AMI Group Research Articles

Identification of Vinculin as a Potential Diagnostic Biomarker for Acute Aortic Dissection Using Label-Free Proteomics.

Acute aortic dissection (AAD) is an emergent vascular disease. Currently, its diagnosis depends on clinical and radiological investigations but lacking of serum biomarkers. In this study, we aimed to identify potential serum biomarkers for AAD using label-free proteomics approach. A total of 90 serum samples were collected from three groups: patients with acute aortic dissection (AAD, n = 30), patients with acute myocardial infarction (AMI, n = 30), and healthy controls (n = 30), and the first four samples from each group were selected for label-free proteomics analysis. Using label-free approach, a total of 22 differentially expressed proteins were identified in the serum samples of the AAD group, of which 15 were upregulated and 7 were downregulated as compared to the AMI and healthy control groups. The most prominent increased protein was vinculin, which was selected to validate in total samples. The level of vinculin was significantly elevated in AAD patients (15.8 ng/ml, IQR: 9.3-19.9 ng/ml) than that in AMI patients (8.6 ng/ml, IQR:5.3-11.4 ng/ml) and healthy volunteers (5.3 ng/ml, IQR:2.8-7.6 ng/ml), P < 0.0001. Furthermore, the concentration of vinculin both increased in type A and B dissection. At the early stage of AAD, vinculin maintained a high level to 48 hours compared with that of AMI. Our study demonstrated that vinculin may play a role in the early diagnosis of AAD.

Patients with Unstable Atherosclerosis Have More Echolucent Carotid Plaques Compared with Stable Atherosclerotic Patients: A 3-D Ultrasound Study

Using a novel 3-D ultrasound system, we aimed to determine differences in carotid plaque size and echogenicity in two atherosclerotic groups. Seventy patients admitted with acute myocardial infarction (aMI) and 69 patients known with chronic peripheral arterial disease (cPAD) were included. The cPAD group had larger plaque volumes (median: 70.24 mm3, interquartile range [40.12–135.61] vs. 55.41 mm3 [4.24–84.31], p = 0.004), thicker plaques (2.45 mm [1.85–3.25] vs. 1.99 mm [1.55 – 2.64], p = 0.005) and higher gray-scale medians (GSMs) (mean: 71.75, standard deviation: 21.55 vs. 60.99 [24.09], p = 0.006) than the aMI group. After adjustment for traditional risk factors, the difference persisted for thickness and volume. The difference in GSM persisted after adjustment for volume only. Patients with stable atherosclerotic disease had larger and brighter carotid plaques compared with unstable atherosclerotic patients. 3-D ultrasound may prove useful in identifying thromboembolic risk.

Cholinergic Stimulation Improve Renal Inflammation After Myocardial Infarction in Spontaneously Hypertensive Rats

IntroductionCardiovascular diseases (CVD) are the leading causes of morbidity and mortality worldwide, and among them, myocardial infarction (MI) has a significant influence on renal function. There is a close relationship between cardiac and renal function, several studies have shown that cardiorenal interactions occur in both directions. This clinical condition, called cardiorenal syndrome, increases the risk of cardiovascular events. It was recently described that the autonomic nervous system (ANS) modulates inflammation, and that vagus nerve stimulation decreases the inflammatory response in different models of septic and aseptic inflammation –this reflex pathway is called as “Cholinergic anti‐inflammatory pathway”. Previous studies by our group have demonstrated that increased vagal activity through administration of pyridostigmine (PY) (acetylcholinesterase pharmacological antagonist) reduces early inflammatory process in myocardial tissue after AMI in normotensive rats, but little is known about vagal modulation and renal inflammation. The aim of this study was to evaluate the effect of cholinergic stimulation on the modulation and expression of the cells inflammatory in renal tissue triggered by AMI in spontaneously hypertensive rats (SHR).Material and MethodsSHR male rats were four groups: SHAM group: S (n = 5), treated group: PY (n=7), infarcted group: I (n = 6) and infarcted and treated group: I + PY (n = 5). All the animals were anesthetized and submitted to thoracotomy and the infarcted and treated groups were subjugated to left coronary artery ligation. Treatment with PY started one hour after thoracotomy, extending until day 7. The total lymphocytes (CD3+) and helper lymphocytes (CD4+) was analysed though immunohistochemistry and expression (TNF‐α, IL‐6, IL‐10) for RT‐qPCR in renal tissue. Statistical analysis, all data were represented as means ± the standard error of the mean (SEM) was performed using GraphPad Prism and one‐way analysis of variance (ANOVA). Values of p&gt; 0.05 were considered statistically significant.ResultsThere were no statistically significant differences in the CD3+ T lymphocytes counts in the renal parenchyma in all four groups. Regarding the CD4+ lymphocytes, the I group showed significant increase lymphocytes than S group (p&lt;0.05). Treatment with PY significantly increased CD4+ lymphocytes group I + PY (p&lt;0.01) when compared with I group. The renal inflammatory profile was confirmed by the significant increase in TNF‐α and IL‐6 mRNA levels (p &lt;0.05), but not IL‐10 when compared to the SHAM group. Treatment with PY significantly decreased the expression of TNF‐α (p &lt;0.01) and IL‐6 (p &lt;0.05) mRNA when compared to the AMI group in renal tissue.ConclusionThe present study demonstrates that cholinergic stimulation with pyridostigmine was able to induces greater anti‐inflammatory cell recruitment and to decrease inflammatory cytokines mRNA expression in renal tissue at day 7 post‐MI in rats.Support or Funding InformationConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Programa de Pós‐Graduação stricto sensu UNINOVE

Serum complement C1q level is associated with acute coronary syndrome

Background and objectivesThe complement system plays an important role in the development of acute coronary syndrome (ACS). Complement C1q is an important initial component of the classical complement pathway and closely related to many chronic inflammatory diseases, including atherosclerosis (AS). We aimed to determine whether there was association between serum complement C1q and the severity of coronary stenosis. Subjects and methods320 patients who underwent coronary arteriography (CAG) were stratified into non-ACS group (control group, n = 74), unstable angina group (UA group, n = 197) and acute myocardial infarction group (AMI group, n = 49) according to the severity of coronary stenosis and clinical manifestations. The severity of coronary stenosis was represented in Gensini score, and serum complement C1q level was compared using immunity transmission turbidity among three groups. ResultsThe level of complement C1q in AMI group was lower significantly than control group and UA group (P < 0.05), but there was no correlation between serum complement C1q and Gensini score (β=-0.086, P = 0.125). In nitrate-taking patients, serum complement C1q had a negative association with Gensini score (r=-0.275, P = 0.001), and in non-smokers, there was also a negative correlation (β=-0.159, P = 0.036). After calibrating smoking, drinking or statins, the serum complement C1q levels of control group, UA group and AMI group decreased in sequence (P < 0.05). Logistic regression analysis showed that the decreasing of serum complement C1q was an unfavorable factor for acute myocardial infarction (OR=0.984, 95 %CI=0.972∼0.997, P = 0.015) and for ACS (OR=0.984, 95 %CI=0.971∼0.984, P = 0.025) in drinking patients. Regrettably, ROC curve suggested that the accuracy in diagnosing coronary atherosclerotic heart disease by serum complement C1q was low (AUC=0.568, 95 %CI= 0.492-0.644, P = 0.076, sensitivity 73.6 %, specificity 58.1 %). ConclusionSerum complement C1q in ACS patients, in particular AMI patients, showed lower level. This finding suggests further decrease of complement C1q level in ACS patients may be a contributory factor to instability or rupture of atherosclerotic plaques. Combined with other clinical indicators, it can be helpful to predict the risk and severity of coronary stenosis.

Inflammation-Related MicroRNAs Are Associated with Plaque Stability Calculated by IVUS in Coronary Heart Disease Patients.

Objectives This study aimed to investigate the association between inflammation-related microRNAs (miR-21, 146a, 155) and the plaque stability in coronary artery disease patients. Methods The expression of miR-21, 146a, and 155 was measured by real-time PCR in 310 consecutive patients. The level of hs-CRP, IL-6, and IL-8 was measured by ELISA. The plaque stability of coronary stenotic lesions was evaluated with intravascular ultrasound (IVUS). Results (1) The levels of hs-CRP, IL-6, and IL-8 were significantly increased in the UAP and AMI groups compared with the CPS group (P < 0.01). (2) The expression of miR-21 and miR-146a in peripheral blood mononuclear cells (PBMCs) and plasma was significantly higher in CAD patients compared with non-CAD patients, whereas the miR-155 expression in PBMCs and plasma was significantly lower in patients with CAD. (3) The miR-21 expression in PBMCs was higher in UAP and AMI groups compared with CPS group. The miR-146a expression in PBMCs was higher in SAP, UAP, and AMI groups than in CPS group. Although the level of miR-155 in PBMCs was lower in SAP, UAP, and AMI groups than in CPS group. The expression patterns of miR-21, miR-146a, and miR-155 in plasma were consistent with those of PBMCs. (4) The expressions of miR-21 and miR-146a in PBMCs and plasma were significantly higher in the vulnerable plaque group than those in stable plaque group. While miR-155 in PBMCs and plasma was significantly lower in vulnerable plaque group compared with stable plaque group. (5) The levels of miR-21 and miR-146a in PBMCs and plasma were significantly higher in soft plaque group than in fibrous plaque group and calcified plaque group. However, miR-155 in PBMCs and plasma was significantly lower in soft plaque group. Conclusions The expression of miR-21 and miR-146a are associated with the plaque stability in coronary stenotic lesions, whereas miR-155 expression is inversely associated with the plaque stability.

Clinical value of ARG1 in acute myocardial infarction patients: Bioinformatics-based approach

BackgroundIn this study, we aimed to explore key genes as biomarker for diagnosis AMI through using Bioinformatics tools. MethodsGSE4648 and GSE60993 were downloaded from Gene Expression Omnibus (GEO). DEGs in GSE4648 and GSE60993 were selected to run GO enrichment, KEGG pathway, and PPI network. Hub genes in DEGS of GSE4648 and GSE60993 were selected out according to Molecular Complex Detection (MCODE) and overlapping genes were further screened out. Finally, the most important gene of coincide genes was used for deeper clinical study of patients with AMI. ResultsA total of 41 and 173 DEGs were screened out in GSE4648 and GSE60993 respectively. GO and KEGG analysis showed similar biological process, cellular Component and molecular function of these two group DEGs. PPI network of these two group DEGs were built and 19 key genes of GSE4648 were selected out according to MCODE, while 48 key genes of GSE60993 were selected out. Overlapping genes of these 19 and 48 genes included PLAUR, ARG1, FOS, and IL1R2, and fold change (FC) of ARG1 was the biggest. Therefore, ARG1 was detected in 46 controls and 115 AMI patients by ELISA, and ARG1 was significantly upregulated in AMI group. Pearson correlation analysis indicated ARG1 was positive correlated with gensini score (R = 0.378). ROC curve revealed that area under ROC curve (AUC) of ARG1 was 77.6%. ConclusionTherefore, ARG1 might play an important role in the development of AMI and could be used as biomarker of AMI.

Comparison between angiotensin-converting enzyme inhibitor and angiotensin receptor blocker after percutaneous coronary intervention

BackgroundThe inhibitors for renin-angiotensin-aldosterone system (RAAS) have different mechanisms of action in coronary artery disease (CAD). This study sought to compare the clinical outcomes between angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) therapy in patients with CAD undergoing contemporary percutaneous coronary intervention (PCI). MethodsBased on the National Health Insurance claims data in South Korea, patients aged 18 years or older who had undergone PCI between July 2011 and June 2015 were enrolled. The study participants were classified either as patients with acute myocardial infarction (AMI, n = 21,747) or angina (n = 28,708). And according to the post PCI discharge medications, patients were categorized into ACEI and ARB therapy groups. The primary endpoint was all-cause death, and the two groups were compared using a propensity-score matching analysis. ResultsThe study population had a median follow-up of 2.2 years (interquartile range, 1.2–3.2). In the propensity-score matched AMI group (8341 pairs), the occurrence of all-cause death was significantly lower in the ACEI group than in the ARB group (hazard ratio [HR] of ACEI, 0.823; 95% confidence interval [CI]: 0.715–0.947; p = 0.006). In the propensity-score matched angina group (10,878 pairs), there was no difference in the incidence of the primary endpoint between the ACEI and ARB groups (HR of ACEI, 1.113; 95% CI: 0.986–1.257; p = 0.084). ConclusionsIn this nationwide Korean cohort study, ACEI therapy in patients with AMI and concomitant PCI showed a significant reduction in all-cause mortality rates when compared to that with ARB therapy.

Interleukin-32 increases in coronary arteries and plasma from patients with coronary artery disease

BackgroundInterleukin-32 (IL-32) is a cytokine associated with higher risk of cardiovascular diseases in inflammatory environments. This study aimed to investigate the IL-32 levels in coronary artery disease (CAD) patients. MethodsIL-32 expression in coronary arteries from both normal donors and CAD patients were analyzed. Plasma IL-32, IFN-γ and IL-17 levels in stable angina pectoris (SAP, n = 80) patients, unstable angina pectoris (UAP, n = 96) patients, acute myocardial infarction (AMI, n = 72) patients and patients exhibiting chest pain unrelated to coronary artery disease (NCAD, n = 72) were measured. Additionally, whether plasma IL-32 levels were independent correlated with the presence of CAD was analyzed. ResultsIL-32 was high expressed in atherosclerotic plaques of CAD patients when compared with normal coronary arteries, and macrophages were the major sources of IL-32. Compared with the NCAD group, IL-32, IFN-γ and IL-17 levels were increased in the CAD group and gradually increased through the SAP, UAP and AMI groups. Plasma IL-32 levels were positively correlated with the Gensini score, IFN-γ levels and IL-17 levels in CAD patients. The results of linear regression showed that IL-32 was independently associated with the occurrence of CAD. ConclusionBoth the coronary artery and circulating IL-32 levels were increased in CAD patients and IL-32 may be a marker of noninvasive diagnosis of CAD.

Effects of intravenous phosphodiesterase inhibitors and corticosteroids on severe meconium aspiration syndrome.

Meconium aspiration syndrome (MAS) is a major cause of severe respiratory failure in near- and full-term neonates. Alleviating inflammation is key to successfully treating severe MAS. Phosphodiesterase (PDE) inhibitors are known to play a role in airway smooth muscle relaxation and alveolar inflammation inhibition. This study aimed to investigate the effects of various intravenous (IV) PDE inhibitors and corticosteroids on MAS. MAS was induced in newborn piglets by instilling human meconium in them. The piglets were randomly divided into five groups (n = 5 in each group): (1) control (sham treatment); (2) dexamethasone (Dex) (IV 0.6 mg/kg of dexamethasone); (3) aminophylline (Ami) (IV 6 mg/kg of aminophylline, followed by continuous infusion of 0.5 mg/kg/h of aminophylline; (4) milrinone (Mil) (IV 50 μg/kg of milrinone, followed by continuous infusion of 0.75 μg/kg/h of milrinone); and (5) rolipram (Rol) (IV 0.8 mg/kg of rolipram). The duration of the experimental period was 4 hours. Compared to the control group, all the four treatment groups revealed better oxygenation 3 hours and more after the start of treatment. The Rol group had a significantly elevated heart beat (p < 0.05) and relatively lower blood pressure compared to the other groups during the first 2 hours of the experiment. The Dex group had significantly lower interleukin (IL)-1β levels in the lung tissue compared to the other groups (p < 0.05) and significantly lower IL-6 levels compared to the Ami and Mil groups (p < 0.05). Lung histology showed slightly less inflammation and atelectasis in the Dex group compared to the other groups, but lung injury scores showed no significant between-group differences. Using IV corticosteroids or any type of PDE inhibitors has some beneficial effects in improving oxygenation in MAS. PDE inhibitors are not superior to IV corticosteroids; in fact, adverse cardiovascular effects occur with the phosphodiesterase type 4 (PDE4) inhibitor. Further investigations are required before using IV corticosteroids and PDE inhibitors in future clinical application.

Effect of Ischemic Preconditioning and Postconditioning on Exosome-Rich Fraction microRNA Levels, in Relation with Electrophysiological Parameters and Ventricular Arrhythmia in Experimental Closed-Chest Reperfused Myocardial Infarction.

We investigated the antiarrhythmic effects of ischemic preconditioning (IPC) and postconditioning (PostC) by intracardiac electrocardiogram (ECG) and measured circulating microRNAs (miRs) that are related to cardiac conduction. Domestic pigs underwent 90-min. percutaneous occlusion of the mid left anterior coronary artery, followed by reperfusion. The animals were divided into three groups: acute myocardial infarction (AMI, n = 7), ischemic preconditioning-acute myocardial infarction (IPC-AMI) (n = 9), or AMI-PostC (n = 5). IPC was induced by three 5-min. episodes of repetitive ischemia/reperfusion cycles (rI/R) before AMI. PostC was induced by six 30-s rI/R immediately after induction of reperfusion 90 min after occlusion. Before the angiographic procedure, a NOGA endocardial mapping catheter was placed again the distal anterior ventricular endocardium to record the intracardiac electrogram (R-amplitude, ST-Elevation, ST-area under the curve (AUC), QRS width, and corrected QT time (QTc)) during the entire procedure. An arrhythmia score was calculated. Cardiac MRI was performed after one-month. IPC led to significantly lower ST-elevation, heart rate, and arrhythmia score during ischemia. PostC induced a rapid recovery of R-amplitude, decrease in QTc, and lower arrhythmia score during reperfusion. Slightly higher levels of miR-26 and miR-133 were observed in AMI compared to groups IPC-AMI and AMI-PostC. Significantly lower levels of miR-1, miR-208, and miR-328 were measured in the AMI-PostC group as compared to animals in group AMI and IPC-AMI. The arrhythmia score was not significantly associated with miRNA plasma levels. Cardiac MRI showed significantly smaller infarct size in the IPC-AMI group when compared to the AMI and AMI-PostC groups. Thus, IPC led to better left ventricular ejection fraction at one-month and it exerted antiarrhythmic effects during ischemia, whereas PostC exhibited antiarrhythmic properties after reperfusion, with significant downregulaton of ischemia-related miRNAs.

Neuregulin-1 protects cardiac electrical conduction through downregulating matrix metalloproteinase-9 and upregulating connexin 43 in a rat myocardial infarction model.

Aims: Neuregulin-1 (NRG-1) is a member of the epidermal growth factor family, and has an important role in cardiomyocyte development and myocardial regeneration. The aim of this study was to determine the protective effect of NRG-1 on cardiac electrical conduction in a rat myocardial infarction (MI) model. Methods: Thirty-three adult male SPF SD rats were randomized into three groups: sham-operated (n=9), acute myocardial infarction (AMI, n=12), and the NRG-1-treated (NRG-1, n=12) groups. All rats were sacrificed on day 8 after inducing MI. The 6-lead electrocardiograms (ECG) were recorded pre-operatively and eight days after operation, and analyzed. The expression levels of matrix metalloproteinase (MMP)-9 and gap junction protein connexin 43 (Cx43) in the infarcted myocardium were measured by Western blotting, and its in-situ distribution was evaluated using immunohistochemistry. Results: The PR, QRS and QT intervals were significantly prolonged in the AMI group compared to the sham operated animals (P<0.05, P<0.01 and P<0.01 respectively), and the PR and QRS intervals were partially restored in the NRG-1-treated rats (P<0.01 and P<0.01 compared to AMI group). Similarly, the increased levels of MMP-9 in the AMI group was restored upon NRG-1 treatment. The myocardial expression of Cx43 was decreased significantly in the AMI group, and was upregulated by NRG-1 treatment. Conclusions: NRG-1 attenuates MI-induced dysfunctional cardiac electrical conduction by downregulating MMP-9 and upregulating Cx43.

Effect of CD14 polymorphisms on the risk of cardiovascular disease: evidence from a meta-analysis

BackgroundCD14 polymorphisms are associated with an increased risk of cardiovascular events. So far, many studies have been conducted, whereas the results were not always consistent.Materials and methodsTwenty-six articles involving thirty-seven datasets were recruited to evaluate the association between rs2569190 (9413 patients and 7337 controls), C-159T (4813 patients and 2852 controls) polymorphisms and cardiovascular diseases in a meta-analysis. The random or fixed effect models were used to evaluate the pooled odds ratios (ORs) and their corresponding 95% confidence intervals.ResultsThe strongest association was observed between rs2569190 and CVD in overall population (T vs. C, OR = 1.169, 95% CI: 1.087–1.257, p = 2.44 × 10− 5). Analysis after stratification by ethnicity indicated that rs2569190 was related to CVD in East Asian population (T vs. C, OR = 1.370, 95% CI; 1.226–1.531, p = 2.86 × 10− 8) and a potential relationship in European (T vs. C, OR = 1.100, 95% CI: 1.019–1.189, p = 0.015). In the stratification of endpoints, the associations were found in CHD subgroup (T vs. C, OR = 1.357, 95% CI: 1.157–1.592, p = 2.47 × 10− 7) and in AMI subgroup (T vs. C, OR = 1.152, 95% CI: 1.036–1.281, p = 0.009). However, we did not find any association between C-159T polymorphism with cardiovascular disease under any model.ConclusionsThe SNP rs2569190 significantly contribute to susceptibility and development of cardiovascular disease, particularly in the East Asian population and in the subtype CHD group, in addition, a potential association was observed in the AMI group, T allele acts as a risk factor for cardiovascular disease.

Impact of diabetes mellitus in patients undergoing contemporary percutaneous coronary intervention: Results from a Korean nationwide study.

ObjectivesDespite an obvious improvement in the treatment of coronary artery disease (CAD) and survival rate of patients with CAD during recent decades, diabetes mellitus (DM) is still considered a risk factor of adverse clinical outcomes in these patients. Therefore, we sought to evaluate the clinical implications of DM in patients with CAD who underwent contemporary percutaneous coronary intervention (PCI).MethodsBased on the National Health Insurance claims data in South Korea, patients aged 18 years or older who had undergone PCI for the diagnosis of CAD between 2011 and 2015 were analyzed. Patients were classified into the DM (n = 26,872) and non-DM (n = 54,243) groups. The primary endpoint was all-cause mortality, and it was compared between the two groups via a propensity score matching analysis.ResultsThe study population was categorized as patients with angina (n = 49,228) or acute myocardial infarction (AMI, n = 31,887). The study population had a median follow-up of 2.1 years (interquartile range, 1.1–3.2). After the propensity score matching analysis, 8,157 and 4,266 pairs of patients with angina and AMI were identified, respectively. In the matched angina group, the incidence of all-cause death was significantly higher in patients with DM (adjusted hazard ratio [aHR]: 1.30; 95% confidence interval [CI]: 1.16–1.47; p<0.001) than in those without DM. Moreover, in the matched AMI group, the incidence of all-cause death was significantly higher in patients with DM (aHR: 1.35; 95% CI: 1.19–1.53; p<0.001) than in those without DM.ConclusionsIn patients undergoing contemporary PCI in Korea, the presence of DM was associated with poorer clinical outcomes.

Rosuvastatin protects acute myocardial infarction rats through autophagy regulation via AMPK signaling

Objective: To investigate the effects of rosuvastatin (RSV)on autophagy and apoptosis of myocardial cells in rats with acute myocardial infarction. Methods: SD rats were divided into control (Sham group), acute myocardial infarction model rats (AMI group), AMI rats treated by RSV with the dose of 5 mg·kg(-1)·d(-1) (RSV group), AMI rats treated by RSV and AMPK inhibitor Compound C at the same time (RSV+ CC group)(n=8) based on simple random sampling methods.Rat myocardial cell line H9c2 was divided into control group, Hypoxia group, Hypoxia+ RSV group, Hypoxia+ RSV+ Compound C group, Hypoxia+ AICAR (AMPK activator)group.After 6 weeks, the rats were examined by hemodynamics, and pathological observation of myocardial tissue by HE staining was also carried out.RT-PCR/Western blot were used to detect the expression of Beclin1, p62, BAX and Bcl-2 mRNA or protein of different groups in vivo and in vitro.Western blot was used to detect the expression of mTOR and AMPK protein and phosphorylation in cardiac tissue of each group. Results: In this study, the rat model of acute myocardial infarction was successfully prepared.Compared with the AMI group, the myocardium inflammation in the RSV group was alleviated, the LVMI decreased significantly, LVSP increased significantly, LVEDP decreased significantly, HR decreased significantly, the absolute value of dP/dTmax and -dP/dTmax increased significantly.The levels of Beclin1 and Bcl-2 mRNA were significantly up-regulated from 0.43 to 2.01 and 0.30 to 0.72, the expression of p62 and BAX mRNA decreased in half, the phosphorylation level of AMPK was significantly up-regulated, and the level of mTOR phosphorylation significantly reduced(P<0.05). These changes were antagonized by AMPK inhibitors in RSV+ CC group.In vitro experiments showed that, after RSV intervening, the levels of Beclin1 and Bcl-2 mRNA and protein in the myocardial cells of Hypoxia group significantly increased in triple, while the expressions of p62 and BAX mRNA and protein significantly decreased above a half.The above changes were consistent with those of the AMPK activator group and were antagonized by Compound C. Conclusion: RSV can effectively promote autophagy and decrease apoptosis in rat heart after myocardial infarction through AMPK/mTOR pathway.

The expression level of miR-155 in plasma and peripheral blood mononuclear cells in coronary artery disease patients and the associations of these levels with the apoptosis rate of peripheral blood mononuclear cells.

The aim of the study was to investigate the expression of miR-155 in plasma and peripheral blood mononuclear cells (PBMCs), the effects of miR-155 on the apoptosis rate of PBMCs and the extent of coronary stenosis in coronary artery disease patients. Seventy chest pain patients were divided into three groups by symptoms, signs, auxiliary examination and coronary arteriography: 21 cases in the acute myocardial infarction group (AMI), 23 cases in the Angor pectoris group (AP) and 26 cases in the control group (CT). The peripheral blood mononuclear cells of the patients in the three groups were separated for cell culture. Annexin V/propidium iodide (PI) was performed to analyze cell apoptosis. RT-qPCR was used to evaluate the expression level of miR-155 in plasma and PBMCs. There were significant differences on the expression of miR-155 in plasma and PBMCs, the apoptosis rate of PBMCs, Gensini score and the extent of coronary stenosis among the three groups (P<0.05). The expression of miR-155 in plasma and PBMCs in AMI and AP group were lower than CT group while the AMI group was lower than the AP group (P<0.05). The apoptotic rate of PBMCs, Gensini score and the extent of coronary stenosis of the AMI and AP groups were higher than CT group while the AMI group was higher than the AP group (P<0.05). The expression of miR-155 in plasma was positively correlated with PBMCs, but negatively correlated with the apoptosis rate of PBMCs, Gensini score and the extent of coronary stenosis. The apoptosis rate of PBMCs in patients with coronary heart disease was positively correlated with the degree of coronary artery stenosis and Gensini score. In conclusion, in the patients with coronary heart disease the apoptosis rate of PBMCs was increased and the expression of miR-155 in plasma and PBMCs cells was decreased, which were correlated with the severity of coronary heart disease.

DIFFERENCE IN PRESCRIBED MEDICATIONS AND 5-YEAR MORTALITY BETWEEN FIRST NATIONS AND NON-FIRST NATIONS ANGIOGRAPHY PATIENTS

Improved development and uptake of pharmacological therapies for the management of cardiovascular disease symptoms has contributed to lower mortality rates. This study sought to explore guideline-recommended prescribing of medications among First Nations (FN) and non-FN patients following angiography and whether any differences in rates of filling prescriptions over the following year (proxy for medication use) is associated with CVD mortality disparities between populations. All index angiography patients (≥18 years) during 2000/0 -2008/09 in Manitoba were identified using health administrative data. Patients were separated by whether or not their angiography occurred during an AMI hospitalization (AMI and non-AMI groups). Medications dispensations were observed for beta-blockers, ACE-inhibitors, statins, and clopidogrel within three-months of angiography. Medication possession ratios (MPR) for each were calculated over a one-year period starting from the date of the first dispensation and patients were assigned to 1 of 4 categories based on their MPR: 1) not dispensed; 2) low MPR (<40% MPR); 3) intermediate MPR (≥40% to ≤79% MPR); 4) high MPR (≥80% MPR). Cox proportional models examined differences in all-cause and cardiovascular mortality using a model that controlled for socio-demographic variables and comorbidities, and a second model that also included the MPR categories. In the AMI group, the proportion of non- FN patients with high MPRs was greater for each medication class except for clopidogrel compared to FN patients. In the non-AMI group, the proportion of FN patients with high MPRs was greater for clopidogrel and ACE-inhibitors compared to the non-FN patients. In the first adjusted model, FN patients had an increased cardiovascular mortality in both groups (HR AMI group = 1.57; 95%CI: 1.05-2.35; HR non-AMI group = 1.50; 95%CI: 1.17-1.94; Table 1). Adding the MPR variable attenuated the relationship in both groups and the hazard was only significantly higher for FN patients in the non-AMI group (HR = 1.40; 95%CI: 1.08-1.80). Similarly, with the all-cause mortality model that included MPR variable, only FN patients in the non-AMI group were significantly higher (HR model 1 = 1.52; 95%CI: 1.28-1.79; HR model 2 = 1.45; 95%CI; 1.23-1.71). There were differences in the patterns the use of prescribed guideline-recommended medications between FN and non-FN patients. FN patients were less likely to have high MPRs for some of the medication classes, but not all. FN patients had higher cardiovascular mortality than non-FN patients, which was consistent with differences in medication utilization only in the AMI group.

The application of intestinal stomas in mesenteric ischemia

Objective: To evaluate the application of intestinal stomas in mesenteric ischemia (MI) according to the concept of damage control surgery. Methods: Clinical data of 59 MI patients received intestinal stomas at Jinling Hospital, Nanjing University School of Medicine from January 2010 to June 2017 were analyzed retrospectively. There were 41 male and 18 female patients aging of (51±14) years (ranging from 20 to 86 years). All the patients were divided to two groups according to the degree of bowel ischemia: acute MI group (AMI, bowel necrosis, n=43) and chronic MI group (CMI, bowel stricture, n=16). The medium time from onset to consult of AMI was 7(12) days (M(Q(R))) and the time of CMI was 80(51) days. After the resection of irreversible ischemic intestine, ostomy was carried out for all 59 patients. Patients received oral anticoagulation, enteral nutrition and succus entericus reinfusion therapy for about 6 months after discharge. Then definite surgery to restore digestive tract was preferred. Results: In AMI group, APACHEⅡ score in admission was (16±3). The length of infarcted intestine resected was (160±95) cm, normal bowel left was (220±106) cm. Twelve patients had complications during first post-operation period including sepsis (n=8), acute renal failure (n=4), acute respiratory distress syndrome (n=4), short bowel syndrome (n=4). 30-day mortality was 18.6%. Total 30 patients received operation to restore the continuity of intestinal tract after 202(42) days and APACHEⅡ score was 4±2. Two patients suffered from sepsis and were cured after anti-infection. In CMI group, APACHEⅡ score was 16±3 and NRS2002 score was more than 3. The length of infarcted intestine resected was (43±33) cm. All patients had restored the continuity of intestinal tract after 176 (47) days. No major complications occurred during the first and second post-operation period. Conclusions: According to damage control surgery, after early revascularization, patients with acute intestinal necrosis should be treated with infarcted bowel resection and stomas. Besides, second operation to restore the continuity of intestinal tract should be conducted after nutritional support for 6 months. Patients with ischemic enteropathy who cannot be corrected with severe malnutrition should achieve stomas during first operation.

Clinical role of serum Copeptin in acute coronary syndrome.

ObjectiveTo assess the role of Copeptin in diagnosis of acute myocardial infarction in troponin-blind period.Subjects and methodsThis study was conducted on 40 patients who presented to emergency department complaining of chest pain and were highly suspicious to have acute cardiac ischemia, in addition to 10 subjects serving as a healthy control group. Blood samples were collected for determination of CK-MB, cTnI and Copeptin. These were measured twice (in patients’ group); at 3 h and then at 6–9 h from admission time.ResultsThe first sample revealed a non-significant difference between UA group and AMI group as regards CKMB and troponin, however, high significant difference was found as regards Copeptin (Z = 5.29, P < 0.001). Moreover, ROC curve analysis of serum Copeptin for discriminating AMI group from UA group in the first sample showed diagnostic sensitivity and specificity of 100%.In conclusionDetermination of copeptin in early diagnosis of AMI has diagnostic value being superior to a conventional cTn-I within the first three hours after acute chest pain.

Death anxiety in patients with myocardial infarction or cancer.

ObjectiveThe aim of this study was to find out the level of death anxiety among 3 groups: patients with acute myocardial infarction, patients with cancer and healthy individuals in two training and research hospitals; also to evaluate its relationship with several sociodemographic and clinical variables.Materials and methodThis study was conducted with one hundred and eighty persons (108 male, 72 female) who have been referred to cardiology or oncology departments and the healthy individuals. Participants completed sociodemographic and clinical data form, State and Trait Anxiety Inventory (STAI-I, STAI-II), Thorson Powell Death Anxiety Scale (TPDAS), Death Depression Scale (DDS).ResultsParticipants included in the present study were 40% female with an average age of 53.48 for whole group. The mean TPDAS score for patients with AMI was 51.60 ± 16.40, for patients with cancer 37.10 ± 10.23 and for healthy individuals 43.40 ± 13.35. In AMI group there were positive correlations between STAI-I and TPDAS, DDS scores and also between STAI-II and DDS. In cancer group positive correlations were between STAI-I, II and TPDAS, DDS. TPDAS and DDS were positively correlated in all three groups. Women and participants who were unemployed scored higher on DDS.ConclusionIn this study patients with AMI had higher death anxiety than patients with cancer or healthy individuals. Generally death anxiety was related with education, employment and socioeconomic status. Prospective studies carefully searching for different variables in different medical groups would reveal and help us to understand the importance of death anxiety and its impact on courses of physical and mental disorders.

Assessment of CD-147 Level in women with coronary heart disease after menopause

In the current study, Seventy menopausal women have CHD were admitted to the Coronary Care Unit of AL-Sadder Teaching Hospital in AL-najaf AL-Ashraf during the period from January to April/2016 for the ages were ranging from 40 to 69 years old. The samples were divided into three groups (SA 25, UA 22, AMI 23), while the healthy group was composed of 20.The current study indicated a significant increase(p 0.05)of serum CD147concentration in AMI group as compare with UA group and SA group of CHD, While serum of E2 concentration showed a significantly decrease (p<0.05)in AMI compare with UA and SA groups of CHD. The result showed also a negative correlation between E2 and CD147.