Effects of trimetazidine on myocardial autophagy in rats with heart failure after myocardial infarction / 天津医药

Objective To observe changes of left ventricular function and the level of autophagy after treatment with trimetazine in rats with heart failure after myocardial infarction(MI). Methods Twenty healthy male Wistar rats with the ligation of the proximal part of the left descending branch were randomly and equally allocated into two groups,model group (M group) and trimetazine group (Q group). A sham group (S group) was made up by 10 sham-operated rats. Rats of trimetazine group were given trimetazine(15 mg/kg)once a day for 4 weeks.Then left ventricular function was measured by echocardiography,and hemodynamics was evaluated by Millar pressure-volume system.Serum levels of NT-proBNP and hs-TnT were tested by ELISA.Pathological changes and fibrosis of myocardium were observed by HE and Masson staining.The myocardial apoptosis level was observed by TUNEL, and expressions of autophagy related protein and gene in myocardial tissue were detected by Western blot assay and RT-PCR. Results Trimetazine treatment significantly improved left ventricular dilatation and dysfunction in rats with myocardial failure. Trimetazine treatment also significantly improved pressure overload and the compliance decrease of left ventricular in rats with heart failure after myocardial infarction. Trimetazidine reduced the edema,necrosis and myocardial fibrosis of cardiac myocytes in rats with heart failure.The results from ELISA showed that serum levels of NT-proBNP and hs-TnT were significantly lower in the trimetazine group than those of model group.Compared with model group,the cardiomyocyte apoptosis decreased significantly in the trimetazine group.The results from Western blot assay and RT-PCR showed that autophagic flow of myocardium was increased remarkably in the trimetazine group than that of model group. Conclusion Autophagy has a protective effect on myocardial cells. Trimetazine can improve cardiac function through up-regulation of autophagy in cardiomyocytes in MI rats with heart failure.

Association between plasma adiponectin and small, dense low density lipoprotein in patients with coronary artery disease / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the association between adiponectin and small dense low-density lipoprotein (sLDL-c) in coronary artery disease (CAD) patients. Furthermore, we sought to determine the association between single nucleotide polymorphisms (SNP) rs1501299 (+276G/T), rs266729 (-11365C/G) and the incidence of CAD.</p><p><b>METHODS</b>Consecutive subjects with chest discomfort were examined by coronary angiography and divided into non-CAD [n = 250, 147 male, mean age (60.26 ± 7.52) years] and CAD [n = 267, 153 male, mean age (60.79 ± 9.63) years] groups. Blood samples were collected from all participants following an overnight fasting for at least 12 hours. Plasma adiponectin levels were measured by competitive enzyme-linked immunosorbent assay (ELISA). The serum levels of sLDL-C and oxidized low-density lipoprotein (ox-LDL) were determined by ELISA. Genotypes in rs1501299 and rs266729 of the adiponectin were determined by polymerase chain reaction (PCR).</p><p><b>RESULTS</b>1. The adiponectin levels were significantly lower [(306.17 ± 74.52) mg/L vs. (321.78 ± 86.28) mg/L], whereas sLDL-C and ox-LDL levels were significantly higher [(276.30 ± 45.55) ng/L vs. (249.00 ± 32.02) ng/L and (545.06 ± 115.46) µg/L vs. (497.74 ± 106.09) µg/L, P < 0.05] in CAD group than non-CAD group. 2. Adiponectin level was negatively associated with sLDL-C, whereas sLDL-C positively correlated with ox-LDL in all subjects. 3. Genotype distribution and allele frequencies of rs1501299 and rs266729 were similar between CAD and non-CAD subjects and not related to the serum levels of adiponectin, sLDL-C and ox-LDL.</p><p><b>CONCLUSIONS</b>Reduced adiponectin and increased sLDL-C were independent risk factors for coronary artery disease. Genetic polymorphisms in rs1501299 and rs266729 were not linked with coronary artery disease.</p>

Association between plasma adiponectin level and in-stent restenosis after coronary stenting / 中华心血管病杂志

<p><b>OBJECTIVE</b>The purpose of the present study was to identify the relationship between the plasma level of adiponectin and in-stent restenosis of patients with coronary heart disease after coronary stenting.</p><p><b>METHOD</b>The study population comprised 119 individuals (92 men) who underwent stent implantation, including 65 subjects without in-stent restenosis (group A) and 54 patients with in-stent restenosis (group B). The level of plasma adiponectin was measured using ELISA. Coronary angiography was performed immediately before and after implanting stent and 9 - 12 months later.</p><p><b>RESULTS</b>Baseline characteristics including drug use after PCI were similar between the groups. The rate of implanting bare metal stent is 8 (12.31%) and 6 (11.11%), TAXUS drug-eluting stent is 11 (16.92%) and 10 (18.52%) and CYPHER drug-eluting stent is 46 (70.77%) and 38 (70.37%) respectively (all P > 0.05). Plasma level of adiponectin in patient of group A was significantly higher than that in group B [(15.16 +/- 5.02) mg/L vs. (10.01 +/- 4.93) mg/L, P < 0.05]. The quantitative coronary angiography (QCA) showed that lesion length was similar between groups [(15.82 +/- 6.67) mm vs. (13.40 +/- 4.20) mm, P > 0.05], minimum lumen diameter (MLD) and stenosis rate were also similar before and after implanting stent (P > 0.05) and acute gain was (1.48 +/- 0.65) mm vs. (1.19 +/- 0.37) mm (P > 0.05). MLD was higher in group A than that in group B [(2.55 +/- 0.53) mm vs. (0.57 +/- 0.60) mm, P < 0.01] at 9 - 12 months follow up. Restenosis rate [(24.2 +/- 11.2)% vs.(81.0 +/- 19.1)%, P < 0.01] and late lumen loss [(0.50 +/- 0.34) mm vs. (1.60 +/- 0.54) mm, P < 0.01] were lower in group A than in group B.</p><p><b>CONCLUSIONS</b>The lower plasma adiponectin level might be associated with in-stent restenosis after coronary stenting.</p>

Clinical analysis of retinoic acid syndrome developed in 11 patients with acute promyelocytic leukemia / 中国实验血液学杂志

To explore the clinical features, risk factors an d treatment of retinoic acid syndrome (RAS) in patients with acute promyelocytic leukemia (APL) treated with retinoic acid, the clinical and laboratory data of 11 APL patients with RAS were retrospectively analysed. The results showed that earlier and more common symptoms of RAS were successively dyspnea (11/11), fever (10/11) and hydrothorax (6/11). Higher WBC count (> or = 15.0 x 10(9)/L) in the course of treatment of all-trans retinoic acid susceptible to develop RAS (9/11). The RAS patients were treated with dexamethasone without discontinuing the treatment of retinoic acid, complete remission was achieved in 10 cases and one patient died from disseminated intravascular coagulation. It is concluded that the identification and dexamethasone treatment of RAS in earlier period are extremely important for obtaining better clinical curative effect, and it does not influence therapeutic effect of continuing application of retinoic acid.