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Abstract:Although the human heart is metabolically one of the most active organs in the body, the heart has a relatively low ATP content. Accordingly, the heart has low tolerance for energy deficiency. The regulation of myocardial metabolism is linked to multiple factors, including substrates concentration, hormone concentrations, coronary blood ?ow and nutritional status of the tissue, etc. Dysglycemia, hyper/hypo-thyroidism and hyperuricemia are all involved in the pathophysiological process of heart energy metabolism. Although hyperglycemia on admission is a powerful independent predictor of survival in patients with coronary heart disease, intervention to normalize glycemia has yielded inconsistent results. Indeed, recent large randomized controlled trials have failed to show a significant decrease in mortality with intensive glycemic control, or have even shown an increased mortality risk. “Heart and metabolism” is a rising discipline. We choose “Heart and Metabolism” as the topic of the special columm in this issue and want to have it account for a modest spur to induce others to come forward with valuable contributions.

Abstract:Objective To compare the different effects of glucose solution and glucose-insulin-potassium (GIK) solutions on myocardial injury after percutaneous coronary intervention (PCI). Methods A total of 100 patients with identified coronary heart disease undergoing PCI in our hospital from October to November 2012 were prospectively enrolled in this study. They were randomly divided into two matched groups, with 50 in each group. They were all given conventional treatment as guideline recommended. Patients in control group received intravenous injection of 500ml 10% glucose solution at 2 to 4h before PCI, while those in experimental group had GIK solutions (containing 500ml 10% glucose, 10ml 10% potassium chloride and 12 U insulin) instead of glucose solution. Serum contents of creatine phosphokinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI) were measured before and one day after PCI. Results There was no significant difference in all baseline clinical data between the two groups. The experimental group had very significant higher blood glucose than control [(11.9±3.6) vs (5.3±3.7)mmol/L, P＜0.001] before PCI, and the value was also higher after PCI [(8.8±4.2) vs (5.1±3.9)mmol/L, P＜0.001]. There was no case from the experimental group with blood glucose ≤5.0mmol/L, but there were 7 (14.0%) found in control group. Both groups had obvious increased CK-MB and cTnI levels after PCI, but control group had more significant increases, with patients had more increased CK-MB by 1- to 3-folds and cTnI by over 3-folds (both P＜0.05). Conclusion Glucose solution applied preoperatively protect patients more significantly against myocardial injury when compared with GIK solutions.

Abstract:Objective To determine the effect of pre-operative blood glucose level on the incidence of contrast-induced nephropathy (CIN) in patients with ST-segment elevation myocardial infarction undergoing urgent percutaneous coronary interventions (PCI). Methods A total of 745 ST-segment elevation myocardial infarction patients undergoing urgent coronary interventions in our department from October 2008 to May 2012 were enrolled in this study. All patients received low osmolar nonionic contrast media. Renal function was evaluated by serum creatinine concentration at baseline and each day for the following 3d to analyze the effect of pre-operative glucose level on the incidence of CIN. Results Among the 745 patients (530 males and 215 females), there were 156 patients having CIN, with an incidence of 20.9%. There was no significant difference in the age, diabetes mellitus, high sensitivity C-reactive protein (hs-CRP), blood glucose level, left ventricular ejection fraction (LVEF), and reperfusion time between the CIN and non-CIN groups (P＜0.05). The patients from the CIN group had significantly higher risk of in-hospital all-cause mortality, cardiac death, and arrhythmias (P＜0.05). Multiple logistic regression analysis showed that blood glucose, hs-CRP, and LVEF were independent risk factors for CIN. Elevated glucose level as variables categorized into quartiles were independently correlated with the development of CIN (P＜0.05). Conclusion Elevated pre-operative glucose level has a close correlation with the development of CIN in patients with ST-segment elevation myocardial infarction undergoing urgent PCI, and increases in-hospital mortality as an independent risk factor for CIN.

Abstract:Objective To observe the features and cause of thyroid hormones changes in acute myocardial infarction(AMI) patients, and evaluate their value in the short-term prognosis the patients. Methods Totally 172 patients diagnosed as AMI patients without previows thyroid disorder in our hospital from October 2010 to October 2012 were enrolled, and 92 unstable angina pectoris patients were included as control group. The levels of free tri-iodothyronine (FT3), free tetra-iodothyronine (FT4), thyroid stimulating hormone (TSH), high sensitivity C-reactive protein (hs-CRP) and blood lipids were determined in all patients on the next day of admission. Cardiovascular mortality events of these patients in hospital were also recorded. Results Serum FT3, FT4 and TSH in the AMI group were (2.33±0.47)ng/L, (12.5±2.4)ng/L and (1.32±0.99)μU/L, respectively. While in the angina group, serum FT3, FT4 and TSH were (2.80±0.54)ng/L, (11.5±1.4)ng/L and (2.19±1.07)μU/L, respectively. The levels of FT3 and TSH were significantly lower in the AMI group than in the angina group (P＜0.05). No significant difference was observed in the level of FT4 between the two groups (P＞0.05). The levels of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and hs-CRP were obviously higher in the AMI group than in the angina group (P＜0.05, P＜0.01). There was a linear correlation of FT3 with age, TC, and hs-CRP in the AMI group. When receiver operating characteristics (ROC) analysis was used to evaluate the prognostic value of FT3 for cardiovascular mortality events in the AMI group during hospitalization, the area under the ROC curve was 0.852, suggesting well prognosis value of FT3. There was no significant difference no matter in lipids and thyroid hormone levels in the AMI group between those with and without ST elevation (P＞0.05). Conclusion AMI patients have decreased levels of FT3 and TSH. Serum change of FT3 is a predictor for in-hospital cardiovascular mortality events.

Abstract:Objective High serum uric acid level (SUA) and chronic kidney disease (CKD) are the risk factors that resulted in coronary heart disease (CHD). It is not clear whether the interaction between SUA and CKD is the risk factor of CHD. This study aimed to assess the correlation between severity of coronary artery stenosis and CKD with different level of SUA [man＞417μmol/L (7.0mg/ml), woman＞357μmol/L (6.0mg/ml)]. Methods A total of 214 randomly selected patients with coronary arteriography-identified CHD who admitted in our center from January 2011 to September 2012 were subjected in this study. The patients with CHD were grouped according to the value of estimated glomerular filtration rate (eGFR). The patients’ serum uric acid, clinical features, serum creatinine, inflammatory factors and some metabolism related variables were analyzed. eGFR was calculated with the formula of MDRD. The definition of CKD was defined as whether the patient’s kidney was impaired or not and GFR＜60ml/(min·1.73m2) for more than 3 months. The severity of coronary artery stenosis was assessed by the result of Gensini scale with coronary angiography. All P values were two-tailed and P＜0.05 was deemed statistically significant. Results Among the 214 patients enrolled, 82 cases (38.3%) had CKD. eGFR was negatively correlated with the severity of coronary artery stenosis (r＝-0.536, P＜0.001). SUA was positively correlated with the severity of coronary artery stenosis in CKD patients (r＝0.29, P＜0.01). Logistic regression analysis showed that the independent risk factors of CKD were SUA (OR＝1.22, 95% CI 1.09-1.37, P＜0.001), age (OR＝1.11, 95% CI 1.10-1.14, P＜0.001), coronary artery stenosis (OR＝0.83, 95% CI 0.79-0.85, P＜0.001), and history of hypertension (OR＝1.90, 95% CI 1.40-2.60, P＜0.001). Conclusion Hyperuricemia may be an important factor of aggravating coronary artery stenosis in CKD, and may be involved in every stage of the disease.

Abstract:Thyroid dysfunctions have close relationship with cardiovascular diseases. As thyrotropin distribution shifts progressively toward higher levels with age, specific reference ranges for thyroid function tests should be established for the elderly. Recently, more and more attention is paid to subclinical thyroid diseases. Some evidence shows that subclinical hyperthyroidism exerts important effects on cardiac structure and functions, and it also increases the risk of atrial fibrillation. However, subclinical hypothyroidism might be a potential risk factor for heart failure, ischemic heart disease and all-cause mortality, although it is still controversial. Cardiovascular disease associated with hyper- and hypothyroidism will be improved when thyroid function returns to normal. Since physiologically decreased thyroid activity to some extent might have favorable effects in the very old patients, more clinical evidence should be provided to illuminate the effects of subclinical thyroid dysfunction on cardiovascular diseases; and large, randomized clinical trials are needed to identify the target populations of individuals with subclinical thyroid dysfunction who will be benefited after thyroid treatment.

Abstract:A number of epidemiological studies and clinical trials had shown that hyperuricemia was an independent risk factor for morbidity and unfavorable prognosis of coronary heart diseases, and it also might contribute to the incidence and development of coronary atherosclerosis (AS); and thus, uric acid lowering drugs had anti-ischemic effects in myocardial ischemia. Therefore, treating hyperuricemia would be a new target to prevent coronary AS. However, some other studies had obtained different conclusions revealing there was no correlation between hyperuricemia and coronary heart disease. Thus, pathogenicity of uric acid was still lack of evidence. Meanwhile, high levels of uric acid were found in atherosclerosis plaque in pathological studies. In some in vitro studies, uric acid induced reactive oxygen species production in endothelial cells and vascular smooth muscle cells (VSMCs), which led to endothelial dysfunction and proliferation of VSMCs, and contributed to the formation of AS. However, uric acid was also proved as antioxidant in some other studies. Therefore, the relationship between hyperuricemia and coronary heart disease was still controversial.

Abstract:A series of large-scale clinical trials have shown that statin therapy has definite clinical benefit in patients with cardiovascular diseases. However, some recent clinical researches indicate that statins increase the risk of developing diabetes mellitus. Therefore, the relationship between diabetes mellitus and statin has raise concerns. Some clinical evidence shows although the patients receiving statins have higher risk of diabetes mellitus, they also gain significant benefit from statin therapy by decreasing cardiovascular events, and the harms of new-onset diabetes are outweighed by reductions in cardiovascular benefit. As the risk of increasing new-onset diabetes is higher in the elderly than in the young, it is needed to monitor blood glucose for the elderly, especially for those using high-dose statins. At present, there is no evidence demonstrating that the development of statin-associated diabetes will result in increased risk of major cardiovascular events.

Abstract:Cell death is the important cytological mechanism for organ injury and repair resulting from various diseases, and its 3 forms, necrosis, apoptosis and autophagy, are all involved in the pathophysical development of myocardial infarction (MI). Dysglycemia, not matter hyperglycemia or hypoglycemia is associated with higher morbidity and mortality in patients with MI. However, there are few studies focusing on the relationships among cell death, dysglycemia and MI. In this review, we summarized the mechanisms of cell death, the role of cell death in MI and the regulatory effects of dysglycemia in myocardial cell death. We brought forward that hyperglycemia and hypoglycemia can induce myocardial cell death, which plays a significant role in the development of MI through different pathways. Dysglycemia might induce poor prognosis after MI through regulating myocardial cell death. Therefore, for the MI patients with dysglycemia, regulation of the pathways of myocardial cell death, might be a new approach to improve prognosis of MI patients.

Abstract:Along with the deepening of the research on cardiovascular disease, the elevation of blood glucose in patients with acute coronary syndrome (ACS) has aroused some attention. The patients with elevated blood glucose usually have diabetes or impaired glucose tolerance, suggesting that they may, more or less, have the potential of insulin resistance and islet beta cell insufficiency. Thus, they have poor prognosis through other mechanisms. However, there were not many reports about ACS accompanied with high blood glucose. In this paper we reviewed the incidence, causes, and adverse effects on the cardiovascular system and the prognosis of ACS accompanied by acute high glucose after our comprehensive review of related studies in recent years.

Abstract:Objective To investigate the clinical relative risk factors of venous thromboembolism (VTE) in systemic lupus erythematosus (SLE) patients. Methods Twenty-seven consecutive SLE patients with VTE in our hospital within January 2008 to February 2012 were enrolled as the thrombosis group, while the control group recruited 27 hospitalized SLE patients without history of thrombosis, whose environmental factors, such as sex, age, body mass index (BMI), and life style, matched to the thrombosis group. Univariate analysis was used to compare the clinical risk factors of venous thrombosis [blood platelet count, immunological function, complement, and whether accompanied with hypoproteinemia, lupus nephritis, renal insufficiency, nephrotic syndrome, renal hypertension, proteinuria, or hematuria], and laboratory indexes [C-reactive protein (CRP), D-dimer, white blood cell count, activated partial thromboplastin time (APTT), prothrombin time (PT), and fibrinogen (FIB)] between the two groups. Results The thrombosis group had significant higher incidence of accompanied hypoproteinemia (70.37%), lupus nephritis (74.07%), renal insufficiency (70.37%), nephrotic syndrome (55.56%), renal hypertension (66.67%) than the control group (P＝0.003, 0.000, 0.000, 0.027, 0.029, respectively). CRP [(7.19±9.23)mg/L] and D-dimer [(6.32±5.75)mg/L] levels were both higher in the thrombosis group than in the control group (P＝0.004, 0.000, respectively). Conclusion Hypoproteinemia, lupus nephritis, renal insufficiency nephrotic syndrome and renal hypertension may be the clinical risk factors of VTE in SLE patients. CRP and D-dimer may contribute to the diagnosis.

Abstract:Objective To investigate the risk factors for severe multiple organ failure (MOF) in acute myocardial infarction (AMI) patients so as to identify the high-risk patients as early as possible. Methods A retrospective study was carried out on 6674 Chinese AMI patients with a mean age of (62.94±13.63) (ranging from 18 to 101) years who were admitted in our hospital in the past 18 years (from January 1993 to June 2011). They were divided into 2 groups according to having severe MOF or not. Logistic regression analysis was used to analyze the development of severe MOF with demographic and comorbidity variables. Results Of 6674 hospitalized AMI patients, 83(1.24%) progressed to MOF. The hospital mortality was significantly higher in the severe MOF group than in the Non-MOF group (49.40% vs 8.13%, P＜0.001). On the basis of logistic regression analysis, age, pneumonia, cardiogenic shock and chronic renal failure were independent risk factors for severe MOF with an adjusted OR of 2.76 (95% CI: 1.26-6.03, P＝0.011 for 65 to 74 years old), 4.85 (95% CI: 2.96-7.94, P＜0.001 for≥75 years old), 4.27 (95% CI: 2.68-6.82, P＜0.001), 2.24 (95% CI: 1.08-4.63, P＝0.030), and 2.09 (95% CI: 1.09-4.01, P＝0.027), respectively. Receiver-operation characteristic (ROC) curve analysis showed the model had good discriminative ability [area under the curve (AUC)＝0.83, 95%CI: 0.75-0.89, P＜0.001). Conclusion Though MOF is less common in AMI patients, it always results in extremely poor prognosis. For high risk patients, early individual treatments for comorbidity and complication can effectively prevent the occurrence of MOF.

Abstract:Objective To investigate the impact of superficial calcification of coronary target lesions on the procedures and outcomes of percutaneous coronary intervention (PCI). Methods A total of 61 consecutive patients with 61 target lesions who underwent intravascular ultrasound (IVUS) to determine the characteristics of lesions before PCI and stent implantation in our department from May to December 2012 were enrolled in this study. According to the results of IVUS, these lesions were divided into 2 groups, superficial calcified group and non-superficial calcified group. The intervention procedures, clinic and imaging features after PCI were compared between the two groups. Results There were 29 lesions in superficial calcified group and 32 in non-superficial calcified group. The stenosis area was higher in superficial calcified group than in the control group [(75.70±7.11)% vs (68.78±5.56)%, P＝0.019]. The postoperative stent symmetry and expansion were significantly lower in the superficial calcified group than in non-superficial calcified group [(0.85±0.06) vs (0.90±0.02), P＝0.016; (0.68±0.14) vs (0.82±0.10), P＝0.021, respectively]. The minimus stent diameter [(2.51±0.43) vs (2.76±0.29)mm], minimum stent area [(5.86±1.82) vs (6.73±1.40)mm2) and relative lumen gain (1.26±0.68) vs (1.37±0.72)] were also tended to be smaller in superficial calcified group than in the non-superficial calcified group, though without significant difference. There was no difference in the procedural complications incidence. No major adverse cardiac event was seen in this cohort of patients. Conclusion Compared with non-superficial calcification of coronary target lesions, the superficial calcification may interfere the appropriate stent symmetry and optimal stent expansion.

Abstract:Objective To investigate the safety of the elderly patients with hypertension during analgesic gastroscopy by monitoring the changes of their vital signs and responses during operation process. Methods A total of 100 hypertension patients with age over 80 undergoing gastroscopy were prospectively divided into experimental group (receiving analgesic gastroscopy) and control group (receiving conventional gastroscopy), with 50 cases in each group. During the process of gastroscopy, the heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), saturation of blood oxygen (SaO2), operating time and adverse reaction were monitored and compared between the two groups. Results The HR, SBP, DBP, and SaO2 were decreased during analgesic gastroscopy (P＜0.01), and all of these indexes returned to normal levels after operation. The SBP, DBP, and HR were increased (P＜0.01) and SaO2 was decreased (P＜0.01) during conventional gastroscopy. The SaO2 was higher in analgesic gastroscopy group than in conventional gastroscopy group, but there was no significant difference between the two groups (P＞0.05). Analgesic gastroscopy group had shorter operating time than in conventional gastroscopy group, but there was no significant difference between the two groups (P＞0.05). Analgesic gastroscopy group had significantly fewer adverse reactions and were more comfortable during operation when compared with conventional gastroscopy group (both P＜0.01). Conclusion Analgesic gastroscopy is safe and comfortable for elderly patients with hypertension.

Abstract:Objective To investigate the relationship of the subcellular localization of calcyclin binding protein (CacyBP/SIP) with cell cycle in gastric cancer cell line SGC7901. Methods Double thymidine block was used to synchronize the cell cycle in SGC7901 cells. Flow cytometry was employed to identify the cell cycle synchronization. The localization of CacyBP/SIP protein was observed at the different phase of cell cycle by immunofluorescence staining. The expression levels of total protein and nucleoprotein CacyBP/SIP were detected by Western blotting at different cell cycles. Results Double thymidine block arrested the SGC7901 cells at G1/S phase, then the cells were at S phase in 4h after drug withdrawal. Most of cells got into G2 phase in 8 to 12h after culture and re-entered G1 phase in 16h. Immunofluorescence staining found that CacyBP/SIP was mainly distributed in the cytoplasm at G1/S phase, but then gathered into the perinuclear or nuclear at G2 phase, which indicates that CacyBP/SIP had the characteristics of nuclear translocation of cell cycle dependence. The total expression level of CacyBP/SIP protein had no obvious change at each phase, but the nuclear CacyBP/SIP protein at G2 phase was highest than at any other phases. Conclusion CacyBP/SIP displays cell cycle dependent translocation, and may participate in regulating G2/M phase.

Abstract:Objective To determine the effect of fibroblast growth factor 2 (FGF2) injection on the behavior and astrocytes activation in the hippocampus in the rats of posttraumatic stress disorders (PTSD). Methods Single prolonged stress (SPS) was used to establish the PTSD rat model. Then a single high dose of FGF2 (50μg/kg) was given by intraperitoneal injection in 7d after the model establishment. Another 7d later, open-field test (OF) and elevated plus maze (EPM) test were used to evaluate rats’ spontaneous activity, anxiety and depression behaviors. Immunofluorescence staining and double immunofluorescence Western blotting were used to detect the expression of glial fibrillary acidic protein (GFAP) in the hippocampus in normal, PTSD, and FGF2 treated rats for astrocytes activation and expression level respectively. Results FGF2 treatment resulted in significantly decreased anxiety and depression behaviors compared with the PTSD rats, and enhanced the expression of GFAP obviously in the hippocampus. Conclusion FGF2 obviously attenuates anxiety and depression behaviors in the rats after SPS, which might be due to its enhancement in astrocyte activity in the hippocampus.

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Abstract:Morbidity and mortality of coronary artery disease associated with type 2 diabetes mellitus (T2DM) are in a rising trend. Some related evidence shows that insulin itself may have a dual role in this situation, and insulin is now still considered as a controversial role in T2DM patients due to its contribution to coronary atherosclerotic lesions. In recent years, results from some major observational studies are not consistent with those of randomized controlled trials. Nowadays, the “dual signal pathway hypothesis” of insulin is more popular in the mechanism of insulin in T2DM accompanied with coronary heart disease. It is of great importance to further elucidate the mechanism of insulin in T2DM with coronary heart disease.