/L] in combined treatment group ,P＜0.05 or ＜0.01.There was no significant difference in SCr level between two groups before and after treatment , P＞0.05 all.Conclusion : Compared with pure benazepril antihypertensive treat-ment ,vitamin D combined benazepril possesses better therapeutic effect on reducing UMA and antihypertensive effect .And it is safe without obvious damage on kidney function ,which is worth extending .

Effect of liver X receptor agonist T0901317 on endothelin-1 induced murine HL-1 cardiomyocytes hypertrophy / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the role of liver X receptors (LXRs) on endothelin-1 (ET-1) induced murine HL-1 cardiomyocytes hypertrophy.</p><p><b>METHODS</b>Cultured murine HL-1 cardiomyocytes were divided into four experiment groups: (1) CONTROL GROUP:treated with DMSO; (2) T0901317 group:treated with LXRs agonist T0901317 (1 µmol/L); (3) ET-1 group:treated with ET-1 (1 nmol/L); (4) T0901317 + ET-1 group:treated with T0901317 (1 µmol/L) for 8 hours, then treated with ET-1 (1 nmol/L). Twenty-four hours later, immunofluorescent staining was performed on HL-1 cells, the surface area of HL-1 cells was analyzed with NIH Image J software, and the synthetic rate of protein in HL-1 cells was detected by (3)H-leucine incorporation. The mRNA level of atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MyHC) was measured by quantitative realtime PCR. The effect of T0901317 on mRNA expression of ANP was also detected after LXRs gene silencing.</p><p><b>RESULTS</b>The surface area of HL-1 cells, mRNA expression of ANP and β-MyHC, and (3)H-leucine incorporation in ET-1 group were 2.00 ± 0.29, 1.98 ± 0.47, 2.13 ± 0.39 and 1.79 ± 0.17, respectively, which were significantly higher than those of control group (1.00 ± 0.26, 1.00 ± 0.21, 1.00 ± 0.31 and 1.00 ± 0.03, respectively, all P < 0.05). Compared with ET-1 group, the surface area of HL-1 cells, mRNA expression of ANP and β-MyHC, and (3)H-leucine incorporation were significantly decreased in T0901317 + ET-1 group (1.24 ± 0.25, 1.19 ± 0.21, 1.48 ± 0.27 and 1.15 ± 0.11, respectively, all P < 0.05). After inhibition of LXRα/β expression in HL-1 cardiomyocytes using the specific siRNAs, the mRNA expression of ANP in T0901317 + ET-1 group was 1.78 ± 0.05, which was similar as that in ET-1 group (1.94 ± 0.17, P > 0.05).</p><p><b>CONCLUSION</b>T0901317, an agonist of LXRs, could inhibit ET-1 induced cardiac hypertrophy in vitro, and LXR ligand-mediated inhibition on ANP mRNA expression by T0901317 is receptor dependent.</p>

Association between adipocyte fatty acid binding proteins/adiponectin and coronary artery stenosis / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the relationship between serum and monocyte-derived-macrophages secreted adipocyte fatty acid binding protein (A-FABP), adiponectin (or A-FABP/adiponectin ratio) and coronary artery disease.</p><p><b>METHODS</b>Three hundred and forty subjects underwent coronary angiography (CAG) were classified into CAD group (n = 211) and non-CAD group (n = 129) according to the CAG results. The severity of coronary artery stenosis was assessed by the numbers of involved coronary artery branches and the sum of the Gensini scores. Fasting venous blood was collected from all subjects and peripheral monocytes were isolated from 20 subjects (10 selected from each group with age-, gender-, and BMI-matched). Peripheral blood monocytes were obtained and stimulated into macrophages with PMA, cell culture supernatant was collected. The concentration of serum/supernatant A-FABP and adiponectin levels were assayed by enzyme-linked immunosorbent assays.</p><p><b>RESULTS</b>(1) A-FABP levels tended to be higher in CAD patients compared to non-CAD subjects [18.3(13.2, 22.8) µg/L vs. 16.4(13.5, 20.4) µg/L, P = 0.088]. The concentration of adiponectin in CAD group was significantly lower than those in non-CAD group [13.9 (9.8, 17.1) mg/L vs. 19.7 (14.5, 27.6) mg/L, P < 0.05]. (2) The A-FABP levels increased and the adiponectin levels decreased as the number of stenotic vessels increased. Gensini scores were positively correlated with serum A-FABP (r = 0.120, P = 0.043) and inversely correlated with adiponectin (r = -0.405, P = 0.007). (3) The difference in A-FABP/adiponectin ratio was more prominent between subjects with CAD and subjects without CAD [(1.51 ± 0.79) µg/mg vs. (0.89 ± 0.30) µg/mg, P < 0.01] and there was a stronger positive correlation of Gensini score to A-FABP/adiponectin ratio(r = 0.531, P = 0.000). (4) Monocyte-derived-macrophages from patients with CAD had higher A-FABP/adiponectin ratio than that in patients without CAD [(0.51 ± 0.19) µg/mg vs. (0.36 ± 0.11) µg/mg, P < 0.05].</p><p><b>CONCLUSIONS</b>Increased levels of serum A-FABP and reduced levels of adiponectin in CAD patients serves as a novel biomarker for the severity of the coronary stenosis. A-FABP/adiponectin ratio is superior to A-FABP or adiponectin alone on predicting CAD risks.</p>