Pathogenesis Of Acute Myocardial Infarction Research Articles

Identifying key genes associated with acute myocardial infarction.

Background:This study aimed to identify key genes associated with acute myocardial infarction (AMI) by reanalyzing microarray data.Methods:Three gene expression profile datasets GSE66360, GSE34198, and GSE48060 were downloaded from GEO database. After data preprocessing, genes without heterogeneity across different platforms were subjected to differential expression analysis between the AMI group and the control group using metaDE package. P < .05 was used as the cutoff for a differentially expressed gene (DEG). The expression data matrices of DEGs were imported in ReactomeFIViz to construct a gene functional interaction (FI) network. Then, DEGs in each module were subjected to pathway enrichment analysis using DAVID. MiRNAs and transcription factors predicted to regulate target DEGs were identified. Quantitative real-time polymerase chain reaction (RT-PCR) was applied to verify the expression of genes.Result:A total of 913 upregulated genes and 1060 downregulated genes were identified in the AMI group. A FI network consists of 21 modules and DEGs in 12 modules were significantly enriched in pathways. The transcription factor-miRNA-gene network contains 2 transcription factors FOXO3 and MYBL2, and 2 miRNAs hsa-miR-21-5p and hsa-miR-30c-5p. RT-PCR validations showed that expression levels of FOXO3 and MYBL2 were significantly increased in AMI, and expression levels of hsa-miR-21–5p and hsa-miR-30c-5p were obviously decreased in AMI.Conclusion:A total of 41 DEGs, such as SOCS3, VAPA, and COL5A2, are speculated to have roles in the pathogenesis of AMI; 2 transcription factors FOXO3 and MYBL2, and 2 miRNAs hsa-miR-21-5p and hsa-miR-30c-5p may be involved in the regulation of the expression of these DEGs.

High expression of long chain acyl-coenzyme A synthetase 1 in peripheral blood may be a molecular marker for assessing the risk of acute myocardial infarction.

The current study aimed to investigate whether the increased expression of long chain acyl-coenzymeA synthetase 1 (ACSL1) in peripheral blood leukocytes (PBL) may be a molecular marker for the genetic evaluation of acute myocardial infarction (AMI). The mechanism of action of ACSL1 in the pathogenesis of AMI was also investigated. A total of 75 patients with AMI and 70 individuals without coronary heart disease were selected to participate in the present study. The demographic and clinical information of the enrolled subjects was recorded. Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to measure the expression of ACSL1 at the mRNA and protein levels. It was demonstrated that the expression of ACSL1 mRNA and protein in PBL was increased in patients with AMI compared with controls. Logistic regression analysis indicated that ACSL1 expression in PBL was an independent risk factor of AMI. There was a significant positive association between the level of ACSL1 expression and the degree of atherosclerosis in the coronary artery. Furthermore, patients with AMI exhibited an increased risk of atherosclerosis due to increased fasting blood glucose, total cholesterol, triglyceride and lipoprotein levels and decreased high-density lipoprotein levels, compared with controls. Therefore, the current study demonstrated that ACSL1 expression was increased in the PBLs of patients with AMI. The elevated expression of ACSL1 acts an independent risk factor of AMI and may act as a potential biomarker when determining the risk of AMI.

心身症の疫学-急性心筋梗塞の発症と心身医学的要因の関連性に関する実態調査(心身症の疫学)

心身症の疫学-急性心筋梗塞の発症と心身医学的要因の関連性に関する実態調査(心身症の疫学)

Development of a novel flow cytometric immunobead array to quantify VWF: Ag and VWF: GPIbR and its application in acute myocardial infarction.

Both von Willebrand disease (VWD) and acute myocardial infarction (AMI) involve quantitative and qualitative changes in von Willebrand factor (VWF). Our objective was to develop a rapid and precise flow cytometric immunobead array (FCIA) to quantify VWF antigen (VWF:Ag) and ristocetin-triggered platelet glycoprotein Ib binding (VWF:GPIbR) and apply it in a clinical setting. Microbeads, coated with monoclonal antibodies for SZ29 or SZ151 IgG, were incubated with diluted plasma. VWF-binding microbeads were detected with FITC-conjugated sheep-anti-human VWF IgG by flow cytometry. Plasma VWF:Ag and VWF:GPIbR levels in normal controls (CTL; n=105), patients with VWD (n=21), and patients with AMI (n=146) were tested by FCIA and ELISA in parallel. ADAMTS13 activity and VWF multimer analyses were also implemented. Our novel FCIA showed a strong correlation with the ELISA results (VWF:Ag, r=.855; VWF:GPIbR, r=.813). The intra-assay coefficient variations (CVs) of VWF:Ag-FCIA and VWF:GPIbR-FCIA were 9.2% and 7.7%, respectively, and the interassay CVs were 12.6% and 13.5%, respectively. Plasma VWF:Ag and VWF:GPIbR levels were significantly higher in patients with AMI than in CTL (P<.0001), whereas the ratios of ADAMTS13/VWF:Ag and ADAMTS13/VWF:GPIbR were significantly lower (P<.0001). Levels of plasma ultra-large VWF (UL-VWF) were dramatically increased in patients with AMI. The novel VWF:Ag and VWF:GPIbR-FCIA assays were found to be simpler, more specific, and more accurate than the classical ELISA method. In addition, elevated VWF:GPIbR and UL-VWF may contribute to the pathogenesis of AMI.

P 129 - Alteration of phospholipidome profile in the heart of an animal model of acute myocardial infarction

Acute myocardial infarction (AMI) is one of the main causes of mortality and health care cost in the world. Development of valuable clinical tools can help in diagnosis in the early stage of disease or predicting recovery. The pathogenesis of AMI is multifactorial and lipids can have an active role in this pathology and be good candidates as biomarkers of initial stages of the disease and extent of tissue damage. Changes in phospholipidome profile were observed in cardiomyoblasts as model of AMI. However, lipidomics studies in AMI are scarce. In this work, a mass spectrometry-based lipidomics approach was used to evaluate changes in phospholipid profile in heart of murine models under ischemia, ischemia-reperfusion and starvation conditions. Differences in fatty acids and phospholipid profiles, related to the course of AMI were observed. An increase of C16:0, C18:0, C20:4 and C22:6, and a decrease of C18:2 were observed in ischemia-reperfusion and starvation. An increment of PL bearing FA 22:6, such as PC(18:0/22:6), PE(16:0/22:6), and PE(18:0/22:6), occurred in the same conditions. These PL can be precursors of anti-inflammatory lipids (e.g. resolvins) involved in AMI recovery. Therefore, lipidomics profiling by mass spectrometry can offer valuable information to understand AMI that can be exploited for diagnosis and prognosis.

Serum Magnesium Levels in Acute Myocardial Infarction

BACKGROUND: Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complication like arrhythmia. Magnesium improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death. It improves vascular tone, peripheral vascular resistance, after load and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen derived free radicals, improves endothelial function and inhibits platelet function including platelet aggregation and adhesion. OBJECTIVE: To know the relationship between the serum magnesium levels and arrhythmias in patients with acute myocardial infarction. METHOD: By using simple random method, 50 cases of acute myocardial infarction, admitted in Coimbatore Medical College and Hospital. RESULTS: There is a significant difference in the magnesium levels in patients with arrhythmias and without arrhythmias. CONCLUSION: In acute myocardial infarction, patients with low magnesium levels are more prone to get arrhythmias. So magnesium treatment can be considered in patients of acute myocardial infarction with low magnesium levels.

Некоторые особенности патогенеза острого инфаркта миокарда при необструктивном поражении коронарных артерий

Некоторые особенности патогенеза острого инфаркта миокарда при необструктивном поражении коронарных артерий

Involvement of Serum Matrix Metalloproteinase-9 in the Pathogenesis of Acute Myocardial Infarction

Objectives: Prior studies indicate that matrix metalloproteinase-9 (MMP-9) plays a key role in pathogenesis of plaque rupture. The objective of this study was to evaluate the involvement of serum MMP-9 enzyme at pathogenesis of the plaque rupture in coronary atherosclerosis. Methods: The study enrolled 80 consecutive patients who underwent percutaneous coronary intervention in our institution. Inclusion in the case group (n = 40) required a ruptured coronary atherosclerotic plaque confirmed by conventional angiography, whereas inclusion in the control group (n = 40) required stable coronary atherosclerosis. Serum MMP-9 levels were determined by ELISA. Cardiac Infarction Injury Score (CIIS) by electrocardiogram and Gensini score (Coronary Angiographic Scoring System) were utilized for assessing the severity of coronary artery disease. Results: The average level of MMP-9 was significantly higher in the case group than in the control group (396±155 ng/mL vs. 223±87 ng/mL, p&lt;0.001) with further demonstration that MMP-9 is an independent predictor of plaque rupture (β = 0.985, p&gt;&lt;0.001). MMP-9 is well correlated with Gensini and CIIS score (r = 0.552, p &gt;&lt;0.01 and r = 0.340, p&gt;&lt;0.01, respectively). Furthermore, serum MMP-9 enzyme significantly increased in accordance with the severity of the myocardium damage (p &gt;&lt;0.01) by CIIS score. Conclusion: MMP-9 plays a role at pathogenesis of plaque rupture in coronary atherosclerosis.&gt;&lt;0.001) with further demonstration that MMP-9 is an independent predictor of plaque rupture (β = 0.985, p&lt;0.001). MMP-9 is well correlated with Gensini and CIIS score (r = 0.552, p &gt;&lt;0.01 and r = 0.340, p&gt;&lt;0.01, respectively). Furthermore, serum MMP-9 enzyme significantly increased in accordance with the severity of the myocardium damage (p &gt;&lt;0.01) by CIIS score. Conclusion: MMP-9 plays a role at pathogenesis of plaque rupture in coronary atherosclerosis.&gt;&lt;0.001). MMP-9 is well correlated with Gensini and CIIS score (r = 0.552, p&lt;0.01 and r=0.340, p&lt;0.01, respectively). Furthermore, serum MMP-9 enzyme significantly increased in accordance with the severity of the myocardium damage (p&lt;0.01) by CIIS score. Conclusion: MMP-9 plays a role at pathogenesis of plaque rupture in coronary atherosclerosis.

Radiofrequency Renal Denervation Protects the Ischemic Heart via Inhibition of GRK2 and Increased Nitric Oxide Signaling.

Rationale:Catheter-based renal denervation (RDN) is currently under development for the treatment of resistant hypertension and is thought to reduce blood pressure via interruption of sympathetic pathways that modulate cardiovascular function. The sympathetic nervous system also plays a critical role in the pathogenesis of acute myocardial infarction and heart failure.Objective:We examined whether treatment with radiofrequency (RF)-RDN would protect the heart against subsequent myocardial ischemia/reperfusion injury via direct effects on the myocardium.Methods and Results:Spontaneously hypertensive rats received either bilateral RF-RDN or sham-RDN. At 4 weeks after RF-RDN (n=14) or sham-RDN (n=14) treatment, spontaneously hypertensive rats were subjected to 30 minutes of transient coronary artery occlusion and 24 hours –7 days reperfusion. Four weeks after RF-RDN, myocardial oxidative stress was markedly attenuated, and transcription and translation of antioxidants, superoxide dismutase 1 and glutathione peroxidase-1, were significantly upregulated compared with sham-RDN spontaneously hypertensive rats. RF-RDN also inhibited myocardial G protein–coupled receptor kinase 2 pathological signaling and enhanced myocardial endothelial nitric oxide synthase function and nitric oxide signaling. RF-RDN therapy resulted in a significant reduction in myocardial infarct size per area at risk compared with sham-RDN (26.8 versus 43.9%; P<0.01) at 24 hours postreperfusion and significantly improved left ventricular function at 7 days after myocardial ischemia/reperfusion.Conclusions:RF-RDN reduced oxidative stress, inhibited G protein–coupled receptor kinase 2 signaling, increased nitric oxide bioavailability, and ameliorated myocardial reperfusion injury in the setting of severe hypertension. These findings provide new insights into the remote cardioprotective effects of RF-RDN acting directly on cardiac myocytes to attenuate cell death and protect against ischemic injury.

Dietary Nitrate and the Epidemiology of Cardiovascular Disease: Report From a National Heart, Lung, and Blood Institute Workshop.

In view of continuing unanswered questions regarding the geographical and demographic distribution of cardiovascular disease, and recent discoveries about the effects of dietary nitrate on cardiovascular physiology, the National Heart, Lung, and Blood Institute (NHLBI) convened a workshop to

Effects of coagulation factors and inflammatory cytokines on development of acute myocardial infarction in patients younger than 60 years

Purpose : To investigate the effects of coagulation factors and inflammatory cytokines on acute myocardial infarction (AMI) development in patients younger than 60 years. Methods : In this study, 60 patients admitted to The First Affiliated Hospital of Dalian Medical University (Dalian, China) with AMI and 30 other subjects matched with the patients for age and ethnicity but without AMI were enrolled. Blood samples were collected from the AMI patients and the control subjects after a 12-h fast. Subsequently, the levels of coagulation factors (F) II (FII), VII (FVII), VIII (FVIII), fibrinogen (Fg) and von Willebrand factor (vWF) in plasma were analyzed by enzyme-linked immunosorbent assay (ELISA). The protein expression levels of these coagulation factors were determined by Western blot analysis. Inflammatory factors including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and interleukin- 6 (IL-6) were also measured by ELISA. Results : FII, FVII, FVIII, Fg and vWF levels in plasm were significantly higher in AMI patients compared with control subjects (p 0.05). However, TNF-α and IL-6 levels in the plasma of AMI patients were significantly higher than those in control subjects (p < 0.05). Conclusion : The results reveal that the pathogenesis of AMI in patients younger than 60 years might be closely related to the high levels of coagulation factors and inflammatory cytokines in the blood. Keywords : Coagulation factor, Inflammatory cytokines, Acute myocardial infarction, C-reactive protein, Tumor necrosis factor-α, Interleukin- 6

ESC working group position paper on myocardial infarction with non-obstructive coronary arteries.

The management of acute myocardial infarction (AMI)1 has evolved over the past century and particularly in the past 50 years. Important milestones include the development of the electrocardiogram, coronary care units, coronary angiography, reperfusion therapies, and troponin assays. These innovations are the foundation of contemporary AMI management strategies that include a diagnosis centred on elevated troponin values associated with corroborative clinical evidence,1 early use of coronary angiography, and reperfusion therapies.2–4 Pivotal in the evolution of these contemporary strategies were the early AMI coronary angiography studies undertaken by DeWood et al. These pioneering studies demonstrated that, in patients presenting with ST elevation myocardial infarction (STEMI), almost 90% had an occluded coronary artery provided that angiography was undertaken within 4 h of chest pain onset.5 In contrast, in AMI patients who did not present with ST elevation (non-ST elevation myocardial infarction or NSTEMI), only 26% had an occluded coronary artery when angiography was performed within 24 h of symptom onset.6 In both of these landmark studies,5,6 >90% of the acute MI patients had angiographic evidence of obstructive coronary artery disease (CAD), underscoring the importance of the atherosclerotic process in the pathogenesis of AMI. Although DeWood's studies underscore the importance of obstructive CAD in AMI, it is fascinating that ∼10% had no significant CAD on coronary angiography. This is confirmed in several large AMI registries7–9 where 1–13% of AMI's occurred in the absence of obstructive CAD thereby eliciting an important set of questions—what is the mechanism of the myocardial damage in these patients? Do these patients differ from those with obstructive CAD? Should they be …

Radiofrequency Renal Denervation Protects the Ischemic Myocardium

The sympathetic nervous system plays a critical role in the pathogenesis of acute myocardial infarction (AMI) and heart failure. This study tested whether pre‐conditioning with radiofrequency renal artery ablation (RF‐ABL) protects the heart against myocardial ischemia/reperfusion (MI/R) in the setting of hypertension. Spontaneously hypertensive rats (SHR) received either bilateral RF‐ABL (n=14) or Sham‐ABL (n=14) (Biosense Webster Stockert 70 RF generator). Four weeks following treatment, hypertensive SHR were subjected to 30 minutes of left coronary artery occlusion. After 24 hours reperfusion, the myocardial infarct size/area‐at‐risk (AAR) were determined. In addition, the left ventricle (LV) was collected for measurement of nitric oxide (NO) metabolites, nitrite (NO2−) and S‐nitrosothiol (RSNO), and oxidative stress. RF‐ABL produced a significant decrease in myocardial infarct size per AAR compared to Sham‐ABL (26.8 vs. 43.9%) and lower plasma cardiac troponin‐I (6.8 vs. 10.3 ng/ml). Cardiac NO2− levels increased from 2.6 to 3.2 nmol/mg and RSNO levels increased from 0.5 to 1.1 nmol/mg following RF‐ABL. Myocardial oxidative stress was markedly attenuated as measured by 8‐Isoprostane, carbonyl content, and MDA levels. Greater transcription (RT‐PCR) of antioxidants, SOD1 and GPX‐1 were also observed following RF‐ABL. These findings translated to a significant increase in 24‐hr survival of RF‐ABL (13 of 14) as compared to Sham‐ABL (8 of 14) SHR to MI/R. Together, these findings demonstrate that in hypertensive SHR, RF‐ABL produced a sustained increase in myocardial NO bioavailability and attenuation of oxidative stress, both of which can contribute to preconditioning the myocardium against subsequent MI/R injury. These findings provide new insights into the remote cardioprotective effects of RF‐ABL in the setting of AMI.Support or Funding InformationBiosense Webster IIS‐175 to DRK &amp; FS; P30 GM103514 to DRK. 1R01 HL092141, 1R01 HL093579, 1U24 HL 094373, &amp; 1P20 HL113452 to DJL.

Matrix Metalloproteinase-9 in the Culprit Coronary Artery and Myocardial No-Reflow

Matrix Metalloproteinases (MMPs) have been implicated in the pathogenesis of acute myocardial infarction (AMI). However, little is known about the association between MMP-9 and myocardial no-reflow. The aim of this study was to evaluate the role of MMP-9 in the culprit coronary artery as a predictor of no-reflow in patients with ST-elevation AMI. Ninety patients with ST-elevation AMI who underwent emergency percutaneous coronary intervention were consecutively recruited in this study. Blood samples were obtained from the extraction catheter placed distal to the culprit lesion at the beginning of percutaneous coronary intervention. No-reflow was defined as a coronary thrombolysis in myocardial infarction flow grade ≤2 after vessel reopening or thrombolysis in myocardial infarction flow 3 with a final myocardial blush grade ≤2. No-reflow was observed in 25 patients (27.8%). Using multiple logistic regression analysis, local MMP-9 levels (odds ratio [OR] = 3.356; confidence interval [CI]: 1.441-5.881; P = 0.007) were found to be a significant risk factor of no-reflow together with lesion length (OR = 6.985; CI: 2.574-11.533; P = 0.009) and time to balloon (OR = 2.143; CI: 1.216-5.901; P = 0.042). Elevation of MMP-9 level in the culprit coronary artery may predict no-reflow in patients with ST-elevation AMI.

English

BACKGROUND: In myocardial infarction, there occurs functional deficit of available magnesium due to trapping of free magnesium in adipocytes. Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complications. Magnesium ions are considered essential for the maintenance of functional integrity of myocardium. The serum magnesium concentration was found to have great significance in acute myocardial infarction. The present study was undertaken to evaluate the prognostic value of serum magnesium in acute myocardial infarction. AIMS AND OBJECTIVES: 1. To evaluate serum magnesium concentration in patients with acute myocardial infarction within 24 hours of presentation and on 7 th day post myocardial infarction. 2. To evaluate validity of serum magnesium as prognostic indicator in acute myocardial infarction. METHODS AND MATERIALS: All cases admitted over a period of 2 years were taken as time bound study (Approximately 50-70 cases by hospital statistics). Serum magnesium was estimated by spectrophotometric method. Difference in serum magnesium levels within 24 hours and on the 7th day were calculated. These values were compared with the control values. RESULTS: We observed statistically significant lower serum magnesium concentration at onset in comparison to control. Serum magnesium gradually raised to normal value by 7 th day. Further, mean serum magnesium on the 1 st and 7 th days in complicated cases was lesser than uncomplicated cases. Difference in serum magnesium levels within 24 hours and on the 7 th day were calculated using Z test and P value was then calculated. These values were compared with the control values. CONCLUSIONS: Serum magnesium levels were found to be lower in acute myocardial infarction cases at presentation within 24 hours as compared to matched controls. Serum magnesium levels were lower in acute myocardial infarction with complication, when compared with acute myocardial infarction without complication. Serum magnesium levels were very low in patients of acute myocardial infarction who expired. Serum magnesium levels raised towards normal values by 7th day. So it can be concluded that measurement

A New Risk Chart of Acute Myocardial Infarction in Men by an Innovative Algorithm: A Pilot Study

Acute myocardial infarction (AMI) is a common and complex disease; pathogenesis of AMI is not completely understood and genetic, clinical and phenotypic variables are involved in the disease’s history. The aim of this paper was to assess: 1) the predictive capacity of Artificial Neural Networks (ANNs) in consistently distinguishing the two different conditions (AMI or control). 2) the identification of the variables with the maximal amount of relevant information for AMI. Genetic variances in inflammatory genes, along with clinical and classical risk factors from 149 AMI patients and 72 healthy subjects were investigated. From the data base of this case/control study 36 genetic, clinical and phenotypic variables were selected. The TWIST system, an evolutionary algorithm able to remove redundant and noisy information from complex data sets, further selected 18 variables. Moreover, fitness, sensitivity, specificity, overall accuracy and areas under the receiver-operating curves (AUC) of the 18 selected variables associated with AMI risk were investigated. Our findings showed that ANNs are useful in distinguishing risk factors selectively associated with the disease. Finally, the new mix of variables, including classical risk factors and genetic markers, generated a new risk cluster of variables able to discriminate between AMI and control subjects with an overall accuracy of 90%. This approach may be used to assess individual AMI risk in unaffected subjects with increased risk of the disease such as, first relative with positive parental history of cardiovascular diseases. Keywords: Acute myocardial infarction, disease’s risk, gender, genotype, phenotype, statistical algorithms.

Plasma angiopoietin-1 level, left ventricular ejection fraction, and multivessel disease predict development of 1-year major adverse cardiovascular events in patients with acute ST elevation myocardial infarction — A pilot study

ObjectivesPatients with acute myocardial infarction (AMI) are frequently complicated with major cardiovascular events (MACEs). Endothelial dysfunction has been found to be involved in pathogenesis of AMI, but its role in development of MACEs after AMI is not clearly investigated. This study aimed to determine whether the plasma markers of endothelial dysfunction could serve as independent predictors for MACEs in patients with AMI. MethodsThis prospective study was conducted from March 2010 to July 2012 and enrolled consecutive 132 patients with acute ST elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (PCI). Plasma levels of thrombomodulin (TM), von Willebrand factor (vWF), angiopoietin (Ang)-1, Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) were measured on day 1 of AMI. The development of MACEs at 1-year follow-up was recorded. ResultPatients with STEMI who developed MACEs had increased heart rate on admission (86±24 vs. 74±20bpm, p=0.006), lower left ventricular ejection fraction (LVEF) (49.0±12.4 vs. 57.2±12.4%, p=0.002), and higher incidence of multivessel disease (66.7% vs. 42.2%, p=0.018) comparing with those without MACEs. Plasma level of Ang-1 was lower in patients with MACEs than in those without (21,165±16,281 vs. 31,411±21,593pg/mL, p=0.018). In multivariate analysis, Ang-1 level<median value (OR 2.977, 95% CI 1.16–7.63, p=0.023), LVEF (OR 0.958, 95% CI 0.92–0.99, p=0.022) and multivessel disease (OR 3.013, 95% CI 1.19–7.60, p=0.019) independently predicted 1-year MACEs. ConclusionDecreased plasma Ang-1 levels on admission, LVEF and multivessel disease independently predicted the development of 1-year MACEs in patients with STEMI. These results suggest that endothelial dysfunction may play an important role in mediating MACEs in patients with STEMI.

Hematological and Biochemical Variations in Myocardial Infarction

Background: The aim of the current study was to assess the hematological and biochemical variations in the serum of myocardial infarction patients and healthy controls. Method: The case-control study included 200 samples collected from Myocardial infarction patients and controls for the analysis the variations of hematological and biochemical. Result: WBC and ESR were increased, whereas, hemoglobin and platelet was decreased in patients as compared with the controls. Serum triglyceride, total cholesterol, LDL increased and decreased HDL in patients as compared with the controls. Copper and potassium showed increased levels whereas, decreased serum albumin, and zinc in patients as compared with the controls. Conclusion: Further detailed investigations on the role of hematological, biochemical, variations in the pathogenesis of acute myocardial infarction are needed.

Levels of thyroid hormone, ferritin and testosterone in Acute Myocardial Infarction (AMI) patients in north India

Background: Thyroid hormone plays a critical role in cardiomyocyte maturation and stress-related cellular responses like AMI. The inhibition of thyroid hormone receptor alfa (TRα) causes down regulation of this hormone in post-ischemic myocardium. On the other hand, ferritin, an inflammatory marker; and testosterone, a hormone which alters lipid profile, also play significant roles in pathogenesis of AMI. The objective of our study was to compare thyroid profile (total T3, T4 and TSH), ferritin, Vitamin B-12, folic acid and testosterone in newly diagnosed male cases of AMI with age-matched controls. We also contrasted these biochemical parameters between AMI subgroups with very low and low left ventricular ejection fraction (LVEF). Methodology: A cross-sectional study was conducted from September, 2012 to February, 2013 at a tertiary care hospital of north India. Newly diagnosed male AMI patients with positive clinical and ECG findings, and CPK MB > 25 U/L (spcetrophotometric method) and Troponin-I ultra > 2ng/ml (chemiimmunofluroscence method) were enrolled as cases (n=43). Cases were further sub-classified into those with very low LVEF ( Result: AMI patients reported significantly lower T3, higher ferritin and lower testosterone level in comparison to control group. On the other hand, cases with lower LVEF ( Conclusion: Our study found down regulation of T3 and testosterone levels, with raised higher ferritin levels in patients suffering from an acute attack of AMI. Key words: AMI, Thyroid hormone, Ferritin, Testosterone.

Proprotein convertase subtilisin/kexin type 9 expression is transiently up-regulated in the acute period of myocardial infarction in rat.

BackgroundThe proprotein convertase subtilisin/kexin type 9 (PCSK9) has been confirmed as a major factor regulating cholesterol homeostasis and has low-density lipoprotein receptor (LDLR) independent effects. In addition, the pathogenesis of acute myocardial infarction (AMI) involves lipids alteration and other acute phase responses. It remains unknown whether the PCSK9 expression is influenced by the impact of AMI. The present study aimed to investigate the changes of PCSK9 concentration using AMI rat model.MethodsAMI (n = 6-8 at each time point) or sham operated (n = 6) adult male rats model were used. Whole blood and liver tissue were collected at 1, 3, 6, 9, 12, 24, 48, and 96 hour (h) post infarction. The plasma PCSK9 concentration was measured by ELISA and lipid profiles were measured by enzymatic assay. The liver mRNA levels of PCSK9, LDLR, sterol response element binding protein-2 (SREBP-2) and hepatocyte nuclear factor 1α (HNF1α) were measured by quantitative real-time PCR.ResultsThe plasma PCSK9 concentration was increased from 12 h to 96 h (P < 0.05 vs. control). Paralleled with the enhanced plasma PCSK9 concentration, the hepatic PCSK9 mRNA expression was up-regulated by 2.2-fold at 12 h and 4.1-fold at 24 h. Hepatic mRNA levels of LDLR, SREBP-2 and HNF1α were all increased and lipid profiles underwent great changes at this acute period.ConclusionsWe firstly demonstrated that PCSK9 was transiently up-regulated in the acute period of AMI, which is also driven by transcriptional factors, SREBP-2 and HNF1α, suggesting that the role of PCSK9 in myocardial injury may be needed further study.