Abstract:The investigation on the biological roles and underlying mechanisms of gaseous signaling molecules such as nitric oxide, hydrogen sulfide and sulfur dioxide provides a new perspective to understand life activities and the occurrence of diseases. In the column of this issue, a few well-established research teams showed their recent work on endogenous AAT2/SO₂ system inhibited myocardial cell autophagy during cardiac hypertrophy, endogenous H₂S/CSE system suppressed inflammation of endothelial cells and increased skin blood flow by exogenous hydrogen and oxygen mixed gas, respectively, which provide both a new understanding of the cardiovascular effects and mechanisms induced by gaseous signaling molecules and new ideas for the prevention and treatment of cardiovascular diseases. Research still needs to be accelerated in the area on exploration of new gaseous transmitters, the function, mechanism, network and determination techniques of gaseous signal molecules in different physiological and pathological states and its clinical significance in vivo.

Abstract:Aim To investigate the role of endogenous sulfur dioxide (SO₂) in inhibiting cardiomyocyte autophagy in angiotensin Ⅱ (AngⅡ)-induced myocardial hypertrophic mice. Methods 16 healthy 9-week-old C57BL mice were randomly divided into wild type control group (WT Con group) and wild type＋AngⅡ group (WT AngⅡ group); 16 cardiac-specific aspartate aminotransferase 2 (AAT2) transgenic mice were randomly divided into AAT2 control group (AAT2 Con group) and AAT2＋AngⅡ group (AAT2 AngⅡ group); 8 mice in each group. The mouse was subcutaneously implanted with a capsule osmotic pressure pump pre-filled with normal saline or AngⅡ in the back for continuous administration for 4 weeks. Total heart weight/body weight (HW/BW) ratio was detected in 4 groups of mice. HE staining was used to observe the changes of myocardial cell structure. The expression of α-myosin heavy chain (α-MHC) was detected by immunohistochemistry staining. The content of SO₂ in myocardial tissue was detected by high performance liquid chromatography. Western blot was used to detect the expressions of endogenous SO₂ producing enzymes AAT1 and AAT2, cardiomyocyte phenotypic markers α-MHC and β-MHC as well as myocardial autophagy indicators Beclin-1, LC3, Atg4B and p62. Results Compared with WT Con group, the SO₂ content was significantly reduced (P＜0.01) but the expression of AAT1 protein had no obvious changes (P＞0.05), the expression of AAT2 protein was significantly decreased (P＜0.05), in the myocardial tissue of the mice in WT AngⅡ group; HW/BW was increased significantly (P＜0.01), and myocardial fibers were thickened; Immunohistochemistry showed that the expression of α-MHC protein was decreased in cardiomyocyte cytoplasm; Western blot results showed that the expression of α-MHC protein in cardiomyocytes was significantly decreased (P＜0.01), the expression of β-MHC protein was significantly increased (P＜0.01), and cardiomyocyte autophagy was significantly increased which was demonstrated by the fact that the ratio of LC3Ⅱ/LC3Ⅰ was significantly increased, the expressions of Beclin-1 and Atg4B protein were significantly increased, and the expression of p62 protein was significantly reduced (all P＜0.01). However, compared with WT Con group, the SO₂ content and AAT2 protein expression in AAT2 AngⅡ group were significantly increased (P＜0.01), AAT1 protein expression did not significantly change (P＞0.05), and the HW/BW ratio was significantly decreased (P＜0.05); The thickness of myocardial fibers was significantly reversed; The conversion of α-MHC protein to β-MHC protein was significantly reduced (P＜0.01), and the level of autophagy was significantly reduced in cardiomyocytes. Conclusion Endogenous SO₂/AAT2 system can inhibit the cardiomyocyte autophagy and myocardial hypertrophy in the AngⅡ-treated mice.

Abstract:Aim That Ox-LDL induced endothelial inflammation response then promoted monocyte and macrophage adhesion is an essential pathophysiological process of atherosclerosis. Hydrogen sulfide is a novel gasotransmitter and exhibits anti-atherosclerotic and anti-inflammation effects. The present study investigated the role of Krüppel-like factor 6 (KLF6) in protection of H₂S on ox-LDL induced endothelial inflammation. Methods Cystathionine γ lyase (CSE) protein expression, H₂S generation by fluorescence probe were assayed after ox-LDL stimulated in human aortic endothelial cells (HAEC). Then, quantitative real-time PCR were used for measuring the changes of Krüppel-like factors mRNA while treated with H₂S donor or overexpression CSE gene by adenovirus. And then, assayed the inflammatory factors changes and monocyte adhesion to HAEC while knockdown the KLF6. At last, chromatin immunoprecipitation (ChIP) assay were used for determining the DNA binding activity of KLF6 after H₂S treatment. Results Using Western blot to measure the CSE protein expression, H₂S fluorescence probe to identify the endogenous H₂S generation, it found that ox-LDL down-regulated endothelial endogenous CSE/H₂S system in a dose-dependent and time-dependent manner.Ox-LDL lowered KLF6 but increased KLF10 mRNA expression; H₂S donor (NaHS) reversed the KLF6 and KLF10 mRNA changes by ox-LDL induction. In this cellular model, other KLF family mRNA is not changed. Next, it confirmed H₂S donor or CSE overexpression up-regulated KLF6 protein expression. H₂S reduced inflammatory factors-ICAM-1, VCAM-1 expression and monocyte adhesion to endothelium induced by ox-LDL, knockdown KLF6 blocked the H₂S action. It confirmed that H₂S donor decreased DNA binding activity of KLF6 to CXCL2, IL-8 and ATG7 promoter. Conclusion Ox-LDL down-regulated endothelial CSE/H₂S system. H₂S donor treatment or overexpression CSE reduced ox-LDL induced inflammation response by KLF6.

Abstract:Aim To investigate the effects of high concentration hydrogen-oxygen mixed gas (HCHOG) on skin blood flow. Methods Using MoorFLPI-2 Laser Speckle blood stream real-time imaging system, the blood flow amount in facial and hand skin before and after the inhalation of HCHOG (66.7% hydrogen gas + 33.3% oxygen gas) were examined in 12 healthy adult volunteers, respectively. Results After 30 minutes of HCHOG inhalation, the facial skin blood flow (FSBF) was increased by 9.7% (P＜0.05) compared with the FSBF before HCHOG inhalation. The dorsum of hand skin blood flow (DHSBF) was increased significantly by 27.1% (P＜0.01) compared with the DHSBF before HCHOG inhalation. Conclusion A short-time inhalation of HCHOG notably enhanced the FSBF and DHSBF in healthy adults, respectively.

Abstract:Hydrogen sulde (H₂S) is a novel endogenous gaseous signal molecule, and plays important role in both physiological and pathophysiological processes including vasodilation, regulation of blood pressure and angiogenesis, anti-oxidation and cardioprotection. The underlying mechanisms involve in induction of S-sulfhydration, modulation of autophagy and miRNA expression, regulation of ion channels, SIRT1 and Nrf2 activity, interaction with NO and CO signaling. It has been shown that decrease of endogenous H₂S level links to a variety of cardiovascular diseases such as hypertension, atherosclerosis, myocardial ischemia and reperfusion injury and heart failure. Increased endogenous H₂S production or administration of exogenous H₂S is a new strategy for prevention and treatment of the cardiovascular diseases. This review mainly focuses on the recent progress about the role and mechanisms of hydrogen sulfide in cardiovascular system.

Abstract:Aim PhiC31 integrase directs foreign DNA containing with attB integration into specific genomic DNA, incurring long-term and stable expression. This study analyzed the effect of LDLR expression mediated by phiC31 integrase on lipoprotein profile and atherosclerosis in family hypercholesterolaemia mice (LDLR－/－). Methods Male LDLR－/－ mice were tail vein co-injected with phiC31 integrase expression plasmid pCMV-int and plasmid pcDNA 3.1-TBG-LDLR-attB carried with LDLR gene and attB sequence. Mice co-injected with pCMV-int and pcDNA3.1-TBG-LDLR lacking attB sequence were used as control. Results LDLR directed by thyroxine binding globulin promoter and mediated by phiC31 integrase maintained higher and persistent expression in H22 cells and specifically in livers from mice injected with pcDNA3.1-TBG-LDLR-attB. The expression reduced serum low density lipoprotein cholesterol (LDLC) levels up to 35%, and resulted in decreases by 19% of plaque size/lumen area in cross section at ascending aorta compared with mice co-injected with pCMV-int and pcDNA3.1-TBG-LDLR. Conclusion The expression of LDLR mediated by phiC31 integrase improved lipoprotein profile and ameliorated atherosclerosis in LDLR－/－ mice.

Abstract:Aim To investigate the effects of deferiprone (DFP) on expressions of iron transmembrane transport proteins concluding iron influx and efflux system in the hippocampus of cerebral ischemia-reperfusion rats. Methods The rats (n＝48) were randomly divided into sham operation group, cerebral ischemia-reperfusion group (I/R group) and DFP＋I/R group. All rats were pretreated by intragastric administration (ig) 1 h before the middle cerebral artery occlusion method for preparing cerebral ischemia-reperfusion model. After the operation, continuous ig administration was performed for days. After cerebral ischemia-reperfusion for 72 hours, the behavioral activity of rat was recorded by Longa's neurobehavioral score standard. Iron accumulation in the hippocampus was measured by DAB-intensified Perl's histochemical staining. Western blot was used to detect the expressions of iron transmembrane transport protein in hippocampus of rats in each group, including iron importin:transferrin receptor (TFR) and divalent metal ion transporter 1 (DMT1), iron exportin:ferroportin (Fpn), hephaestin (Heph), feline leukemia virus subgroup C receptor (FLVCR) and breast cancer resistance protein (BCRP). Results Compared with I/R group, the Longa's neurobehavioral score was significantly decreased (P＜0.01), the number of aggregated iron particles was reduced, the protein expressions of TFR and DMT1 were significantly decreased (P＜0.05 or P＜0.01), and the protein expressions of Heph, FLCVR and BCRP were up-regulated (P＜0.05 or P＜0.01), in the DFP＋I/R group. Conclusions Deferiprone can reduce the expressions of iron importin TFR and DMT1, increase the expressions of iron exportin Heph, FLVCR and BCRP, promote the efflux of heme iron and non-heme iron and reduce brain iron deposition. Thus it can decrease nerve damage after cerebral ischemia-reperfusion and improve the disease prognosis.

Abstract:Aim To investigate the protective effect of capsaicin on renal ischemia reperfusion injury in rats and its mechanism. Methods 50 male SD rats were divided into sham operation group (Sham), renal ischemia-reperfusion injury group (IRI) and low, middle and high dose capsaicin group. The model of renal ischemia reperfusion injury was established by clamping bilateral renal pedicle for ischemia 45 min, and reperfusion 24 h. Then rats were killed by excessive anesthesia and kidney and serum were collected. Serum creatinine (SCr), urea nitrogen (BUN), cell apoptosis and pathologic renal tissue were detected, mitochondrial adenosine triphosphate (ATP), malondialdehyde (MDA) content, Ca²⁺-ATP enzyme,Na⁺-K⁺-ATP enzyme, catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity were measured. Results Capsaicin intervention can reduce BUN, SCr, cell apoptosis and the pathological change of kidney tissue, increase Ca²⁺-ATP, Na⁺-K⁺-ATP, CAT, GPx and SOD enzyme activity and ATP content and decrease the level of MDA in mitochondria. Conclusion Capsaicin has protective effects on renal ischemia-reperfusion injury in a concentration dependent-manner and its mechanism is related to the inhibition of lipid peroxidation.

Abstract:Aim To investigate whether the anti-fibrosis effect of spironolactone in heart is associated with the expression of silent information regulator 1 (SIRT1). Methods 40 male Sprague-Dawley rats were randomly assigned to 4 groups:control group, model group, low-dose spironolactone group, and high-dose spironolactone group. The latter 3 groups were injected subcutaneously with isoproterenol [5 mg/(kg·d) for 7 days] to establish rat myocardial fibrosis model. The rats of low-dose spironolactone group and high-dose spironolactone group were given 30 and 60 mg/(kg·d) spironolactone intragastric administration at the same time of injecting isoproterenol, while the control group was given the same volume of normal saline for 21 days. Changes of left cardiac function were detected by Powerlab physiological recorder, and pathological changes of myocardium were evaluated by HE staining and Masson staining. Western blot and real-time fluorescence quantitative PCR were used to detect the expression of SIRT1 in rat myocardium. Results The left ventricular weight index (LVWI), right ventricular weight index and left ventricular end-diastolic pressure (LVEDP) in the model group were significantly higher than those in the control group (P＜0.05). Left ventricular systolic pressure (LVSP), maximum change rate of left ventricular pressure rise (＋dp/dt_max) and maximum change rate of left ventricular pressure drop (－dp/dt_max) in model group were significantly lower than those in control group (P＜0.05). Compared with the control group, the myocardial arrangement was disorder, collagen fiber proliferation was obvious, and the expressions of SIRT1 mRNA and protein was down regulated in the model group rats (P＜0.05). After giving spironolactone, the levels of LVWI and LVEDP in rats were significantly lower than those in model group (P＜0.05), and LVSP, ＋dP/dt_max and －dp/dt_max were significantly higher than those in model group (P＜0.05). Compared with the model group, the degree of myocardial arrangement disorder decreased, the collagen content decreased, and the mRNA and protein expressions of SIRT1 increased in the spironolactone group (P＜0.05). Conclusion Spironolactone can alleviate myocardial fibrosis induced by isoproterenol in rats, and its anti-fibrosis effect may be related to the up-regulation of SIRT1 expression.

Abstract:Aim To investigate the effect of asiatic acid (AA) on angiogenesis and ventricular remodeling in acute myocardial infarction (AMI) rats and its mechanism, based on the changes of silent information regulator 3 (SIRT3)/β-catenin/peroxisome proliferator activated receptor γ (PPARγ) signaling pathway during the development of AMI. Methods A total of 72 SD rats was randomly divided into groups according to the principle of weight balance. 12 of them were in the blank control group, and the AMI model was made in the remaining rats. After successful modeling, according to the random number table method rats were randomly divided into 5 groups:model group, positive control group, AA high dose group, AA medium dose group and AA low dose group, 12 rats in each group. The blank control group and the model group were given normal saline, the positive control group was given aspirin enteric-coated tablets, and the drug intervention group was given different doses of AA. 28 days later, Doppler ultrasound was used to detect angiogenesis and ventricular remodeling in each group. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expressions of SIRT3, β-catenin and PPARγ mRNA in rat myocardium. The levels of inflammatory factors interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), nuclear factor κB (NF-κB) were detected by enzyme linked immunosorbent assay.Results Compared with the blank control group, the cardiac function was worse, the microvascular density (MVD) increased, the expressions of SIRT3, β-catenin, PPARγ mRNA and the serum levels of IL-6, TNF-α, NF-κB were all increased, in the model group (P＜0.05). Compared with the model group, the cardiac function was obviously improved, MVD increased, the expressions of SIRT3, β-catenin and PPARγ mRNA increased, and the levels of serum IL-6, TNF-α and NF-κB decreased, in each AA drug adiministration group (P＜0.05). Compared with the positive control group, the cardiac function was improved, the MVD increased, the expressions of SIRT3, β-catenin and PPARγ mRNA in the myocardium increased, and the levels of serum IL-6, TNF-α and NF-κB decreased, in the high, middle and low dose groups of AA (P＜0.05). Conclusion Asiatic acid inhibits SIRT3/β-catenin/PPARγ signaling pathway in infarcted myocardium of rats, and has protective effect on myocardial tissue of AMI rats.

Abstract:Aim To investigate the change of serum small and dense low density lipoprotein cholesterol (sdLDLC) level in patients with coronary heart disease (CHD) after lipid-lowering therapy. Methods Blood samples were collected from 1065 patients with CHD and 469 healthy controls from March to July 2016. Serum low density lipoprotein cholesterol (LDLC), high density lipoprotein cholesterol (HDLC) and sdLDLC levels were measured by direct assay, and serum triglyceride (TG) and total cholesterol (TC) levels were measured by enzyme method. The reference interval of the healthy control group was established. According to the serum LDLC level of CHD patients after lipid-lowering therapy, lipid-lowering LDLC standard group and intensive lipid-lowering LDLC standard group were determined. The blood lipid indexes were compared in each group, and the changes of sdLDLC level and sdLDLC/LDLC ratio were analyzed and compared. Results (1)After lipid-lowering therapy, CHD group compared with the healthy control group, there were significant differences in TG, HDLC and sdLDLC/LDLC ratio between the two groups (P＜0.05), and there were no significant differences in the levels of TC, LDLC and sdLDLC between the two groups (P＞0.05). (2)Compared with the healthy control group, the sdLDLC/LDLC ratio increased in lipid-lowering LDLC standard group (P＜0.05), and there was no significant difference in sdLDLC level between the two groups (P＞0.05). Among the patients who had reached the standard of lipid-lowering, the sdLDLC level of 2.3% CHD patients and the sdLDLC/LDLC ratio of 7.7% CHD patients were higher than the reference interval established by this study. (3)Compared with the healthy control group, SdLDLC level reduced and sdLDLC/LDLC ratio increased in intensive lipid-lowering LDLC standard group (P＜0.05). Among the patients who had reached the standard of intensive lipid-lowering, the sdLDLC level of 0.8% CHD patients and the sdLDLC/LDLC ratio of 15.3% CHD patients were higher than the reference interval established by this study. ConclusionsIn the lipid-lowering therapy and intensive lipid-lowering therapy for CHD patients, the changes of serum sdLDLC level and sdLDLC/LDLC ratio are of great significance for risk analysis of residual cardiovascular events. Lowering sdLDLC level may be one of the important indicators that ultimately reduce the risk of CHD.

Abstract:Aim To investigate the relation between change of the number and functional activity of circulating endothelial progenitor cells and endothelial function in overweight and postmenopausal women. Methods Eighty volunteers were divided into four groups:healthy postmenopausal women (n＝20), overweight postmenopausal women (n＝20), healthy men (n＝20) and overweight men (n＝20). Flow cytometry analysis was used to detect the number of CD34 and KDR double-positive labeled circulating endothelial progenitor cells in the four groups, and acetylated low density lipoprotein (ac-LDL) and lectin fluorescent staining method were explored to detect the number of cultured endothelial progenitor cells. In addition, the migration and proliferation of endothelial progenitor cells were detected respectively with MTT and Transwell method. Finally, vascular endothelial function was investigated by brachial artery-based flow-mediated dilatation (FMD). Results No significant differences were found among the number of circulating endothelial progenitor cells in the four groups (P＞0.05). There was no conspicuous difference in activity of circulating endothelial progenitor cells as well as FMD between overweight men and postmenopausal overweight women (P＞0.05). Compared with the normal weight group, the FMD, migration, and proliferation of circulating endothelial progenitor cells were remarkably decreased in overweight group (P＜0.05). A strong significant correlation was found between the migration and proliferation of circulating endothelial progenitor cells and FMD(r＝0.45, P＜0.05; r＝0.52, P＜0.05, respectively) in overweight group. Conclusion The number and functional activity of circulating endothelial progenitor cells and endothelial function in overweight postmenopausal women were not preserved, and which were significantly declined.

Abstract:Aim To evaluate the clinical efficacy and safety of ticagrelor's antiplatelet therapy for patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing direct percutaneous coronary intervention (PCI).Methods A total of 164 patients diagnosed with STEMI who underwent direct PCI was randomly divided into two groups:ticagrelor group (40 cases) and clopidogrel group (124 cases). According to the results of platelet aggregation rate on the fifth day after treatment, clopidogrel group was divided into two subgroups:non-clopidogrel resistance (CPGR) group (81 cases) and CPGR group (43 cases). The patients in group CPGR were changed to oral administration of ticagrelor. The patients were followed up for 3 months. 5 days, 1 month, 3 months after medication, platelet aggregation rate, main adverse cardiovascular events (MACE) (including cardiac death, nonfatal myocardial infarction, stroke, revascularization of target vessels, stent thrombosis, recurrent angina pectoris, cardiac insufficiency) and adverse drug reactions (including haemorrhage and dyspnea) were analyzed and compared between ticagrelor group and non-CPGR group. Change of platelet aggregation rate before and after the change of medicine was analyzed in CPGR group. Results Platelet aggregation rates in ticagrelor group were significantly lower than that in non-CPGR group at 5 days, 1 month and 3 months after treatment (33.94%±14.90% vs 53.13%±14.07%, 25.26%±8.89% vs 35.51%±9.45%, 24.91%±7.55% vs 31.57%±9.53%), and differences were statistically significant (P＜0.05). In CPGR group, the platelet aggregation rate decreased significantly after 1 month's change to ticagrelor (28.33%±8.11% vs 64.50%±11.38%), and difference was statistically significant (t＝18.944, P＜0.05). Followed up for 3 months, the incidences of MACE and mild to moderate dyspnea in ticagrelor group were significantly lower than those in non-CPGR group, and the differences were statistically significant (P＜0.05). There was no significant difference in mild bleeding between the two groups (P＞0.05). There were no severe bleeding and severe dyspnea in the two groups. Conclusion The antiplatelet effect of ticagrelor is superior to clopidogrel, and it is safe and effective for CPGR patients with mild adverse reactions and good safety.

Abstract:Aim To investigate the correlation between blood pressure variability and heart rate variability in patients with hypertension and diabetes. Methods 90 cases of essential hypertension were selected as hypertension group, 92 cases of hypertension combined with diabetes mellitus were selected as hypertension combined with diabetes group, 90 cases of healthy people were selected as control group at the same time. Glycated hemoglobin (HbA1c), serum creatinine (Cr) and fasting plasma glucose (FBG) were determined. 24 h dynamic electrocardiogram (ECG) and ambulatory blood pressure (BP) were synchronously measured, and each index was calculated automatically by computer. The differences of general condition, heart rate variability and blood pressure variability in the three groups were compared, and the correlation between the indexes was analyzed by Pearson. Results The differences of HbA1c and FBG in the three groups were statistically significant, there was no significant difference in gender, age, blood lipid and Cr. The indexes of heart rate variability of hypertension group and hypertension combined with diabetes group were lower than those of the control group (P＜0.05), and the indexes of heart rate variability of hypertension combined with diabetes group were lower than those of the hypertension group (P＜0.05). The differences of SBP, DBP, SSD, dSSD, nSSD, sCV and dCV in the three groups were statistically significant (P＜0.05), which were higher in the hypertension group and the hypertension combined with diabetes group than those in the control group (P＜0.05), and which were higher in the hypertension combined with diabetes group than those in the hypertension group (P＜0.05), and the differences of DSD, dDSD and nDSD had no significance in the three groups (P＞0.05). There was a negative correlation between 24 h mean systolic blood pressure standard deviation SSD and SDNN, SDANN, rMSSD, SDNNIndex and PNN50 in hypertension group and hypertension combined with diabetes group. Conclusions Compared with hypertensive patients, the impairment of autonomic nervous function in patients with hypertension combined with diabetes group is more obvious. The blood pressure variability and heart rate variability of follow-up patients are helpful to assess the condition and improve the prognosis.

Abstract:Aim To investigate the relationship between serum phospholipid transfer protein (PLTP) activity levels and severity of coronary artery lesions in patients with coronary heart disease (CHD). Methods 202 patients with chest pain were recruited in the Xishan People’s Hospital of Wuxi from June 2015 to June 2016, and these patients were divided into two groups based on coronary angiography (CHD group and non-CHD group). PLTP activity was measured with an assay kit, and the severity of coronary artery disease assessed by Gensini score was analyzed. Results PLTP activity levels and Gensini score in CHD group were significantly higher than that in non-CHD group (90.3(67～118)mg/dL vs 77.4 (54.6～103.3)mg/dL, P<0.05; 29(8～48) vs 2(0～6), P<0.001). PLTP activity levels and Gensini score were higher in patients aged 70～79 years old,male and diabetes than patients aged 60～69 years old, female and non-diabetes. Multiple linear regression analysis showed that PLTP activity levels were predictor for Gensini score after adjusting for the other risk factors (Beta=0.356, P<0.001). ROC curve was for PLTP activity levels to detect CHD patients with upper Gensini score quartile, and the area under the curve was 0.749(P<0.001). Conclusion Serum PLTP activity levels were predictive for the severity of coronary artery lesions in patients with CHD.

Abstract:Aim To explore the value of adenosine triphosphate (ATP) stress ^99mTc-Methoxyisobutylisonitri(^99mTc-MIBI) gated myocardial single-photon tomography (SPECT) imaging for making risk stratificatioin in the patients with intermediate coronary lesions. Methods In this study, 100 patients with intermediate coronary lesions, diagnosed by coronary angiography (CAG) were involved. The short axis and vertical long axis slices of left ventricular myocardial were divided into 17 segments by ATP stress ^99mTc-MIBI gated myocardial SPECT examination. We evaluated radionuclide distribution of each segment sections of left ventricular myocardium with semiquantitative visual method, calculated summed stress score (SSS), summed rest score (SRS), summed difference score (SDS), and ischemia segment number of left ventricular, analyzed the severity myocardial ischemia, and made risk stratificatioin, compared with the severity and vessel narrowness of intermediate coronary lesions. Results A total of 100 patients with intermediate coronary lesions were enrolled in this study, including 62 patients with single intermediate coronary lesion, 33 patients with double-vessel lesions, and 5 patients with three. The risk stratification of patients with intermediate coronary lesions was divided into 45 cases (45.0%) in low risk group, 34 cases in middle risk group (34.0%) and 21 cases in high risk group (21.0%). The proportion of high-risk patients in multi-vessel disease group was higher, SSS and SDS were higher than those in single-vessel disease group. And there were significant differences of SSS and SDS between the two groups (P＜0.05), but there was no significant difference of SRS (P＞0.05). All patients had a total of 143 intermediate coronary lesions, including 84 LADs, 29 LCXs, 30 RCAs. SSS, SDS, SRS were not significantly different between the three groups (P＞0.05). There was no significant difference in risk stratificatioin between patients with mild stenosis and moderate stenosis. Narrowness has no correlation with SSS, SRS and SDS in all intermediate coronary lesions regardless LAD, LCX or RCA. The result of ATP stress ^99mTc-MIBI gated myocardial SPECT was significantly higher than that in dynamic electrocardiogram (76.0% vs 39.0%, P＜0.05). Conclusion ATP stress ^99mTc-MIBI myocardial SPECT imaging could make risk stratification more precisely in the patients with intermediate coronary artery lesions, and guide clinical treatment.

Abstract:polyunsaturated fatty acids can play an anti-atherosclerosis effect by regulating blood lipid profile, improving endothelial function, anti-inflammatory, improving plaque stability and other mechanisms. This study reviewed the structure, metabolism and the possible anti-atherosclerosis mechanisms of ω-3 polyunsaturated fatty acid.

Abstract:After reperfusion, the condition of the ischemic myocardium aggravates, which causes the irreversible change of myocardium ultrastructure, resulting in the further damage of cardiac function, metabolism and electrophysiology; It is called myocardial ischemia reperfusion injury (MIRI). Cell apoptosis is closely related to the development of most cardiovascular diseases. There is cell apoptosis in many heart diseases, such as heart failure, myocardial infarction, arrhythmia, cardiomyopathy and so on. Cell poptosis plays an important role in the progress of MIRI. ATP-sensitive potassium channel (KATP) participates in a variety of activity and function regulation of cells, and it has the role of dilating blood vessels and myocardial protection, so increasingly becoming a hot spot of concern. However, the detailed mechanism of KATP regulating cell apoptosis is not yet clear. This review summarizes the recent progress in the role and possible mechanisms of KATP mediated MIRI.