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The lipid endocannabinoid system has recently emerged as a novel therapeutic target for several inflammatory and tissue-damaging diseases, including those affecting the cardiovascular system. The primary targets of cannabinoids are cannabinoid type 1 (CB1) and 2 (CB2) receptors. The CB2 receptor is expressed in the cardiomyocytes. While the pathological changes in the myocardium upregulate the CB2 receptor, genetic deletion of the receptor aggravates the changes. The CB2 receptor plays a crucial role in attenuating the advancement of myocardial infarction (MI)-associated pathological changes in the myocardium. Activation of CB2 receptors exerts cardioprotection in MI via numerous molecular pathways. For instance, delta-9-tetrahydrocannabinol attenuated the progression of MI via modulation of the CB2 receptor-dependent anti-inflammatory mechanisms, including suppression of pro-inflammatory cytokines like IL-6, TNF-α, and IL-1β. Through similar mechanisms, natural and synthetic CB2 receptor ligands repair myocardial tissue damage. This review aims to offer an in-depth discussion on the ameliorative potential of CB2 receptors in myocardial injuries induced by a variety of pathogenic mechanisms. Further, the modulation of autophagy, TGF-β/Smad3 signaling, MPTP opening, and ROS production are discussed. The molecular correlation of CB2 receptors with cardiac injury markers, such as troponin I, LDH1, and CK-MB, is explored. Special attention has been paid to novel insights into the potential therapeutic implications of CB2 receptor activation in MI.

Background: Concentrations of cardiac troponin predict risk of cardiovascular disease and death in the general population. There is limited evidence on changing patterns of cardiac troponin in the years preceding cardiovascular events., Methods: We analyzed cardiac troponin I (cTnI) with a high-sensitivity assay in 3272 participants in the Trøndelag Health (HUNT) Study at study visit 4 (2017-2019). Of these, 3198 had measurement of cTnI at study visit 2 (1995-1997), 2661 at study visit 3, and 2587 at all 3 study visits. We assessed the trajectories of cTnI concentrations in the years prior to cardiovascular events using a generalized linear mixed model, with adjustment for age, sex, cardiovascular risk factors, and comorbidities., Results: At HUNT4 baseline, median age was 64.8 (range 39.4-101.3) years, and 55% were women. Study participants who were admitted because of heart failure or died from cardiovascular cause on follow-up had a steeper increase in cTnI compared with study participants with no events (P < .001). The average yearly change in cTnI was 0.235 (95% confidence interval, 0.192-0.289) ng/L for study participants with heart failure or cardiovascular death, and -0.022 (95% confidence interval, -0.022 to -0.023) ng/L for study participants with no events. Study participants who experienced myocardial infarction, ischemic stroke, or noncardiovascular mortality exhibited similar cTnI patterns., Conclusions: Fatal and nonfatal cardiovascular events are preceded by slowly increasing concentrations of cardiac troponin, independently of established cardiovascular risk factors. Our results support the use of cTnI measurements to identify at-risk subjects who progress to subclinical and later overt cardiovascular disease., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

The cardiac mitochondrial damage and cardiac hypertrophy pathways are intimately associated with the pathology of myocardial infarction (MI). The protective effects of β-caryophyllene on mitochondrial damage and cardiac hypertrophy pathways in isoproterenol-induced myocardial infarcted rats were investigated. Isoproterenol (100 mg/kg body weight) was administered to induce MI. The ST-segment, QT interval, and T wave were widened, and the QRS complex and P wave were shortened in the electrocardiogram (ECG) and the serum cardiac diagnostic markers and heart mitochondrial lipid peroxidation products, calcium ions, and reactive oxygen species (ROS) were elevated and the heart mitochondrial antioxidants, tricarboxylic acid cycle, and respiratory chain enzymes were lessened in isoproterenol-induced myocardial infarcted rats. The heart mitochondrial damage was noted in the transmission electron microscopic study. The whole heart weight was increased and the subunits of nicotinamide adenine dinucleotide phosphate - oxidase 2 (Nox 2) genes such as cybb and p22-phox and cardiac hypertrophy genes such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), β -myosin heavy chain (β-MHC), and actin alpha skeletal muscle-1(ACTA-1) were highly expressed in the rat's heart by reverse transcription-polymerase chain reaction study. The β-caryophyllene (20 mg/kg body weight) pre- and co-treatment orally, daily for 21 days reversed changes in ECG and lessened cardiac diagnostic markers, ROS, and whole heart weight and ameliorated mitochondrial damage and Nox/ANP/BNP/β-MHC/ACTA-1cardiac hypertrophy pathways in isoproterenol-induced myocardial infarcted rats. The observed effects might be due to the antioxidant, anti-mitochondrial damaging, and anti-cardiac hypertrophic mechanisms of β-caryophyllene., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Scopoletin is a phenolic coumarin isolated from a variety of plants and was originally used to treat various diseases including arthritis as well as bone-related diseases. The goal of this study was to determine scopoletin's therapeutic potential in an animal model of myocardial infarction induced with ISO. There were five groups of albino male rats. Group I (control) animals were orally treated with olive oil. Group II (scopoletin) animals were pre-treated orally with a 50-mg dosage of scopoletin for 28 days. Group III (ISO-treated) animals were treated with 85 mg/kg of ISO subcutaneously for 2 consecutive days (29th and 30th day). Group IV (scopoletin and ISO) animals were pre-treated orally with 25 mg of scopoletin for 28 days before exposure to ISO. Group V (scopoletin and ISO) animals were pre-treated with 50 mg of scopoletin for 28 days before exposure to ISO. In the ISO-administered animals, a wider heart-to-body weight ratio, a higher heart weight, higher cardiac diagnostic markers, higher MDA levels and related antioxidant levels, inflammatory, and apoptotic markers were observed. Scopoletin pre-treatment with ISO (25 and 50 mg/kg b.wt) significantly reduced heart-to-body weight ratio, cardiac diagnostic markers, MDA, inflammatory markers, and apoptotic markers. Meantime, a pre-treatment with scopoletin increased the levels of antioxidant enzymes. Inflammation and necrosis were observed in the histopathology of heart tissue of ISO-treated animals and these histopathological conditions were reversed by scopoletin pretreatment. The antioxidant and anti-inflammatory properties of ISO-treated rats were shown to be increased by scopoletin, showing its therapeutic potential against cardiovascular diseases. Through the use of its antioxidant and anti-inflammatory properties, scopoletin exhibited anti-myocardial infarction properties. However, further preclinical studies will be required to demonstrate the mechanism of action of scopoletin involved in anti-myocardial infarction., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

We developed a new plasmonic nanostripe microcone array (PNMA) substrate-integrated microfluidic chip for the simultaneous surface-enhanced Raman scattering (SERS)-based immunoassay of the creatine kinase MB isoenzyme (CK-MB) and cardiac troponin (cTnI) cardiac markers. The conventional immunoassay usually employs a microtiter plate as the solid capture plate to form the immunocomplexes. However, the two-dimensional (2D) surface of the microtiter plate limits the capture efficiency of the target antigens due to the steric hindrance effect. To address this issue, a gold film-coated microcone array with nanostripes was developed that can provide a large surface area for capture antibody conjugation and serve as a SERS-active substrate. This unique nano-microhierarchical structure showed an excellent light trapping effect and induced surface plasmon resonance to further enhance the Raman signals of the SERS nanoprobes. It significantly improved the sensitivity and applicability of SERS-based immunoassay on the microfluidic chip. With this integrated microfluidic chip, we successfully performed the simultaneous detection of CK-MB and cTnI, and the detection limit can reach 0.01 ng mL -1 . It is believed that the PNMA substrate-integrated microfluidic chip would play a critical role in the rapid and sensitive diagnostics of cardiac diseases.

Background: Stem cell therapy has emerged as a novel treatment for heart failure after myocardial infarction (Ml). Bone marrow-derived mesenchymal stem cells (BM-MSCs) are commonly considered because of their accessibility and usability. However, their therapeutic potential remains controversial. In our previous in vitro study, chorion-derived mesenchymal stem cells (C-MSCs) and umbilical cord-derived mesenchymal stem cells (UC-MSCs) demonstrated an ability to differentiate into cardiomyocytes and neural cells, respectively. Thus, we examined whether C-MSCs had a better differentiation potential in an MI animal model., Methods: MI was induced by ligation of the left anterior descending artery, and DiI-labeled MSCs were injected into the border of the infarcted myocardium. The left ventricular ejection fraction (LVEF) and fractional shortening (FS) were measured using echocardiograms. Masson's Trichrome staining was performed to evaluate the viable myocardium. Alpha-sarcomeric actin (α-SA), cardiac troponin-T (cTnT), and isolectin were immunolabeled to evaluate differentiation and capillary formation., Results: After 8 weeks, the LVEF and FS significantly increased to a greater extent in the C-MSC-injected group with maintenance of viable myocardium, as compared to in the control, UC-MSC-, and BM-MSC-injected groups (p < 0.05). Compared to UC-MSCs and BM-MSCs, C-MSCs significantly increased the capillary density (p < 0.05) and demonstrated higher expressions of cTnT and α-SA., Conclusions: In conclusion, compared to UC-MSCs and BM-MSCs, C-MSCs showed a better therapeutic efficacy in a rat MI model., Competing Interests: Conflict of interest None., (Copyright © 2022 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.)

Express and highly sensitive immunoassays for the quantitative registration of cardiac troponin I (cTnI) are in high demand for early point-of-care differential diagnosis of acute myocardial infarction. The selection of antibodies that feature rapid and tight binding with antigens is crucial for immunoassay rate and sensitivity. A method is presented for the selection of the most promising clones for advanced immunoassays via simultaneous characterization of interaction kinetics of different monoclonal antibodies (mAb) using a direct label-free method of multiplex spectral correlation interferometry. mAb-cTnI interactions were real-time registered on an epoxy-modified microarray glass sensor chip that did not require activation. The covalent immobilization of mAb microdots on its surface provided versatility, convenience, and virtually unlimited multiplexing potential. The kinetics of tracer antibody interaction with the “cTnI—capture antibody” complex was characterized. Algorithms are shown for excluding mutual competition of the tracer/capture antibodies and selecting the optimal pairs for different assay formats. Using the selected mAbs, a lateral flow assay was developed for rapid quantitative cTnI determination based on electronic detection of functionalized magnetic nanoparticles applied as labels (detection limit—0.08 ng/mL, dynamic range > 3 orders). The method can be extended to other molecular biomarkers for high-throughput screening of mAbs and rational development of immunoassays.

Background: This study determined the effect of Biochanin A (BCA) on isoproterenol (ISO) induced Myocardial Infarction (MI) in male Wistar rats., Methods: Animals (weighing 150-180 g) were divided into four groups, with six animals in each group and pretreated with BCA (10mg/kg Body Weight [BW]) and ɑ-tocopherol (60mg/kg BW) for 30 days; and ISO (20mg/kg BW) was administrated subcutaneously on the 31st and 32nd day., Results: ISO-induced MI rats demonstrated the significant elevation of serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, creatine kinase-MB and cardiac troponin; however, concomitant pretreatment with BCA protected the rats from cardiotoxicity caused by ISO. Activities of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and glutathione reductase significantly reduced in the heart with ISO-induced MI. Pretreatment with BCA produced a marked reversal of these antioxidant enzymes related to MI-induced by ISO., Conclusion: In conclusion, this study suggested that BCA exerts cardioprotective effects through modulating lipid peroxidation, enhancing antioxidants, and detoxifying enzyme systems., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Context: Lutein (LU) is a major carotenoid with various pharmacological activities including anti-inflammatory, antioxidant and anti-apoptosis. Objective: The cardioprotective efficacy of LU was determined by evaluating the biochemical and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) rat model. Materials and methods: Healthy male albino rats ( n  = 40) were segregated into 4 equal groups. Group I (control) rats were administered with olive oil, Group II (LU) rats were orally pre-treated with only 40 mg of LU for 28 days, Group III (MI induced) rats were injected (subcutaneously; s.c) with 85 mg/kg of ISO for 2 consecutive days, whereas Group IV (LU + ISO) rats were pre-treated with 40 mg of LU for 28 days before ISO induction. Results: ISO-induced group showed increased infarct size and cardiac/inflammatory/apoptotic markers. However, pre-treatment with LU (28 days) considerably reduced ( p  < 0.01) the infarct size (14%), lipid peroxidation product (MDA;42%), cardiac markers [(lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), cardiac troponin T (cTn T)], inflammatory markers [IL-1β, IL-6, tumour necrosis factor alpha (TNF-α), nuclear factor kappa B p65 subunit (NF-κB p65)] and apoptotic markers (caspase-3 and -9). Also, LU significantly improved ( p  < 0.01) the antioxidants [catalase (CAT), superoxide dismutase (SOD)] as well as markedly upregulated ( p  < 0.01) the protein expression of HO-1 and Nrf2. Moreover, LU considerably reversed all the histopathological changes and thus exhibits its cardioprotective activity. Conclusion: LU exhibits potent cardioprotective activity against ISO-induced cardiotoxicity and might be recommended with standard cardioprotective agents for treating various MI-related complications.

Aims: Myocardial injury (MI) is the principal cause of death from cardiovascular disease (CVD). The present study was conducted to investigate the ameliorative and antioxidant effects of cerebrolysin (CBL) on isoproterenol-induced MI in rats., Methods: MI was induced in the rats by subcutaneously injecting 100 mg/kg of isoproterenol (ISO) in the first two days. The serum levels of creatine phosphokinase (CK-MB) and cardiac troponin I (cTnI) were measured on the third day to confirm MI. The post-treatment involved intraperitoneally injecting 5 ml/kg of CBL for 7 days. Nitric oxide (NO), malondialdehyde (MDA) in the heart tissue and catalase (CAT) and serum levels of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured on the 10th day using the enzyme-linked immunosorbent assay (ELISA). Histopathological examinations of the heart tissue were also performed., Findings: The present results suggested significant increases in CK-MB, cTnI, MDA and NO. A significant decrease was also observed in the ISO-treated rats in certain antioxidant enzymes, including CAT and GPX. CBL administration showed a significant ameliorative increase against the oxidative ISO-induced damage. Moreover, the histopathological findings showed lower levels of the infiltration of inflammatory cells and edema and vascular proliferation in the CBL-treated rats., Significance: The present histopathological and biochemical findings attributed antioxidant properties to CBL in the rat myocardium and suggested protective effects on ISO-induced MI., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Myocardial infarction (MI) is one of the most important reason of mortality into worldwide. Visfatin is a novel adipokine which was reported increased in metabolic syndrome and obesity. Moreover, it is known that visfatin increases in aterosclerotic endotelial dysfunction. In our study we want to demonstrate how visfatin changes in isoproterenol (ISO) induced MI. Rats were allocated into 4 groups in which each group included 6 rats in this study. 200 mg/kg ISO was administered into rats except control group to induce MI. I. and II. Group rats in 6th hour, III. Group rats in 24th hour and IV. Group rats in 7th day were decapitated. Visfatin was searched in cardiac tissues of all groups by immunohistochemistry stainning. Visfatin and cardiac markers' levels were measured in serum samples. Serum visfatin levels gradually increased in 6th and 24th hour in MI rats compared to controls. In 7th day visfatin levels decreased to control levels. These changes correlated with serum troponin T levels. These findings were supported by immunohistochemistry stainning of visfatin in cardiac tissues. It has been shown that visfatin could be useful in diagnosing MI and may be a biomarker for cardiac ischemia because of increasing in systemic circulation and cardiac tissues in MI like troponins., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The present study aimed to investigate the expression of microRNA (miR)‑133a in patients with or without acute myocardial infarction (AMI) following radical surgery for gastric cancer, and to explore its underlying mechanisms. Blood samples were collected from patients with or without AMI in order to detect the expression levels of miR‑133a and endothelial injury markers. In addition, an AMI rat model was established. Reverse transcription‑quantitative polymerase chain reaction was used to detect the mRNA expression levels of miR‑133a and B‑cell lymphoma 2‑like 1 (Bcl2l1). In addition, an ELISA assay was used for endothelial injury marker analysis. To investigate the effects of miR‑133a on human umbilical vein endothelial cells (HUVECs), a miR‑133a inhibitor was used. Cell proliferation and apoptosis were subsequently detected using an MTT assay and flow cytometry. Western blot analysis was also conducted to detect Bcl2l1 protein expression. The results suggested that patients with AMI exhibited significantly increased expression of endothelial injury markers (von Willebrand factor, heart‑type fatty acid‑binding protein and cardiac troponin I) and miR‑133a in blood samples compared with patients without AMI. In addition, treatment with a miR‑133a mimic was able to upregulate the expression of endothelial injury markers in an AMI rat model, whereas treatment with a miR‑133a inhibitor had the opposite effect. Furthermore, cellular experiments indicated that a miR‑133a inhibitor could promote HUVEC proliferation and reduce cell apoptosis. The present results also confirmed that miR‑133a directly targets Bcl2l1 and negatively regulates Bcl2l1 expression. In conclusion, the results of the present study suggested that miR‑133a was involved in the endothelial injury process after AMI by targeting Bcl2l1.

The detection of cardiac markers is critical to the diagnosis of acute myocardial infarction, and immunochromatographic assays are a common tool for point-of-care analysis. Methods : We report a multiplexed lateral flow test strip for simultaneous quantitative detection of cardiac troponin I (cTnI), creatine kinase isoenzyme MB (CKMB), and myoglobin (Myo). Hydrophilic, monodisperse, stable, and carboxyl-modified (COOH-) magnetic nanobeads (MNBs) were used to construct immunomagnetic probes specific to the three cardiac markers. The detection area of the sandwich-style complexes contained three test lines for cTnI, CKMB, and Myo. The magnetic signal intensity of the detection area in the nitrocellulose membrane was measured via a magnetic immunochromatography reader developed in house. Results : To optimize the assay, a modified working buffer was also investigated to improve the detection sensitivity, decrease the background noise, and shorten the detection time. The MNB-based immunochromatography test (MICT) strip offers a wide linear dynamic detection range, rapid detection, high sensitivity, and specificity. The limit of detection was 0.0089 ng/mL for cTnI, 0.063 ng/mL for CKMB, and 0.05 ng/mL for Myo with minimal cross-reactivity. There were 110 clinical human serum samples that were used to evaluate this platform with high correlation. Conclusion : MICT shows great potential as a supplemental method for in vitro diagnostics in the laboratory or in other point-of-care testing (POCT) applications., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.

Cardiac mitochondrial oxidative stress causes mitochondrial damage that plays an important role in the pathology of myocardial infarction. The preventive effects of diosmin on cardiac mitochondrial oxidative stress in isoproterenol-induced myocardial infarcted rats were evaluated. Rats were pretreated with diosmin (10 mg/kg body weight) daily for 10 days. Myocardial infarction was induced in rats by isoproterenol (100 mg/kg body weight) injection twice at an interval of 24 h (on 11th and 12th day). Isoproterenol-induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium ion, and a significant decrease in the levels of heart mitochondrial glutathione peroxidase, reduced glutathione, glutathione-S-transferase, isocitrate, malate, α-ketoglutarate, and succinate dehydrogenases. Transmission electron microscopic findings revealed damaged mitochondria with loss of cristae, swelling, and vacuolation in isoproterenol-induced rats' heart. Diosmin pretreatment showed significant preventive effects on all the biochemical parameters, and the structure of mitochondria was evaluated. Furthermore, the transmission electron microscopic study confirms the biochemical findings. The antioxidant and negative inotropic effects of diosmin inhibited cardiac mitochondrial oxidative stress and prevented mitochondrial damage in myocardial infarcted rats.

Background: Zinc is one of the most important microelements in the body and zinc homeostasis plays a critical role in maintaining cellular structure and function. Zinc dyshomeostasis can lead to many diseases, such as cardiovascular disease. Our aim was to investigate whether there is a relationship between zinc and cardiac markers, and the risk of acute myocardial infarction (AMI) by zinc quartiles., Methods: We enrolled a total of 529 patients and measured their serum zinc levels and cardiac markers. We performed further studies after dividing subjects into four groups according to their concentrations of zinc by quartile to clarify the relationship between zinc levels and risk of increased acute myocardial infarction prevalence rate., Results: We observed that there was a significant inverse linear relationship between zinc and Lg(creatine kinase) (p=0.011), Lg(creatine kinase-MB) (p=0.002) and Lg(cardiac troponin T) (p=0.045). In addition, the acute myocardial infarction prevalence rates were 28.8%, 24.8%, 20.5%, and 18.2% by patients with zinc quartiles, respectively. Multivariate logistic regression analysis showed that the odds ratio between the lowest and highest zinc quartile groups was 1.92 (1.019-3.604) (p<0.05)., Conclusions: The present study revealed a relationship between serum zinc levels in that zinc levels were significantly inversely correlated with serum creatine kinase (CK), creatine kinase-MB (CKMB) and cardiac troponin T (cTnT) levels. Furthermore, we found that the prevalence rate of acute myocardial infarction decreased with increasing zinc quartiles., (Copyright © 2017 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

The present study aims to evaluate the preventive effects of vanillic acid on altered ion pumps, ions and Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with vanillic acid (5 mg/kg and 10 mg/kg body weight) daily for 10 days. After the pretreatment, isoproterenol (100 mg/kg body weight) was injected into rats at an interval of 24h for 2 days to induce myocardial infarction. Isoproterenol induced rats significantly increased activities/levels of serum cardiac markers, plasma lipid peroxidation products, serum uric acid and significantly decreased plasma non-enzymatic antioxidants. Furthermore, isoproterenol significantly altered the activities/levels of ion pumps and ions in the heart. The myocardial expressions of apoptotic genes such as Fas-receptor, caspases-8, -9, and -3 were increased in isoproterenol induced rats. There was a significant increase in cardiomyocyte apoptosis observed in isoproterenol induced rats. Pretreatment with vanillic acid (5 mg/kg and 10 mg/kg body weight) to isoproterenol induced rats showed significant effects on all the biochemical and molecular parameters evaluated. Isolated cardiomyocyte viability by trypan blue exclusion staining also correlated with these biochemical findings. Thus, vanillic acid prevented altered ion pumps, ions and inhibited Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Our study also revealed that pretreatment with vanillic acid at the dose of 10 mg/kg body weight was more effective than 5 mg/kg body weight. The cardioprotective effects of vanillic acid are associated with its antioxidant mechanisms., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Myocardial infarction continues to be a major public health problem, not only in western countries but also increasingly in developing countries and makes significant contribution to the mortality statistics. Reduction in mortality rate and prevention of myocardial infarction are of utmost importance. Tachycardia, left ventricular hypertrophy (LVH), altered adenosine triphosphatases (ATPases), and shifts in electrolyte balance play a vital role in the pathogenesis of myocardial infarction. This study was designed to evaluate the preventive effects of zingerone (vanillyl acetone) on tachycardia, LVH, altered electrocardiogram (ECG), altered activities of membrane bound ATPases, electrolyte imbalance and myocardial infarct size in isoproterenol induced myocardial infarcted rats. Rats were pretreated with zingerone (vanillyl acetone) 6 mg/kg body weight daily for a period of 14 days and were then induced myocardial infarction with isoproterenol (100 mg/kg body weight) on 15th and 16th day. Isoproterenol induced myocardial infarcted rats showed tachycardia, LVH, altered ECG, serum cardiac troponin-T, plasma myoglobin, heart ATPases, heart sodium ion, calcium ion, potassium ion, and increased myocardial infarct size. Pretreatment with zingerone (vanillyl acetone) revealed preventive effects on tachycardia, LVH, ECG, and all the above mentioned biochemical parameters evaluated in isoproterenol induced myocardial infarcted rats. The 2, 3, 5-triphenyl tetrazolium chloride staining on myocardial infarct size confirmed the prevention of myocardial infarction. Further, the in vitro study revealed a very convincing free radical scavenging of zingerone (vanillyl acetone). Thus, the observed effects of zingerone (vanillyl acetone) are due to its antioxidant and free radical scavenging activities in isoproterenol induced myocardial infarcted rats., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Differentiation between procedure-related necrosis and postprocedural myocardial infarction (MI) is challenging because of the inherent association of these procedures to varying levels of myocardial injury. To improve risk stratification of patients at risk of an acute MI, the universal definition of MI implemented cardiac biomarker thresholds. The cutoff points for these thresholds, however, are largely arbitrary and lack therapeutic implications. Measurement of cardiac marker concentrations after percutaneous coronary intervention and cardiac surgery should, therefore, be used as a marker of baseline risk, atherosclerosis burden, and procedural complexity rather than a conclusive marker to diagnose acute MI., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Measurement of circulating cardiac troponins I and T has become integral to the diagnosis of myocardial infarction. This article discusses the structure and function of the troponin complex and the release of cardiac troponin molecules from the injured cardiomyocyte into the circulation. An overview of current cardiac troponin assays and their classification according to sensitivity is presented. The diagnostic criteria, role, and usefulness of cardiac troponin for myocardial infarction are discussed. In addition, several examples are given of the usefulness of high-sensitivity cardiac troponin assays for short-term and long-term prediction of adverse events., (Copyright © 2014 Elsevier Inc. All rights reserved.)

This article examines the use of high-sensitivity cardiac troponin (hs-cTn) assays to rule out non-ST elevation myocardial infarction (NSTEMI). Despite concerns about assay imprecision, studies have shown that the single sample rule out (SSRO) method is safe. The article provides data on the imprecision of hs-cTnT assays and calculates the probability of misclassification for different troponin values. The risk of misclassification is low, particularly when the initial troponin value exceeds 7 ng/L. An alternative SSRO threshold of 6 ng/L has also been found to be clinically safe. The article also discusses the misclassification issue with the Roche elecys e801 hs-cTnT assay, which had a low rate of misclassification, with less than 0.08% of results in the range of 6-7 ng/L being misclassified. The study concludes that despite the imprecision, the assay is precise enough to ensure that misclassifications are rarely clinically significant. [Extracted from the article]

Background and objectives. Myocardial infarction (MI) is a severe cardiac event associated with plaque formation in arteries, leading to reduced blood flow to the heart. Arrhythmias, such as bradyarrhythmia or tachyarrhythmia, commonly accompany MI, contributing to its morbidity and mortality. Electrolyte disturbances, particularly potassium and magnesium imbalances, can exacerbate arrhythmic risks in MI patients. This study aimed to assess the incidence of alterations in serum potassium and magnesium levels during acute MI and their correlation with rhythm disturbances. Material and methods. A prospective analytical study was conducted with 150 patients diagnosed with acute MI based on ECG changes and elevated cardiac markers. Serum potassium and magnesium levels were measured, and rhythm disturbances were assessed using continuous cardiac monitoring and standard ECG. Spearman correlation analysis was performed to evaluate the association between serum potassium, serum magnesium, and rhythm changes. Results. The study investigated the demographic and clinical characteristics of participants and the potential relationship between serum electrolyte levels and arrhythmic changes. The mean age of the participants was 54.3 years, with a male predominance (76% male, 24% female). Among the participants, 50.67% had diabetes, 52% had hypertension, and 28% had both conditions. Serum electrolyte analysis showed elevated magnesium levels in 6.66% and elevated potassium levels in 12.66% of patients. Notably, arrhythmic changes in ECG were present in 62% of patients, with sinus tachycardia being the most prevalent (17%). However, statistical analysis revealed no significant correlation between serum magnesium, serum potassium, and rhythm changes (p >0.05). These findings suggest that while arrhythmic changes are common, they are not directly associated with elevated levels of these electrolytes, indicating the need for further investigation into other potential factors influencing arrhythmias in this population. Conclusion. Despite the prevalence of electrolyte disturbances in acute MI patients, this study found no significant association between serum magnesium, serum potassium levels, and rhythm disturbances. Further research is warranted to elucidate the complex interplay between electrolyte imbalances and arrhythmias in MI. [ABSTRACT FROM AUTHOR]

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Ludwig's angina was first described in 1839 by German physician, Wilhelm Frederick Von Ludwig as a rapidly and fatal progressive gangrenous cellulitis and edema of the soft tissues of the neck and floor of the mouth with rapid spread to other places like anterior mediastinum. However, Type 2 acute myocardial infarction (MI) due to Ludwig's angina has not been documented. A 62‐year‐old male presented to the emergency department with visible anterior neck swelling for 1 week, which was preceded by a tooth arch 1 week prior, the patient presented with a high grade fevers, dysphonia, dysphagia, and facial swelling. No history of trauma. He reported in the past 24 h prior to evaluation, a steady progression of pain intensity with rapid progression and anterior neck skin erythema and swelling. The pain was exacerbated by rotation of the neck, tongue protrusion, and speaking. On examination, there was a visible anterior neck swelling measuring 10.0 × 3.0 cm in widest dimensions, exquisitely tender to palpation with a positive temperature gradient, skin hyperpigmentation and firm in consistency, no crepitus, fluctuance, or induration. Tongue appeared elevated with sublingual edema and pooling of secretions. No stridor. A chest and neck ultrasound scan revealed an extensive abscisic mass from the submandibular, neck, sternal notch, and right clavicular region with the largest pockets measuring 2.11 × 0.8 cm, 2.03 × 0.62 cm, 1.50 × 1.1 cm, with noted submandibular, subclavicular and deep and superficial cervical lymph nodes, the largest measuring 1.23 × 1.63 cm in dimensions. A neck‐CT scan with contrast revealed a pronounced subcutaneous tissue localized collection extending to both submandibular spaces measuring about 5.5 × 12.5 × 9.5 cm with mural enhancement. The upper chest cuts showed moderate pleural effusions and a paracardial hypodense well‐defined lesion measuring 7.5 × 2.5 cm with mild pericardial effusion. The patient was referred to the ear, neck and throat, ENT surgeon for urgent drainage of the abscess, which was done successfully and about 300 mL of hemorrhagic pus was drained. Then transferred to highly dependent unit, (HDU) for IV antibiotic administration and vital observations, prior to that electrocardiogram, ECG showed a normal sinus rhythm. The following day in HDU, the patient started experiencing a chest pain of sudden onset radiating to the upper jaws, left forearm and throbbing in nature, palpitations and started becoming diaphoretic. Blood pressure was 150/70 mmgh and pulse of 120 bpm. ECG readings demonstrated ST‐elevation, at lead 11, V2, and V3, cardiac Troponin I and CK‐MB were elevated 10.0 ng/mL, (<0.4 ng/mL) and 150.0 IU/L, (5‐25 IU/L) respectively. The patient was started on medications to relief acute ischemic pain these included, sublingual nitroglycerin 0.6 mg, morphine 5 mg intravenous slowly, antithrombotic, and beta‐adrenergic blockade. He was kept in HDU later with heparin 80 U/kg bolus and 8 U/kg continuous infusion and was taken for coronary angiogram which demonstrated no any coronary artery occlusion. The patient later on started to register improvement and later discharged on medications for follow‐up. On follow‐up, the subsequent ECG showed persistent atrial fibrillation and patient was discharged on P2Y12 inhibitor, clopidogrel, 75 mg, and beta‐blocker, metoprolol 50 mg. Over the past three decades, mortality rates for acute MI have increased significantly, One common subtype, type 2 MI is noted and driven by a myocardial oxygen supply and demand mismatch in the absence of coronary thrombosis. T2MI can occur with or without obstructive coronary disease like in this patients with angiographically normal coronary arteries. T2MI is increasingly recognized because of various septic pathophyisologies that cause increased myocardia oxygen demand. Evidence of myocardial ischemia especially those with sepsis are likely to develop myocardial injury. T2MI is frequent and explains a significant increase in clinical practice. A consensus is needed about how the diagnosis is established, to facilitate evidence‐based therapies geared toward improving outcomes. [ABSTRACT FROM AUTHOR]

Objective: To discuss the diagnosis and treatment of one patient with ruptured intracranial aneurysm complicated with acute myocardial infarction (AMI), and to provide the reference for the clinical diagnosis, treatment, and anesthesia of the disease. Methods: The clinical data, imaging findings, and anesthesia methods of one patient with ruptured intracranial aneurysm complicated with AMI were retrospectively analyzed, and the analysis was performed combined with the relevant literatures. Results: The patient was admitted to hospital due to sudden severe headache with nausea and vomiting for 4 h. A total of 1 h and 10 min after admission, the multi-slice CT results showed subarachnoid hemorrhage (SAH). There was little bilateral ventricular effusion, and the intracranial angiography results showed a tumor in the posterior communicating segment of the right internal carotid artery. A total of 2 h 52 min after admission, the myoglobin was 483. 6 μ g·L-1, the troponin I was 4. 990 μg·L-1, the creatine kinase isoenzyme-MB (CK-MB) was 45. 70 μg·L-1. A total of 16 h 31 min after admission, the ECG results showed sinus bradycardia, left ventricular hypertrophy, and ST-T segment changes. The initial diagnosis of the patient was SAH, AMI, and hypertension grade 3 (very high risk). After early comprehensive treatment, the patient underwent emergency clipping of cerebral aneurysm after 3 d. The anesthesia method was tracheal intubation ansthesia, and the anesthetic drugs were carefully selected to achieve the best blood flow and anesthesia effect. The vital signs of the patient were stable during the operation, and the condition of the patient was improved and discharged after 7 d. Conclusion: For the patients with intracranial aneurysm rupture complicated with AMI, CT, intracranial angiography, and myocardial markers are the important examinations for the diagnosis and differential diagnosis; controlling the blood pressure is the key point for the treatment and anesthesia. [ABSTRACT FROM AUTHOR]

Abstract Ludwig's angina was first described in 1839 by German physician, Wilhelm Frederick Von Ludwig as a rapidly and fatal progressive gangrenous cellulitis and edema of the soft tissues of the neck and floor of the mouth with rapid spread to other places like anterior mediastinum. However, Type 2 acute myocardial infarction (MI) due to Ludwig's angina has not been documented. A 62‐year‐old male presented to the emergency department with visible anterior neck swelling for 1 week, which was preceded by a tooth arch 1 week prior, the patient presented with a high grade fevers, dysphonia, dysphagia, and facial swelling. No history of trauma. He reported in the past 24 h prior to evaluation, a steady progression of pain intensity with rapid progression and anterior neck skin erythema and swelling. The pain was exacerbated by rotation of the neck, tongue protrusion, and speaking. On examination, there was a visible anterior neck swelling measuring 10.0 × 3.0 cm in widest dimensions, exquisitely tender to palpation with a positive temperature gradient, skin hyperpigmentation and firm in consistency, no crepitus, fluctuance, or induration. Tongue appeared elevated with sublingual edema and pooling of secretions. No stridor. A chest and neck ultrasound scan revealed an extensive abscisic mass from the submandibular, neck, sternal notch, and right clavicular region with the largest pockets measuring 2.11 × 0.8 cm, 2.03 × 0.62 cm, 1.50 × 1.1 cm, with noted submandibular, subclavicular and deep and superficial cervical lymph nodes, the largest measuring 1.23 × 1.63 cm in dimensions. A neck‐CT scan with contrast revealed a pronounced subcutaneous tissue localized collection extending to both submandibular spaces measuring about 5.5 × 12.5 × 9.5 cm with mural enhancement. The upper chest cuts showed moderate pleural effusions and a paracardial hypodense well‐defined lesion measuring 7.5 × 2.5 cm with mild pericardial effusion. The patient was referred to the ear, neck and throat, ENT surgeon for urgent drainage of the abscess, which was done successfully and about 300 mL of hemorrhagic pus was drained. Then transferred to highly dependent unit, (HDU) for IV antibiotic administration and vital observations, prior to that electrocardiogram, ECG showed a normal sinus rhythm. The following day in HDU, the patient started experiencing a chest pain of sudden onset radiating to the upper jaws, left forearm and throbbing in nature, palpitations and started becoming diaphoretic. Blood pressure was 150/70 mmgh and pulse of 120 bpm. ECG readings demonstrated ST‐elevation, at lead 11, V2, and V3, cardiac Troponin I and CK‐MB were elevated 10.0 ng/mL, (

Recently, pharmaceutical scientists' interest has increased to find novel pharmaceutical natural substances with potent antioxidant capacity and very low side effects to be used safely in preventive medicine. One of the most common types of diseases with a large spread globally is cardiovascular diseases, which cause a high rate of deaths annually. The present study evaluated the use of Artemisia herba alba leaves' extract (AHALE) and AHALE zinc oxide nanoparticles (AHALE – ZnONPs) against isoproterenol (ISO) inducing myocardial infarction (MI) in male rats. Several groups of Wistar male rats fed a high-fat diet (HFD) were pretreated with several doses of AHALE or AHALE – ZnONPs for one month followed by exposure to ISO for two days. After treatment, samples of the rats' heart tissues and blood were collected for several molecular biological and biochemical analyses. Heart enzymes, antioxidant enzymes, lipid peroxidation compounds, lipid markers, activities, ROS generation, apoptosis, DNA damage and expression of lipid metabolism genes were analyzed in rats pretreated with AHALE or AHALE – ZnONPs followed by exposure to ISO. The results showed an increase in the levels of AST, ALT, LDH, CK, CK-MB, and cTnT (heart markers), elevation in TG, TC, and LDL levels (lipid profile markers), levels of TBARS and LOOH (lipid peroxidation products), ROS generation, DNA damage, apoptosis, and upregulation of PPAR-α, ADD1, FASN, and ACC genes in animals exposed to ISO in comparison with the control animals. Moreover, a decrease in antioxidant enzyme activities, including GPx, GRx, and GST, was observed in animals exposed to ISO in comparison with control rats. In male rats pretreated with AHALE or AHALE – ZnONPs followed by exposure to ISO, the oxidative stress induced by ISO was prevented. The results suggest that Artemisia extract could be considered for use as one of the natural compounds for prevention of atherosclerosis and heart diseases due to its high antioxidant and hypolipidemic activities. The reduced oxidative stress of Artemisia extract may be a result of the existence of flavonoids and phenolic substances. [ABSTRACT FROM AUTHOR]

The present study aimed at determining the effect polyphenolic extract for tubers cyperus rotundus on myocardial infarction in female rats. In this study, 36 female rats were used and the animals were divided into 6 groups of each group containing (6 rats). Myocardial infarction was induced by injection of isoproterenol at (85 mg/kg) in the intraperitoneally of female rats at an interval of 24 h for two days. The results showed that the injection of isoproterenol in the intraperitoneally of female rats has caused a significant increase in levels of Troponin-I, lactate dehydrogenase(LDH), creatine phosphokinase (CPK), alanine transferase (ALT), aspartic transferase (AST) and necrosis in the second group compared to the first group. It was found in the current study that treatment of female rats with myocardial infarction with phenolic extract of tubers of cyperus rotundus has caused a significant decrease in levels of Troponin-I, lactate dehydrogenase (LDH), creatine phosphokinase (CPK), alanine transferase (ALT), aspartic transferase (AST). Necrosis decreased in the group treated with phenolic extract of tubers of cyperus rotundus. From this we conclude that the phenolic extract of cyperus rotundus of tubers has protective role against myocardial infarction. [ABSTRACT FROM AUTHOR]

Context: Lutein (LU) is a major carotenoid with various pharmacological activities including anti-inflammatory, antioxidant and anti-apoptosis. Objective: The cardioprotective efficacy of LU was determined by evaluating the biochemical and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) rat model. Materials and methods: Healthy male albino rats (n = 40) were segregated into 4 equal groups. Group I (control) rats were administered with olive oil, Group II (LU) rats were orally pre-treated with only 40 mg of LU for 28 days, Group III (MI induced) rats were injected (subcutaneously; s.c) with 85 mg/kg of ISO for 2 consecutive days, whereas Group IV (LU + ISO) rats were pre-treated with 40 mg of LU for 28 days before ISO induction. Results: ISO-induced group showed increased infarct size and cardiac/inflammatory/apoptotic markers. However, pre-treatment with LU (28 days) considerably reduced (p

Objectives: The present study is focused to evaluate cardioprotective activity of ethanolic extract of Amaranthus cruentus. Methods: Amaranthus cruentus extract (Dose 200mg/kg and 400mg/kg) in isoprenaline induced myocardial infarction in rats. The ethanolic extract of Amaranthus cruentus was prepared and subjected to acute toxicity in albino rats. The extract was given orallyat two different doses 200mg/kg and 400mg/. Isoprenaline was administered subcutaneously (85mg/kg s.c.). Results: The histopathological examination revealed mild infarction and inflammation in isoprenaline treated rats. The ethanolic extract of Amaranthus cruentus showed significant cardio protective effect by decreasing the serum level of LDL and VLDL cholesterol levels. The biochemical parameters (AST, ALT and ALP) and HDL cholesterol levels were restored. Conclusion: The outcome of the present study suggested cardioprotective activity of Amaranthus cruentus extract. [ABSTRACT FROM AUTHOR]

Purpose: Hospitals and outpatient clinics are now using point-of-care testing (POCT) devices that contract for the use of diagnostic analyses at the site of patient care delivery, so, facilitating earlier decision-making besides proper treatment. In our study, the aim was to assess the quantitative Nano-Ditech (Cranbury, NJ, USA), CK-MB, cTnIandmyoglobin POC assays and to compare them with the Getein 1100 (Nanjing, China) CK-MB, cTnI and myoglobin POC assays. Materials and Methods: Lithium heparin plasma samples (Terumo Europe N.V. Leuven, Belgium,) for Getein 1100 and Nano-Ditech cardiac marker samples were randomly collected from among routine samples from 100 patients (53 male and 47 female) with chest pain complaint who admitted to BilecikGolpazarı Government Hospital between August-September 2017 and all analyses were performed using the Nano-Ditechanalyzer and comparative analyses were performedby the Getein 1100) assays. Results: In our study, the correlation between the two devices was found to be r = 0.023 and p=0.017 for troponin, r = 0.130 and p=<0.001 for CK-MB and there is no correlation for myoglobin. Conclusion: According to evaluation of both devices' analytical performances, it was found that the comparison of the all values of troponin, CK-MB and myoglobin, which are important for the diagnosis and exclusion of acute myocardial infarction(AMI), is discordant with the method comparison protocol proposed by the Clinical and Laboratory Standards Institute (CLSI) (EP-9). [ABSTRACT FROM AUTHOR]

The objective of this study is to appraise the cardioprotective properties of Gomphrena globosa flowers on isoproterenol-induced myocardial infarction in albino rats. The experimental rats were divided into four groups with six rats in all the groups. Group 1 and group 2 animals were treated with standard diet for 45 days and will serve as a normal control group and positive control group respectively. Group 3 Rats were administered 2.5 mg/Kg body weight metoprolol succinate by oral route for duration of 45 days. Group 4 Rats received 500 mg/Kg body weight of Gomphrena globosa extract via oral route for duration of 45 days. All the groups except group 1 were then administered 85 mg/kg body weight of isoproterenol by subcutaneous route in two doses on 44th and 45th day at gap of twenty four hrs. At the end of the study period, from all groups blood was collected for the estimation of biochemical parameters by puncturing the retro-orbital plexus and the rats were sacrificed. Serum cardiac marker enzymes for instance creatine kinase (CK), lactate dehydrogenase (LDH), creatine kinase muscle-brain (CK-MB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein, lipid profile which includes high density lipoprotein (HDL), low density lipoprotein (LDL), total cholesterol (TC), triglycerides (TG), and very low density lipoprotein (VLDL) levels were measured. In heart tissue homogenate antioxidant activity was assessed for catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. Histopathological and ultrastructural studies were then carried out. The present results indicated that ethanolic extract of flowers Gomphrena globosa showed myocardial retrieval by ameliorating the levels of cardiac marker enzymes to normal and increasing the levels of HDL and decreasing the lipid profile. Furthermore, myocardial antioxidants levels were enhanced along with a lessening in the levels of malondialdehyde. The cardioprotective effect was correlated with standard Metoprolol. Following pretreatment with Gomphrena globosa there was reduction in the degree of inflammation and necrosis which was confirmed by histopathological findings. This study concludes that Gomphrena globosa extract exerts cardioprotective activity against isoproterenol-induced cardiac damage in rats. [ABSTRACT FROM AUTHOR]

Abstract In the present study, 45 children in Upper Egypt (less than 16 years old) were admitted to the Pediatric Intensive Care Unit for scorpion envenomation (SE). They were compared with 30 apparently healthy children of matching age and sex as controls. Out of the studied victims, 35 children (78%) showed signs of severe envenomation, while 10 victims (22%) showed signs of mild envenomation. The case fatality was 33%. The serum levels of cardiac markers, cardiac troponin T (cTnT) and I (cTnI), as well as the enzymatic activities of creatine kinase-MB (CPK-MB) and lactate dehydrogenase (LDH) were determined for both victims and controls. In addition, the serum levels of oxidative stress markers, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH) and zinc (Zn) were measured. Electrocardiography and echocardiography were done. All the envenomed victims showed significantly higher mean values of cTnT, cTnI, CPK-MB and LDH than control group. These cardiac markers were elevated in severe cases and in non survivors in comparison with mild cases and survivors respectively. Furthermore, the serum levels of NO and MDA were significantly higher while the serum levels of SOD, GSH and Zn were significantly lower in all envenomed victims than the controls (p < 0.05 for all). There were no significant differences in the serum levels of oxidative stress markers among severe and mild cases or between survivors and non survivors victims. There were no significant correlations between the serum levels of cardiac markers and the oxidative stress markers in envenomed victims. In conclusions, oxidative stress occurs in scorpion envenomed children, but does not determine prognosis. Cardiac markers, but not the oxidative stress, remain the most important determining factor for the severity and the outcome of SE. Highlights • Oxidative stress occurs in scorpion envenomed children. • Cardiac markers are essential determining factor for envenomation severity and the outcome. • Oxidative stress not correlated to cardiac markers in scorpion envenomed children. • Oxidative stress not related to the envenomation severity and the outcome. [ABSTRACT FROM AUTHOR]

Kombucha (Bio-tea) is a beverage produced by the fermentation of sugared black tea using a symbiotic association of bacteria and yeasts. Traditional claims about Kombucha report beneficial effects such as antibiotic properties, gastric regulation, relief from joint rheumatism and positive influence on the cholesterol level, arteriosclerosis, diabetes, and aging problems. The present investigation was carried out to understand the preventive effect of Kombucha on heart weight, blood glucose, total protein, lipid profile and cardiac markers in rats with myocardial damage induced using Isoproterenol. As Bio-tea is produced by fermenting tea, the parameters were compared in rats pre-treated with normal black tea and Bio-tea for 30 days followed by subcutaneous injection of Isoproterenol (85 mg/kg body weight). Normal rats as well as Isoproterenol induced myocardial infarcted rats were also used, which served as controls. Isoproterenol induced myocardial infarcted control rats showed a significant increase in heart weight, blood glucose and cardiac markers and a decrease in plasma protein. Increased levels of cholesterol, triglycerides, low density lipids (LDL) and very low density lipids (VLDL) were also observed, while the high density lipid (HDL) content decreased. Bio-tea showed a higher preventive effect against myocardial infarction when compared to tea, as was observed by the significant reduction in heart weight, and blood glucose and increase in plasma albumin levels. Bio-tea significantly decreased cholesterol, triglycerides, LDL and VLDL while simultaneously increasing the levels of HDL. Similarly a decrease in leakage of cardiac markers from the myocardium was also observed. [ABSTRACT FROM AUTHOR]

We measured the level of cardiac markers (high-sensitivity troponin T and MB fraction of creatine kinase) in children of the first year of life with congenital heart disease in the perioperative period. After cardiac surgery, plasma levels of the above markers exceed the reference limits in the examined children. The diagnosis of myocardial ischemia using biochemical markers in the postoperative period is possible only by dynamic monitoring of the cardiac marker level. The preoperative concentration of high-sensitivity troponin T in children of the first year of life with congenital heart disease can be regarded as a predictor of postoperative complications. [ABSTRACT FROM AUTHOR]

Abstract: Cardiac mitochondrial damage plays an important role in the pathology of myocardial infarction. The protective effects of (−) epicatechin on cardiac mitochondrial damage in isoproterenol induced myocardial infarction were evaluated in rats. Rats were pretreated with (−) epicatechin (20mg/kg body weight) daily for a period of 21days. After the pretreatment period, isoproterenol (100mg/kg body weight) was injected subcutaneously into rats twice at an interval of 24h to induce myocardial infarction. Isoproterenol induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase and adenosine triphosphate. (−) Epicatechin pretreatment showed significant protective effects on all the biochemical parameters evaluated. The in vitro study revealed the superoxide and hydroxyl radical scavenging activity of (−) epicatechin. The possible mechanisms for the beneficial effects of (−) epicatechin on cardiac mitochondria could be attributed to scavenging of free radicals, decreasing calcium, increasing multi-enzymes (antioxidant, tricarboxylic acid cycle and respiratory chain enzymes), reduced glutathione and adenosine triphosphate. Thus, (−) epicatechin attenuated mitochondrial damage in isoproterenol induced myocardial infarcted rats. [Copyright &y& Elsevier]

Abstract: This study investigates the antihyperlipidemic effect of ursolic acid (UA) on isoproterenol (ISO) induced male albino Wistar rats. Myocardial ischemia was induced by subcutaneous injection of ISO (85mg/kg BW) twice at an interval of 24h, for two consecutive days. A significant increase in the activities of the serum marker enzymes [creatine kinase, creatine kinase-MB and lactate dehydrogenease (LDH)], a prominent expression of LDH 1 and LDH 2 isoenzymes, increased levels of plasma total cholesterol (TC), low density lipoprotein-cholesterol, very low density lipoprotein-cholesterol, triglycerides (TG), free fatty acids (FFA), phospholipids (PL) and atherogenic index and decreased level of high density lipoprotein-cholesterol were observed in ISO-induced rats. The levels of TC, TG and FFA increased and the level of PL decreased in the heart tissue of ISO-induced rats. Further, there was an increased DNA damage (Comet assay) and myocardium infarct size as observed by staining with triphenyltetrazolium chloride (TTC). UA was administered subcutaneously for 7days at a dose of 40mg/kg BW. UA administration to ischemic rats brought all these parameters to near normality showing the protective effect of UA on ISO-induced rats. [Copyright &y& Elsevier]

The present study evaluates the effect of aqueous extract of coconut haustorium on isoproterenol-induced myocardial infarction in Sprague Dawley rats. Rats were pretreated with aqueous extract of coconut haustorium (40 mg/100 g) orally for 45 days. After pretreatment, myocardial infarction was induced by injecting isoproterenol subcutaneously (20 mg/100 g body weight) twice at an interval of 24 h. Activity of marker enzymes like lactate dehydrogenase, creatinine kinase-MB, aspartate transaminase and alanine transaminase were increased in the serum and decreased in the heart of isoproterenol treated rats indicating cardiac damage. These changes were significantly reduced in haustorium pretreated rats. Moreover, an increase in the activities of antioxidant enzymes and decrease in the levels of peroxidation products were observed in the myocardium of coconut haustorium pretreated rats. Histopathology of the heart of these rats showed almost normal tissue morphology. From these results, it is clear that aqueous extract of coconut haustorium possess significant cardioprotective and antioxidant properties during isoproterenol-induced myocardial infarction in rats. [ABSTRACT FROM AUTHOR]

Abstract: The present study was designed to evaluate the protective effect of ursolic acid (UA) against isoproterenol-induced myocardial infarction. Myocardial infarction was induced by subcutaneous injection of isoproterenol hydrochloride (ISO) (85 mg/kg BW), for two consecutive days. ISO-induced rats showed elevated levels of cardiac troponins T (cTn T) and I (cTn I) and increased activity of creatine kinase-MB (CK-MB) in serum. Lipid peroxidative markers (thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and lipid hydroperoxides (HP)) elevated in the plasma and heart tissue whereas decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR)) in erythrocytes and heart tissue of ISO-induced rats. Non-enzymatic antioxidants (vitamin C, vitamin E and reduced glutathione (GSH)) levels were decreased significantly in the plasma and heart tissue of ISO-induced rats. Furthermore, ISO-induced rats showed increased DNA fragmentation, upregulations of myocardial pro-apoptotic B-cell lymphoma-2 associated-x (Bax), caspase-3, -8 and -9, cytochrome c, tumor necrosis factor-α (TNF-α), Fas and down-regulated expressions of anti-apoptotic B-cell lymphoma-2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL). UA-administered rats showed decreased levels/activity of cardiac markers, DNA fragmentation and the levels of lipid peroxidative markers in the plasma and heart tissue. Activities of enzymatic antioxidants were increased significantly in the erythrocytes and heart tissue and also non-enzymatic antioxidants levels were increased significantly in the plasma and heart tissue in UA-administered rats. UA influenced decreased DNA fragmentation and an apoptosis by upregulation of anti-apoptotic proteins such as Bcl-2, Bcl-xL and down-regulation of Bax, caspase-3, -8 and -9, cytochrome c, TNF-α, Fas through mitochondrial pathway. Histopathological observations were also found in line with biochemical parameters. Thus, results of the present study demonstrated that the UA has anti-apoptotic properties in ISO-induced rats. [Copyright &y& Elsevier]

Abstract: Background: High-sensitive Troponin I (hsTnI) facilitates the early diagnosis of myocardial infarction (MI). However, since hsTnI has not been well characterized in non-ischemic cardiac conditions, the predictive value of hsTnI for MI remains unclear. Methods: hsTnI (ADVIA Centaur, Siemens) on admission was analyzed in 929 patients with acute cardiac condition and invasive ascertainment of coronary status by catheterization. Results: Hs-TnI upon presentation was higher in patients with STEMI (median 1.27ng/mL, IQR 0.13–14.5ng/mL) as compared to patients with Non-STEMI (0.66ng/mL, IQR 0.10–4.0ng/mL, p <0.001) whereas it did not differ from STEMI in Tako-Tsubo cardiomyopathy (2.57ng/mL, IQR 0.17–8.4ng/mL) and myocarditis (9.76ng/mL, IQR 2.0–27.0ng/mL). In patients with resuscitation of non-ischemic cause (0.31ng/mL, IQR 0.06–1.3ng/mL), acute heart failure (0.088ng/mL, IQR 0.035–0.30ng/mL) and hypertensive emergency (0.066ng/mL, IQR 0.032–0.34ng/mL), hs-TnI was elevated above the recommended threshold of 0.04ng/mL. At this cutpoint of 0.04ng/mL, hsTnI indicated acute MI (STEMI or Non-STEMI) with a sensitivity of 88% and a specificity of 45% (ROC–AUC 0.748). When patients with STEMI were excluded, hsTnI indicated Non-STEMI with a sensitivity of 87% and a specificity of 45% (ROC–AUC 0.725). When sequential measurements were taken into account in a restricted cohort, a maximum hsTnI of ≥0.40ng/mL provided a sensitivity of 89% and a specificity of 85% (ROC–AUC 0.909) for Non-STEMI. Conclusions: HsTnI is a sensitive, albeit unspecific marker of MI. In patients with mildly elevated hsTnI and without evidence for STEMI, we suggest serial assessment of hsTnI and a 10-fold higher cutpoint of 0.40ng/mL before Non-STEMI is assumed. [Copyright &y& Elsevier]

Abstract: Background: Studies of cardiac markers in diagnosing acute myocardial infarction (AMI) have mostly been performed using central laboratory platforms. The AQT90 FLEX TnI (troponin I) assay is designed for quantitative point of care testing (POCT). This study evaluated clinical performance in diagnosing AMI of the AQT90 FLEX TnI POCT assay compared with central laboratory troponin assays. Methods: The study included 458 chest pain patients. Blood samples were obtained on admission and after 6–9h. Blood was analyzed using the following assays: AQT90 FLEX TnI, Access AccuTnI, Abbott AxSYM ADV, Roche cTnT, Roche CKMBmass. Patients were diagnosed with AMI according to the new universal definition of AMI. Results: The performance of the AQT90 FLEX TnI assay on admission was equivalent to the Abbott AxSYM ADV cTnI but inferior to the AccuTnI. After 6–9h both laboratory based assays were superior. The AQT90 FLEX TnI had a negative predictive value (NPV) of 90 and 96% (admission; 6–9h). No statistical differences were seen in receiver operating characteristics analysis. Conclusions: The AQT90 FLEX TnI POCT assay was marginally inferior to the two laboratory based assays of cTnI in diagnosing AMI. A high (NPV) may make this assay suitable as a rule out marker. [Copyright &y& Elsevier]

Eur J Clin Invest 2010; 40 (10): 874–882 Background Despite its proposed cardioprotective effect, the role of plasma urocortin in acute myocardial infarction (AMI) remains unknown. We investigated plasma profile of urocortin in AMI patients and evaluated its long-term prognostic performance. Material and methods Sixty-six AMI patients and 21 healthy subjects were included in this study. Blood samples for urocortin were collected on days 0 (onset), 1, 3 and 5 and at 3 and 6 months. Primary endpoint was mortality within 1 year of follow-up. Secondary endpoint was combined death and nonfatal adverse cardiac events (i.e. myocardial reinfarction, urgent revascularization or hospitalization due to heart failure) within 1 year. Results During follow-up at 1 year, 38 (57·6%) patients were alive without cardiac events, nine (13·6%) had nonfatal cardiac events and 17 (25·8%) died. Plasma urocortin in AMI patients were increased on days 0, 1, 3 and 5 ( P < 0·05 vs. control). The receiver-operating characteristic curve showed an area under curve (AUC) of day 0 urocortin to be 0·750 with 95% confidence interval (CI) of 0·619–0·881 ( P = 0·004), whereas AUC of NT-proBNP was 0·857 (95% CI, 0·722–0·992; P = 0·003). Sensitivity values for predicting the mortality of urocortin NT-proBNP and a combined urocortin and NT-proBNP were 0·81 (95% CI, 0·54–0·95), 0·86 (95% CI, 0·42–0·99) and 1·0 (95% CI, 0·56–1·0), respectively. Conclusions Plasma urocortin level is elevated in AMI patients for 5 days from onset. High plasma urocortin within 24 h after the onset is associated with increased mortality. Combined urocortin and NT-proBNP enhance prognostic performance in AMI patients. [ABSTRACT FROM AUTHOR]

Sudden cardiac deaths because of acute myocardial infarction (MI) constitute a significant percentage of the caseload for death investigators, coroners, and forensic pathologists. Clinicians use cardiac markers, highly sensitive and specific for myocardial damage, to screen living patients for acute MI; however, to this point, the utility of these markers in the autopsy setting has not been fully established. The current study included 10 decedents, five who died of acute MI, and five subjects who died of noncardiac disease. Samples of pericardial fluid and blood from multiple sites were tested for creatine kinase, creatinine kinase MB, and troponin-I. Three main conclusions were drawn: the levels of cardiac markers from all patients are significantly higher than the reference range for living patients, there are significant differences in cardiac marker levels between samples from different anatomic locations, and only three cardiac marker/anatomic site combinations were significantly different between the control and study groups. [ABSTRACT FROM AUTHOR]

The contractile sarcomeric pool of skeletal muscle and heart consists of a highly-ordered arrangement of actin thin filaments, tropomyosin and proteins of the troponin complex: troponin I (TnI), troponin T (TnT) and troponin C (TnC). The cardiac myocyte expresses specific isoforms of both TnI and TnT (cTnI and cTnT, respectively), which can be distinguished from skeletal muscle isoforms by rapid and reliable immunoassays. Due to their superior cardiac specificity, cTnI and cTnT have become the recommended biomarkers for the diagnosis of myocardial injury. The most common applications are for risk stratification and diagnosis of acute coronary syndromes, albeit they can also be used for assessing a variety of other myocardial disorders. However, the excellent diagnostic efficiency of cardiac troponin testing is jeopardized by some pre-analytical issues (unsuitable specimens for testing, analyte stability, handling, transportation and storage of specimens prior to analysis), as well as by analytical concerns related to standardization or harmonization of cTnI immunoassays, imprecision at low concentrations, antibody specificity, immunoreactivity of plasma isoforms released in the blood after myocardial injury, interference from autoantibodies, heterophilic antibodies, rheumatoid factor, and human anti-mouse antibodies. In addition, although the influence of some known mutations in cTnT and cTnI on calcium sensitivity and force generation have been readily demonstrated, their influence on current immunoassays is unknown. Most mutations in these proteins may contribute to the development of certain cardiomyopathies, namely hypertrophic and restrictive. In these situations, the phenotype is characterized by the underlying diseases, and the ability to detect cTnT or cTnI is of relatively little clinical significance. However, the cTnT Arg129Lys polymorphism and those observed in the stable domain of cTnI do not significantly alter the functional properties of the molecule within the myocardium and thus are predictably asymptomatic. While the actual prevalence of these polymorphisms in the general population is still unknown, they might be a source of potential analytical problems; modifying the immunogenicity of the molecule and leading to potential false negative results. The goal of this article is to provide an overview on the potential technical and analytical challenges in the measurement of cardiac troponins, along with the significance of polymorphisms in the genes encoding for cTnI and cTnT in both health and disease. Clin Chem Lab Med 2009;47:1183–94. [ABSTRACT FROM AUTHOR]

Abstract: Background: Release kinetics of ischaemia modified albumin (IMA) have not been described in detail and never in ongoing acute coronary syndrome. We compared IMA kinetics with early necrosis biomarkers during ST-segment elevation myocardial infarction (STEMI) and in different populations with ischaemic heart disease and healthy subjects. Methods: We investigated 1. patients with ongoing STEMI (n =25), 2. patients with non-ST segment elevation MI (n =5), 3. patients with stable angina (n =5), and 4. healthy subjects (n =5). Groups 1–3 underwent percutaneous coronary intervention (PCI). Fourteen blood samples were collected, of which 11 were obtained during the first 24 h following PCI. Samples were analyzed for IMA, cardiac troponin T, CKMB mass, myoglobin, and heart-type fatty acid binding protein. Results: In the STEMI group, mean IMA increased to 16% above upper limit of normal, peaking 40 min after PCI, and nearly normalizing within 2.5 h. Relative concentrations of IMA were low compared to other cardiac biomarkers. In all other groups, changes were non-significant. Conclusions: IMA is a marker of cardiac ischaemia with rapid clearance and a narrow diagnostic time window that may decrease NPV and clinical usefulness due to its dependency of short symptoms duration. Sensitivity of the assay was low compared to other markers. [Copyright &y& Elsevier]

Abstract: Background: Cardiac markers are a cornerstone for assessment of suspected acute coronary syndrome (ACS) patients. The National Academy for Clinical Biochemistry has recently developed practice guidelines for clinical, analytical and point-of-care (POC) testing in the context of ACS. Several technologies have become available for POC applications. Setting: Cardiac troponin is the preferred biochemical marker for diagnosis, risk stratification and guiding management of suspected ACS patients. Samples must be collected with proper timing, typically on presentation and then 6 to 9 h later. Assays should work toward a goal of total CV <10% at the 99th percentile cutpoint, and should adhere to specifications defined by professional organizations. A 1-h or less turnaround time is specified; quantitative POC testing should be implemented if this timing cannot be met consistently by the central laboratory. The same quality criteria for assays apply regardless of testing venue. Implementation/management: Laboratory medicine personnel must have active role in implementation, choice of technology and management of POC cardiac marker testing. Conclusions: Cardiac troponin measurements at POC are a viable alternative when testing needs cannot be met by the central laboratory. Laboratory medicine must be involved in implementation and ongoing service. Quality of testing must not be compromised by performance at POC. [Copyright &y& Elsevier]