Stress In Acute Myocardial Infarction Research Articles

Global research trends on psychosocial rehabilitation in patients with cardiovascular diseases: A bibliometric analysis using CiteSpace

Cardiovascular diseases (CVDs) pose a serious threat to global public health due to its high prevalence and mortality. Meanwhile, psychosocial rehabilitation (PSR) has gained popularity due to its beneficial effects on the cardiovascular system. There is substantial evidence that PSR is effective in lessening cardiovascular morbidity and mortality in CVD patients. To learn more about the development of PSR, 3,759 publications about PSR and related research were retrieved from the Web of Science (WoS) Core Collection from 1989 to 2022. Then, these publications were analysed using CiteSpace 6.1.R3 (64-bit) W version software in terms of country and institution-based analysis, author co-citation analysis (ACA), keyword analysis, and document co-citation analysis (DCA). The outcomes were elaborated in four aspects. First, the number of annual publications related to PSR has consistently increased in last three decades. Second, country and institution-based analysis showed that a few developed countries such as the United States, England and Canada, and institutions such as the Harvard University, the University of California, and the University of Toronto were the most active countries and institutions in carrying out PSR-related studies. Third, author co-citation analysis (ACA) revealed that Sherry L. Grace from York University had the highest number of publications (35). Her research majorly focused on optimizing post-acute cardiovascular care and its outcomes that contribute to the field of PSR. Frasure-Smith had the highest burst count of 41.39. His research mainly emphasized on the impact of psychological stress in acute myocardial infarction which is related to CVD. Document co-citation analysis (DCA) revealed that epidemiologic evidence was the predominant cluster in the domain of PSR. Fourth, Keyword based analysis showed that keywords such as coronary heart disease, cardiovascular disease, acute myocardial infarction and major depression made outstanding contribution to the PSR field. In conclusion, this study has provided useful information for gaining knowledge about PSR such as identifying potential contributors for researchers interested in the field of PSR, and discovering research trends in PSR, which can provide guidance for more extensive studies related to PSR in the future.

Inflammation and Oxidative Stress Role of S100A12 as a Potential Diagnostic and Therapeutic Biomarker in Acute Myocardial Infarction.

Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases with high morbidity and mortality. Numerous studies have indicated that S100A12 may has an essential role in the occurrence and development of AMI, and in-depth studies are currently lacking. The purpose of this study is to investigate the effect of S100A12 on inflammation and oxidative stress and to determine its clinical applicability in AMI. Here, AMI datasets used to explore the expression pattern of S100A12 in AMI were derived from the Gene Expression Omnibus (GEO) database. The pooled standard average deviation (SMD) was calculated to further determine S100A12 expression. The overlapping differentially expressed genes (DEGs) contained in all included datasets were recognized by the GEO2R tool. Then, functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were carried out to determine the molecular function of overlapping DEGs. Gene set enrichment analysis (GSEA) was conducted to determine unrevealed mechanisms of S100A12. Summary receiver operating characteristic (SROC) curve analysis and receiver operating characteristic (ROC) curve analysis were carried out to identify the diagnostic capabilities of S100A12. Moreover, we screened miRNAs targeting S100A12 using three online databases (miRWalk, TargetScan, and miRDB). In addition, by comprehensively using enzyme-linked immunosorbent assay (ELISA), real-time quantitative PCR (RT-qPCR), Western blotting (WB) methods, etc., we used the AC16 cells to validate the expression and underlying mechanism of S100A12. In our study, five datasets related to AMI, GSE24519, GSE60993, GSE66360, GSE97320, and GSE48060 were included; 412 overlapping DEGs were identified. Protein-protein interaction (PPI) network and functional analyses showed that S100A12 was a pivotal gene related to inflammation and oxidative stress. Then, S100A12 overexpression was identified based on the included datasets. The pooled standard average deviation (SMD) also showed that S100A12 was upregulated in AMI (SMD = 1.36, 95% CI: 0.70-2.03, p = 0.024). The SROC curve analysis result suggested that S100A12 had remarkable diagnostic ability in AMI (AUC = 0.90, 95% CI: 0.87-0.92). And nine miRNAs targeting S100A12 were also identified. Additionally, the overexpression of S100A12 was further confirmed that it maybe promote inflammation and oxidative stress in AMI through comprehensive in vitro experiments. In summary, our study suggests that overexpressed S100A12 may be a latent diagnostic biomarker and therapeutic target of AMI that induces excessive inflammation and oxidative stress. Nine miRNAs targeting S100A12 may play a crucial role in AMI, but further studies are still needed. Our work provides a positive inspiration for the in-depth study of S100A12 in AMI.

MiR-124-3p targeted SIRT1 to regulate cell apoptosis, inflammatory response, and oxidative stress in acute myocardial infarction in rats via modulation of the FGF21/CREB/PGC1α pathway.

To investigate whether miR-124-3p influences cell apoptosis, inflammatory response, and oxidative stress in rats with acute myocardial infarction (AMI) by mediating the SIRT1/FGF21/CREB/PGC1α pathway. A dual-luciferase reporter gene assay was performed to verify the relationship between miR-124-3p and SIRT1. AMI rats were established via coronary artery ligation after injection with agomiR-124-3p, antagomiR-124-3p, and/or SIRT1 siRNA, and triphenyltetrazolium chloride (TTC), HE, and TUNEL stainings were performed. Bio-Plex rat cytokine assays were performed to determine proinflammatory factor levels. qRT-PCR and Western blotting were used to examine the mRNA and protein expression, respectively. The activity levels of antioxidant enzymes in myocardial tissues were also measured. miR-124-3p was confirmed to target SIRT1 in the H9C2 cells. AMI rats exhibited increased miR-124-3p expression and decreased SIRT1 expression in myocardial tissues. HE staining showed a disorganized cell arrangement and inflammatory cell infiltration in the myocardial tissues of the AMI rats, which was more severe in the rats injected with SIRT1 and agomiR-124-3p but was ameliorated in those treated with antagomiR-124-3p. Moreover, the AMI rats in the antagomiR-124-3p group presented with a reduction in infarct area with an increase in antioxidant enzyme activity, Bcl-2 expression, and activation of the FGF21/CREB/PGC1α pathway, as well as a decrease in cell apoptosis rate, Bax and Caspase-3 expression, and levels of proinflammatory factors, effects that were reversed by si-SIRT1. Inhibiting miR-124-3p expression may activate the FGF21/CREB/PGC1α pathway to reduce cell apoptosis, alleviate the inflammatory response, and attenuate oxidative stress in AMI rats by targeting SIRT1. Graphical abstract.

Early reductive stress followed by a late onset oxidative stress in acute myocardial infarction

Early reductive stress followed by a late onset oxidative stress in acute myocardial infarction

P-148 - Early reductive stress followed by a late onset oxidative stress in acute myocardial infarction

Introduction The idea that the cells might suffer from reductive rather than oxidative stress and that such stress may be relevant in pathophysiology has gained momentum. Aim We aimed at studying markers of oxidative stress and damage as well as the expression of antioxidant enzymes in a swine model of acute myocardial infarction (AMI) followed by reperfusion. Results and Discussion We found an increase in the GSH to GSSG ratio, a decrease in protein glutathionylation and a decrease in p38 MAPK phosphorylation after 90 minutes of ischaemia in heart samples. It was accompanied by an increase in the expression of Thioredoxin (TrX) and Peroxiredoxin (PrX) and a decrease in the expression of Glutathione Peroxidase (Gpx). One week after reperfusion an increase in lipid peroxidation, protein glutathionylation and protein carbonylation was accompanied by a massive increase in the expression of TrX, PrX, GPx, Glutathione Reductase (GR) and Glucose 6 Phosphate Dehydrogenase (G6PD). These increments seemed to be Nrf-2 independent and most of them were maintained in the heart samples one month after reperfusion. Conclusion We have found an early reductive stress followed by a late onset oxidative stress in AMI followed by reperfusion.

Essential role for EGFR tyrosine kinase and ER stress in myocardial infarction in type 2 diabetes.

We previously reported that EGFR tyrosine kinase (EGFRtk) activity and endoplasmic reticulum (ER) stress are enhanced in type 2 diabetic (T2D) mice and cause vascular dysfunction. In the present study, we determined the in vivo contribution of EGFRtk and ER stress in acute myocardial infarction induced by acute ischemia (40min)-reperfusion (24h) (I/R) injury in T2D (db-/db-) mice. We treated db-/db- mice with EGFRtk inhibitor (AG1478, 10mg/kg/day) for 2weeks. Mice were then subjected to myocardial I/R injury. The db-/db- mice developed a significant infarct after I/R injury. The inhibition of EGFRtk significantly reduced the infarct size and ER stress induction. We also determined that the inhibition of ER stress (tauroursodeoxycholic acid, TUDCA, 150mg/kg per day) in db-/db- significantly decrease the infarct size indicating that ER stress is a downstream mechanism to EGFRtk. Moreover, AG1478 and TUDCA reduced myocardium p38 and ERK1/2 MAP-kinases activity, and increased the activity of the pro-survival signaling cascade Akt. Additionally, the inhibition of EGFRtk and ER stress reduced cell apoptosis and the inflammation as indicated by the reduction in macrophages and neutrophil infiltration. We determined for the first time that the inhibition of EGFRtk protects T2D heart against I/R injury through ER stress-dependent mechanism. The cardioprotective effect of EGFRtk and ER stress inhibition involves the activation of survival pathway, and inhibition of apoptosis, and inflammation. Thus, targeting EGFRtk and ER stress has the potential for therapy to overcome myocardial infarction in T2D.

The ankle‐brachial pressure index and it's correlation with oxidative stress in Acute Myocardial Infarction

BackgroundIn recent years significant attention has been paid in identifying markers of increased cardiovascular risk, in particular the coronary artery disease. The ankle‐brachial pressure index (ABI), an easily accessible, inexpensive bedside test can be a significant tool to assess the vascular risk in symptomatic and asymptomatic cardiovascular patients. Oxidative stress and lipid peroxidation is thought to play a crucial role in the generation of atherosclerotic lesions of Acute Myocardial Infarction (AMI).ObjectiveTo determine the association between an abnormal ankle brachial index (ABI) and oxidative stress in coronary artery disease (CAD).MethodThe study population included 160 subjects divided in two groups, 90 patients with AMI and 70 age and sex matched healthy subjects as controls. Ankle Brachial Pressure Index (ABI) was measured in all the subjects along with their LDH level. Antioxidant status of the individuals was determined by measuring the serum levels of Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD). Estimation of Malondialdehyde (MDA), a marker of lipid peroxidation was used as a surrogate marker of free radical activity.ResultA significantly low ABI (<0.9) was observed among the AMI patients as compared to healthy controls. Moreover the ABI showed negative correlation with the level of LDH amd MDA in the AMI patient. GPx and SOD were positively correlated with ABI.ConclusionABI calculation would be able to identify more patients at high risk and as such it should be considered routine investigation for cardiovascular risk prediction.Support or Funding InformationTRAVEL GRANT AND REGISTRATION GRANT FINANCIAL ASSISTANCE REQUIRED TO TRAVEL TO CHICAGO.REQUEST TO ORGANIZERS TO PROVIDE ASSISTANCE.

A COMPARATIVE ANALYSIS OF SERUM MALONDIALDEHYDE LEVELS AS A MARKER OF OXIDATIVE STRESS IN ACUTE MYOCARDIAL INFARCTION CASES WITH AND WITHOUT T2DM.

30Jun 2016 A COMPARATIVE ANALYSIS OF SERUM MALONDIALDEHYDE LEVELS AS A MARKER OF OXIDATIVE STRESS IN ACUTE MYOCARDIAL INFARCTION CASES WITH AND WITHOUT T2DM. M.A.Raheem , M.Siraj , Rajashekar Reddy , Syed Azhar Ali , Priyanka T N and M Ishaq. 1. Department of Medicine, Princess Esra Hospital (PEH), Deccan College of Medical Sciences (DCMS), Hyderabad, India. 2. Department of Cardiology, Princess Esra Hospital, DCMS, Hyderabad, India. 3. Prof and HOD, Salar-E-millat Research Centre for Cellular and Molecular Medicine, PEH, DCMS, Hyderabad, India.

Oxidative Stress and Antioxidant Status in Patients of acute Myocardial Infarction before and after Regular Treatment

In acute myocardial infarction (AMI), generation of free radicals contribute to its pathogenesis. We evaluated the extent of oxidative stress and its amelioration in AMI patients after regular treatment and assessed its association with risk factors like dyslipidemia and diabetes mellitus (DM). Plasma MDA level increased (p<0.001) and erythrocyte GSH and plasma vitamin E levels decreased (p<0.001) in AMI patients. On the 5th day of regular treatment MDA level reduced (p<0.001) and erythrocyte GSH and vitamin E levels increased (p<0.001). The rise in MDA and fall in vitamin E levels were significant (p<0.001) in patients with both dyslipidemia and DM in comparison to patients without dyslipidemia or DM. It is concluded that an imbalance exists between oxidant and antioxidant molecules in AMI patients which shifts towards oxidative side and treatment restores this balance. There may be some association between oxidative stress in AMI and risk factors like dyslipidemia and diabetes mellitus.University Heart Journal Vol. 10, No. 2, July 2014; 60-65

Association of Depression and Stress in Acute Myocardial Infarction: a case-control study

<p><strong>Background: </strong>Psychosocial factors have been reported to be independently associated with coronary artery disease (CAD). However, the stress variable is still sub detailed and there are few studies that used coronary angiography (CA) to assess CAD.</p><p><strong>Objectives: </strong>To compare levels of depression, stress and stressful life events in three groups of individuals: post-MI (Myocardial Infarction) patients; patients presenting symptoms and no previous MI, who underwent cardiac catheterization and had non-significant obstructive CAD and individuals with no symptoms of cardiac disease or others diseases.</p><p><strong>Methods:</strong> We conducted a case-control study, with two cases groups and one control group. The study included 105 patients with recent Myocardial Infarction (MI group), 101 patients with cardiac symptoms and normal CA (CS group), and 100 patients without symptoms of disease (NS group). Multivariate logistic regression was used to assess, stress and vital events, with an Odds Ratio of 95% confidence interval (CI), controlling for age, sex, education level, income, social support group, Body Mass Index (BMI), sedentary lifestyle and family history of MI or sudden death.</p><p><strong>Results: </strong>MI patients group showed depression with an OR= 4.47(95% CI, 2:36 to 8:46, p<.001), and stress OR= 5.37(95%CI, 2.94-9.78, p <.001) whereas CS group showed depression: OR= 6.95(95%CI, 3.64-13.28, p <.001) and stress: OR = 9.18 (95%CI, 4.73-17.82, p <.001) compared to patients without symptoms. After adjusting for risk factors: age, sex, education, income, social support, obesity, sedentary lifestyle, family history of MI or sudden death, the OR showed the following variation: in the MI group, depression OR= 2.51 (95%CI, 1:05 to 5:98, p = .038), stress, OR= 8.76(95%CI, 3:48 to 22:01, p <.001), and CS group, depression OR= 3.25(95%CI, 1.40-7.55,p <01) and stress OR= 12.24 (95%, CI, 4.81-31.14, p <.001). The raised effect of variable stress after adjustment was promoted by the age, sex and physical inactivity variables, and did not affect the significance level (p <.001).</p><p><strong>Conclusions: </strong>This study has demonstrated that subjects with cardiac symptoms without overt CAD, present similar depression and/or stress levels than post-MI patients. And also, post-MI patients and CS patients have more stress and depression than controls, even when adjusted for age, sex, education level, family income, social support, obesity, sedentary lifestyle and family history of MI and / or sudden death.</p>

Impact of smoking on erythrocyte indices and oxidative stress in acute myocardial infarction

Context: The free radicals generated by cigarette smoke are responsible for the production of excessive oxidative stress, causing damage to the cellular and subcellular components in acute myocardial infarction (AMI). Aims: The present study is aimed to evaluate the impact of smoking on erythrocytic oxidative stress and erythrocyte indices in patients with AMI. Materials and Methods: Two hundred consecutively admitted male patients with AMI were enrolled in our study and were subsequently divided into two groups, smokers and nonsmokers. All the subjects were evaluated for lipid profile, red blood cell (RBC) indices and the antioxidant enzyme activities-catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) were studied. Statistical Analysis Used: The independent sample t-test was used, and P values were calculated. Results: We found significantly high (P Conclusions: Along with altered RBC indices, the erythrocyte GPX activity is more reliable and sensitive indicator of oxidative stress than CAT and SOD activities for the assessment of oxidative stress in AMI patients who are smokers.

Abstract P124: Perceived Stress in Acute Myocardial Infarction: Associations with Long-Term Health Status Outcomes

Background: Chronic stress is associated with adverse prognosis in cardiovascular disease, but little is known about its link with health status. We studied the association between chronic stress and health status following acute myocardial infarction (AMI). Methods: In the 24 center US TRIUMPH registry, 4204 AMI patients completed the Perceived Stress Scale-4 (scores range 0-16) during hospitalization. Moderate/high stress over the prior month was defined as scores in the top 2 quintiles (scores=6-16). Patients were assessed at 1 year for disease-specific health status with the Seattle Angina Questionnaire (SAQ) and for generic health status with a Visual Analog Scale (VAS) and the SF-12. Multivariable logistic regression evaluated the independent association between moderate/high stress and poor health status (defined as SAQ angina frequency <100; SAQ physical limitations <75; SAQ QOL <75; VAS <65; SF-12 physical <35; and SF-12 mental <45). Results: After extensive adjustment for demographic, socio-economic and clinical characteristics (including depressive symptoms), AMI patients with moderate/high stress had a greater likelihood of angina and poor disease-specific and generic health status (Figure; p<0.01 for all). Conclusion: Moderate/high stress at the time of an AMI is associated with poor post-AMI health status, even after adjustment for important confounders. Future studies need to examine whether stress mediates observed racial and socio-economic disparities, and whether novel interventions targeting chronic stress can improve post-AMI health status.

Endogenous CGRP protects retinal cells against stress induced apoptosis in rats

Acute stress can provoke apoptosis of the retina cells, and up-regulation of calcitonin gene related peptide (CGRP) in retina. However the role of CGRP in the pathology of the stress induced apoptosis of the retina cells is still elusive. The aim of this study was to investigate the endogenous of CGRP on retinal cell apoptosis induced by the stress of acute myocardial infarction induced by permanent coronary artery occlusion (CAO) in rats. The acute myocardial infarction model was established by ligating the left anterior descending branch of coronary artery in male Sprague-Dawley rats. The rats were randomized into two groups, the CGRP8-37 group and a control group, pretreated with CGRP8-37 (10−7mol/L, 1μL/g, intravenously injected), a specific antagonist of CGRP receptor, and 0.9% saline respectively, at 15min prior to the CAO. The samples of the retina were collected at 3h of CAO for the assays of TUNEL and caspase-3 activity respectively. The total apoptosis ratio of retinal cells in CGRP8-37 group was significantly higher than that in the control group (P<0.05). The capase-3 activity was significantly greater in the CGRP8-37 group, compared with the control group (P<0.05) at 3h of CAO. The vacuolar degeneration of retinal ganglion cells was observed in the CAO animals. The results suggest that the endogenous CGRP may play a protective role in the retinal cell apoptosis induced by the stress of acute myocardial infarction.

Adaptive response to stress of acute myocardial infarction leads to apoptosis of retinal cells of rats

Evidence indicates that adaptive responses to systemic stress occur in retina, as indicated by the changes in sympathetic and sensory afferent neurotransmitters in the retina when under stressful stimulation, such as acute myocardial infarction. The aim of this study was to investigate the potential association of the adaptive responses with retina injury, indicated as apoptosis of retinal cells of the rats suffering from acute stress evoked by coronary artery occlusion (CAO). The apoptotic rate of retinal cells and activity of caspase-3 in retina were examined and analyzed over 6 h of CAO using TUNEL and caspase assay. It was observed that the rate of apoptosis of the retinal cells was significantly increased to 16.8% ± 6% ( n = 10, vs. control, p < 0.05) and 26.9% ± 6.1% ( n = 10, vs. control, p < 0.05), mainly in ganglion cells of the retina, at 3 and 6 h of CAO, respectively. And the activity of caspase-3 was also up-regulated to 2.16 ± 0.77 at 3 h of CAO (vs. 1.00 ± 0.32 of the control, p < 0.05, n = 10) and 2.72 ± 1.11 at 6 h of CAO (vs. 1.37 ± 0.76 of control, p < 0.05, n = 10). The findings may indicate that the adaptive responses to acute stressful simulation, such as acute myocardial infarction, could result in retinal cell injury, presented as increase in apoptosis of retinal cells.

Markers of oxidative stress in acute myocardial infarction treated by percutaneous coronary intervention

Abstract In the current study, we evaluated the dynamics of oxidative stress markers in patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI). Thirty consecutive patients with AMI with ST elevation were included. Plasma lipid peroxidation end product malondialdehyde (MDA) and total antioxidant capacity (TAC) in blood plasma were evaluated. Peripheral venous blood samples were obtained prior to reperfusion and at five time points after reperfusion. The control group consisted of 20 ischemic patients without acute coronary syndrome. TAC in the AMI group at admission was lower than in control patients (1.26 + 0.32 vs. 1.52 + 0.24 mmol/l). Within 1 h after reperfusion, in most cases, values significantly declined (1 min, 1.10 + 0.33 mmol/l; 1 h, 1.06 + 0.21 mmol/l [p= 0.03]). After 3 h, values began to increase (1.14 + 0.29 mmol/l) and returned to basal values after 3 d (1.29 + 0.24 mmol/l). MDA levels in AMI patients at admission were higher than in control patients (1.66 + 0.55 vs. 1.44 + 0.55 mmol/l) but showed a sustained decrease over the 3 h after reperfusion of the occluded artery (1 min, 1.57 + 0.37 mmol/l; 1 h, 1.50 + 0.35 μmol/l; 3 h, 1.35 + 0.59 μmol/l [p = 0.03]). Reperfusion of the occluded coronary artery by PCI in AMI lead to an immediate decrease in TAC, suggesting formation of reactive oxygen species. However, the MDA level significantly decreased after reperfusion. This may suggests less reperfusion injury after PCI.

Elevation of the glycoxidation product Nε-(carboxymethyl)lysine in patients presenting with acute myocardial infarction

An important role in the acceleration of vascular disease has been previously suggested for advanced glycation end products. N(epsilon)-(carboxymethyl)lysine (CML) is an advanced glycation end product formed on protein by combined non-enzymatic glycation and glycoxidation reactions. CML reacts with the receptor of advanced glycation end products inducing impairment of endothelium dependent relaxation and is a marker of oxidative stress. A total of 40 patients with acute myocardial infarction (17 patients with ST-elevation myocardial infarction, 23 patients with non-ST-elevation myocardial infarction) and 40 patients with stable coronary artery disease were included consecutively in this study. During coronary angiography, peripheral venous blood sample was taken for measuring CML. Serum levels of CML were significantly increased in patients with acute myocardial infarction [17.9+/-10.7 vs. 6.6+/-3.1 arbitrary units (AU)/mg protein, p<0.001]. A cut-off value of CML>9.5 AU/mg protein was associated with an odds ratio of acute myocardial infarction of 39.7 [95% confidence interval (CI): 11.1-142, p<0.001], a sensitivity of 0.85 (95% CI: 0.70-0.94) and a specificity of 0.88 (95% CI: 0.73-0.96). CML levels are significantly elevated in patients presenting with acute myocardial infarction. These results suggest the involvement of endothelial dysfunction (through receptor interaction) and oxidative stress in acute myocardial infarction.

Association between serum paraoxonase activity and oxidative stress in acute coronary syndromes

Objective — The oxidation of low-density lipoprotein (LDL) is believed to have a central role in atherogenesis. Under oxidative stress not only LDL, but all other serum lipids are exposed to oxidation. High-density lipoprotein (HDL)-associated paraoxonase (PON1) was shown to inhibit LDL andHDL oxidation.We investigated the relationship between PON1 and oxidative stress in acute myocardial infarction and unstable angina in a comparative fashion.Methods and results — Activities of PON1, concentrations of malondialdehyde (MDA), lipids and lipoproteins were measured in patients (38 subjects with acute myocardial infarction and 33 subjects with unstable angina pectoris) and in age- and sex-matched controls (32 subjects). Serum PON1 activity was significantly lower in patients than in controls (p < 0.001). Patients had significantly increased serum MDA concentrations (p < 0.001) and there were strong negative correlations (p < 0.001) between serum PON1 and MDA levels in the acute myocardial infarction group (r = –0.673), in the unstable angina pectoris group (r = –0.868) and in healthy controls (r = –0.778). Serum HDL-cholesterol (HDL-C) concentrations were lower in patients than controls (p < 0.05). No correlation was observed between PON1 and HDL-C levels in patients or controls. Apo A I concentrations were significantly lower in the patient groups (p < 0.01), but were insignificant between patients with AMI and UAP. Apo A-I and PON1 levels did not show any correlation. Apo B concentrations were lowest in the healthy controls, higher in the UAP group and highest in the AMI group (p < 0.001). In the acute myocardial infarction group LDL/apo B ratio was lower than in healthy controls and in the UAP group, suggesting smaller LDL particle size.Conclusions — Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.

Increased platelet aggregability in response to shear stress in acute myocardial infarction and its inhibition by combined therapy with aspirin and cilostazol after coronary intervention

Although antiplatelet therapy with a specific inhibitor of phosphodiesterase-3 cilostazol improves stent patency compared with use of aspirin (ASA) alone, the specific role of cilostazol on platelet aggregation in patients with acute myocardial infarction (AMI) is less well understood. Thirty-six patients with AMI who were successfully treated with primary angioplasty were randomized to 3 antiplatelet regimens: ASA alone (n = 12), ASA + ticlopidine (n = 12), and ASA + cilostazol (n = 12). We measured shear stress-induced platelet aggregation (SIPA) using a modified cone-plate viscometer on admission and on day 7, and evaluated the inhibitory effects of combination therapy with ASA + cilostazol on SIPA. Compared with cases of stable coronary artery disease, significant increases in SIPA and plasma von Willebrand factor activity were observed in patients with AMI before they received antiplatelet therapy. On day 7 after primary angioplasty, ASA did not inhibit SIPA (65 ± 15% vs 57 ± 11%, p = 0.086), whereas both combination therapies of ASA + ticlopidine and ASA + cilostazol significantly inhibited SIPA in patients with AMI (ASA + ticlopidine: 61 ± 15% vs 45 ± 13%, p <0.0001; ASA + cilostazol: 64 ± 14% vs 43 ± 9%, p <0.005). There was a significant correlation of SIPA with adenosince diphosphate (ADP)-induced platelet aggregation (r = 0.412, p = 0.003) and with plasma von Willebrand factor activity (r = 0.461, p = 0.0008). These data suggest that patients with AMI have increased platelet aggregability in response to high shear stress. Combined antiplatelet therapy with ASA + cilostazol appears to be as effective as therapy with ASA + ticlopidine for reducing SIPA in patients with AMI who are undergoing primary angioplasty.

Beneficial effects of vitamin E treatment in acute myocardial infarction.

Vitamin E (Vit E), an antioxidant, is considered to prolong survival in patients and animals after myocardial infarction. Because myocardial infarction is associated with arrhythmia and heart dysfunction, this study tested the hypothesis that early treatment with Vit E reduces mortality because of its protective effects against arrhythmia and cardiac dysfunction induced by acute myocardial infarction. Rats were randomly divided into 4 groups: sham control, myocardial infarcted, Vit E-treated sham control, and Vit E-treated infarcted animals. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. Treated animals received Vit E (25 mg/kg/d) through a gastric tube beginning 1 hour after the coronary occlusion, whereas control rats received tap water. Electrocardiograms (lead II) at 1, 3, 7, and 21 days after coronary occlusion in the untreated animals showed ST-segment elevation, abnormal Q waves, premature ventricular complex (PVC), and QTc prolongation. Conversely, Vit E-treated rats showed attenuated ST-segment changes, fewer abnormal Q waves, and decreased incidence of PVC after coronary occlusion. Total mortality was reduced from 38% to 16%, whereas the infarct size was decreased from 44.2% to 22.3% in infarcted rats treated with Vit E. The depression in left ventricular function as well as elevation of malondialdehyde content and conjugated diene formation in the 21-day infarcted rat hearts were prevented by Vit E treatment. These results indicate that Vit E may exert beneficial effects on the heart by reducing oxidative stress in acute myocardial infarction.

Role of oxidative stress in acute myocardial infarction

Role of oxidative stress in acute myocardial infarction