Serum Levels Of Cardiac Enzymes Research Articles

Circ-0006332 stimulates cardiomyocyte pyroptosis via the miR-143/TLR2 axis to promote doxorubicin-induced cardiac damage

ABSTRACT Doxorubicin (DOX)-mediated cardiotoxicity can impair the clinical efficacy of chemotherapy, leading to heart failure (HF). Given the importance of circRNAs and miRNAs in HF, this paper intended to delineate the mechanism of the circular RNA 0006332 (circ -0,006,332)/microRNA (miR)-143/Toll-like receptor 2 (TLR2) axis in doxorubicin (DOX)-induced HF. The binding of miR-143 to circ -0,006,332 and TLR2 was assessed with the dual-luciferase assay, and the binding between miR-143 and circ -0,006,332 was determined with FISH, RIP, and RNA pull-down assays. miR-143 and/or circ -0,006,332 were overexpressed in rats and cardiomyocytes, followed by DOX treatment. In cardiomyocytes, miR-143 and TLR2 expression, cell viability, LDH release, ATP contents, and levels of IL-1β, IL-18, TNF-α, and pyroptosis-related molecules were examined. In rats, cardiac function, serum levels of cardiac enzymes, apoptosis, myocardial fibrosis, and levels of IL-1β, IL-18, TNF-α, TLR2, and pyroptosis-related molecules were detected. miR-143 diminished TLR2 expression by binding to TLR2, and circ -0,006,332 bound to miR-143 to downregulate miR-143 expression. miR-143 expression was reduced and TLR2 expression was augmented in DOX-induced cardiomyocytes. miR-143 inhibited DOX-induced cytotoxicity by suppressing pyroptosis in H9C2 cardiomyocytes. In DOX-induced rats, miR-143 reduced cardiac dysfunction, myocardial apoptosis, myocardial fibrosis, TLR2 levels, and pyroptosis. Furthermore, overexpression of circ -0,006,332 blocked these effects of miR-143 on DOX-induced cardiomyocytes and rats. Circ -0,006,332 stimulates cardiomyocyte pyroptosis by downregulating miR-143 and upregulating TLR2, thus promoting DOX-induced cardiac injury.

Carbon Dots Derived from Curcumae Radix and Their Heartprotective Effect.

Acute myocardial infarction (AMI) is a common cardiovascular disease in clinic. Currently, there is no specific treatment for AMI. Carbon dots (CDs) have been reported to show excellent biological activities, which hold promise for the development of novel nanomedicines for the treatment of cardiovascular diseases. In this study, we firstly prepared CDs from the natural herb Curcumae Radix Carbonisata (CRC-CDs) by a green, simple calcination method. The aim of this study is to investigate the cardioprotective effect and mechanism of CRC-CDs on isoproterenol (ISO) -induced myocardial infarction (MI) in rats. The results showed that pretreatment with CRC-CDs significantly reduced serum levels of cardiac enzymes (CK-MB, LDH, AST) and lipids (TC, TG, LDL) and reduced st-segment elevation and myocardial infarct size on the ECG in AMI rats. Importantly, cardiac ejection fraction (EF) and shortening fraction (FS) were markedly elevated, as was ATPase activity. In addition, CRC-CDs could significantly increase the levels of superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT), and reduce the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in myocardial tissue, thereby exerting cardioprotective effect by enhancing the antioxidant capacity of myocardial tissue. Moreover, the TUNEL staining image showed that positive apoptotic cells were markedly declined after CRC-CDs treatment, which indicate that CRC-CDs could inhibit cardiomyocyte apoptosis. Importantly, The protective effect of CRC-CDs on H2O2 -pretreated H9c2 cells was also verified in vitro. Taken together, CRC-CDs has the potential for clinical application as an anti-myocardial ischemia drug candidate, which not only provides evidence for further broadening the biological application of cardiovascular diseases, but also offers potential hope for the application of nanomedicine to treat intractable diseases.

Protective effects of epigallocatechin-3-gallate counteracting the chronic hypobaric hypoxia-induced myocardial injury in plain-grown rats at high altitude

Exposure to hypobaric hypoxia (HH) environment causes stress to the body, especially the oxygen-consuming organs. Chronic HH conditions have adverse effects on the myocardium. Thus, we conducted this experiment and aim to evaluate such adverse effects and explore the therapeutic role of epigallocatechin-3-gallate (EGCG) in rats’ heart under chronic HH conditions. For that purpose, we transported rats from plain to a real HH environment at high altitude for establishing the HH model. At high altitude, animals were treated with EGCG while the salidroside was used as the positive control. General physiological data were collected, and routine blood test results were analyzed. Cardiac magnetic resonance (CMR) was examined to assess the structural and functional changes of the heart. Serum levels of cardiac enzymes and pro-inflammatory cytokines were examined. Oxidative markers in the left ventricle (LV) were detected. Additionally, ultrastructural and histopathological changes and apoptosis of the LV were assessed. Furthermore, the antioxidant stress-relevant proteins nuclear factor E2-related factor 2 (Nrf2) and the heme oxygenase-1 (HO-1) were detected. The experiment revealed that EGCG treatment decreased HH-induced elevation of cardiac enzymes and relieved mitochondrial damage of the LV. Notably, EGCG treatment significantly alleviated oxidative stress in the LV and inflammatory response in the blood. Western blot confirmed that EGCG significantly upregulated Nrf2 and HO-1. Therefore, EGCG may be considered a promising natural compound for treating the HH-induced myocardial injuries.

Toxoplasma gondii Reactivation Aggravating Cardiac Function Impairment in Mice.

Toxoplasma gondii (T. gondii) reactivation is common, especially among immunocompromised individuals, such as AIDS patients. The cardiac involvement associated with toxoplasmosis, however, is usually obscured by neurological deterioration. The aim of this study was to observe the alterations in cardiac functions in various landmark periods after infection and to assess whether reactivation more seriously damages the heart. We established three infection models in mice using TgCtwh6, a major strain of T. gondii prevalent in China. The groups included an acute group, chronic latent group, and reactivation group. We evaluated the cardiac function impairment via H & E staining, Masson staining, echocardiography, myocardial enzyme profiles, and cardiac troponin, and detected the expression of inflammatory factors and antioxidant factors with Western blotting. Immunofluorescence was used to detect the expression of the macrophage marker F4/80. Our results showed that damage to the heart occurred in the acute and reactivation groups. Impaired cardiac function manifested as a decrease in heart rate and a compensatory increase in left ventricular systolic function. Serum levels of cardiac enzymes also increased dramatically. In the chronic phase, myocardial fibrosis developed, diastolic functions became severely impaired, inflammation persisted, and macrophage expression was slightly reduced. Ultimately, reactivation infection exacerbated damage to cardiac function in mice, potentially leading to diastolic heart failure. Macrophages were strongly activated, and myocardial fibrosis was increased. In addition, the antioxidant capacity of the heart was severely affected by the infection. Taken together, these results suggested that the reactivation of T. gondii infection could aggravate injury to the heart, which could be associated with a host-cell-mediated immune response and strong cytokine production by macrophages, thus representing a novel insight into the pathogenic mechanism of toxoplasmosis.

Comparative study between conventional crystalloid cardioplegic solution with modified del nido cardioplegia in mitral valve regurgitation surgery

Background: Cardioplegia is crucial for protecting the heart. Long-term cardiac protection is offered by the Del Nido Cardioplegia solution (dNCS). Aim: To compare conventional crystalloid cardioplegia with modified del Nido cardioplegia in mitral valve regurgitation replacement surgery. Objectives and Methods: This randomized clinical study included 80 patients undergoing to elective mitral regurgitation replacement surgery of both sex and age from 21 to 60 years with ASA (III and IV). All 80 patients were randomly assigned to receive conventional cardioplegia (St. Thomas’ cardioplegic solutions) or to obtain a modified del Nido cardioplegia (using normal saline) (groups A and B, respectively). The laboratory data for assessment of myocardial protection were obtained through measurements of preoperative serum levels of cardiac enzymes as, CK-MB, troponin, and lactate, immediately after operation, 12 and 24 hours postoperatively. Results: There was a significant increase in CK-MB only after 1 h (p < .001) in group (A) and after 12 h. CK-MB and lactate levels were significantly increased (p < 0.05). Also, after 24 h. CK-MB and Troponin T levels were significantly increased (p < .001). Regarding complications, one patient had atrial fibrillation and one case had permanent stroke in group (A), and two patients died in group (A), while one patient died in group (B) without a significant difference between the groups. Conclusions: We report that Modified Del Nido Cardioplegia has better postoperative chemical parameters as CK-MB, Troponin T and Lactate in mitral valve surgery in adults. DNC is a safe alternative to conventional cardioplegia and has achieved at least the same results.

The role of myocarditis in the acute phase of Kawasaki as a predictor of the future coronary aneurysm: a case–control study

BackgroundThis study aimed to evaluate the relationship between cardiac troponin I and T (cTnI, cTnT) and creatine kinase (CK)-MB during the acute phase of Kawasaki disease (KD) and the development of coronary artery involvement (CAI).ResultsNinety children diagnosed with KD and 38 attending ambulatory clinics as controls were enrolled in this study. Serum levels of cardiac enzymes were measured in all case and control groups. Serial echocardiograms were performed in KD patients during the acute, subacute and convalescence phases. Thirty-six percent of patients had CAI during the acute phase of KD; this rate was 21% and 18% in the echocardiography in the sub-acute and convalescent-phase, respectively. Elevated serum cTnI and cTnT levels were seen in 15.5% and 10% of KD patients, respectively, but not in the controls (P < 0.01). Patients with abnormal echocardiography had significantly higher levels of CK-MB but cTnI and cTnT. Cardiac troponins have high specificity, and CK-MB had a high sensitivity for predicting CAI in KD.ConclusionSubclinical myocarditis occurs during KD, and serum cardiac troponin levels are significantly elevated, but cardiac biomarkers cannot predict CAI in the future.

Cardioprotective effect of silymarin nanoemulsion on 5-fluorouracil-induced cardiotoxicity in rats.

5-Fluorouracil (5-FU)-associated cardiotoxicity has been ranked as the second most common cause of cardiotoxicity induced by chemotherapeutic drugs after anthracyclines. In the present study, we investigated the protective impacts of silymarin (SIL) and silymarin nanoemulsion (SLN) against cardiotoxicity caused by 5-FU in rats. Thirty male Wistar rats were divided into six groups as follows: control, SLN (5 mg/kg), SIL (5 mg/kg), 5-FU + SLN, 5-FU + SIL, and 5-FU. Cardiotoxicity was induced by a single intraperitoneal injection of 5-FU (100 mg/kg). The control group received an intraperitoneal injection (ip) of normal saline and the treatment groups received ips of SIL and SLN for 14 days. 5-FU resulted in significant cardiotoxicity, represented by an increase in the serum levels of cardiac enzymes and malondialdehyde, as well as cyclooxygenase-2 (COX-2) and tumor necrosis factor-α (TNF-α) expression, and histopathological degeneration. 5-FU treatment also induced a decrease in body weight, total antioxidant capacity (TAC), and catalase values. Evaluation of electrocardiographic parameters in 5-FU-treated rats showed increases in the ST segment, QRS duration, and RR interval. Treatment with SIL and SLN reduced oxidative stress, cardiac enzymes, histopathological degeneration, and the expression of TNF-α and COX-2 in cardiac tissue. Our results demonstrated that treatment with SIL and SLN significantly improved cardiotoxicity induced by 5-FU in rats.

Akut koroner sendromlarda sistemik immün-inflamasyon indeksi ve yüksek duyarlılıklı kardiyak troponin T

Aim: Acute coronary syndromes (ACSs) are classified as ST-segment elevated myocardial infarction (STEMI), non-ST-segment elevated myocardial infarction (NSTEMI) and unstable angina pectoris (USAP). Cardiac troponins constitute the cornerstone biomarkers for the laboratory diagnosis of ACS. In this study, we aimed to investigate whether systemic immune-inflammation index (SII) is associated with peak cardiac troponin T (TnT) levels in ACS.Methods: Consecutive patients with ACS whose coronary angiography was performed were included in the present study (n=397). Admission SII was determined as platelet count x neutrophil count/lymphocyte count. Serum levels of cardiac enzymes, including high-sensitivity TnT and creatine kinase-myocardial band (CK-MB), were measured at the time of admission and repeated daily during patients’ hospital stay.Results: Patients were categorized as namely STEMI (n=92) and NSTEMI/USAP (n=141). The findings obtained in this study showed that the median of SII levels was higher in STEMI than NSTEMI/USAP at a significant level. Correlation analysis of SII with various clinical and laboratory parameters demonstrated a significant correlation with C-reactive protein, peak CK-MB (r=0.52, p&amp;lt;0.001), peak TnT (r=0.49, p&amp;lt;0.001) and left ventricular ejection fraction (r= -0.48, p&amp;lt;0.001). Multivariate linear regression analysis identified age and log-SII (Beta Coefficient: 1.29, 95% Confidence Interval: 0.93-1.66, p&amp;lt;0.001) as independent predictors of peak TnT levels.Conclusion: SII is an independent predictor of peak TnT levels and significantly correlates with peak CK-MB levels in patients with ACS. SII significantly and inversely correlates with left ventricular systolic functions.

Evaluation of inflammatory miRNA155 and 146a expression in heart tissue of ovalbumin-sensitized male rats

Introduction: Asthma is a chronic pulmonary inflammation occurred in response to different allergens, leading to respiratory system insufficiency. The production of different inflammatory factors and enhanced immune system response may affect the function of other organs. The aim of this study was to investigate the expression of inflammatory microRNAs in cardiac tissue in asthmatic rat model. Methods: In this study, the animals were allocated into Control and Asthmatic rats (n=8). To induce asthma, rats were challenged with ovalbumin. 14 days after induction of asthma, rats were euthanized and Hematoxylin-Eosin staining was performed to assess pathological changes in pulmonary tissue. Serum levels of cardiac enzymes were measured using ELISA kits. Finally, transcription level of inflammatory miRNAs, miRNA-146a and -155, were measured using real-time PCR analysis. Results: Based on our findings, histological examination indicated the existence of pathological changes in pulmonary tissue after asthma induction. Bright-field analysis revealed an existence of inflammatory response and cytotoxicity in cardiac tissue. Also, the serum levels of CpK-MB, ALT, and AST were significantly higher in the serum of asthmatic group compared to control group (p&lt;0.05). Finally, asthmatic condition induced the expression of (2-fold) miRNA-146a and (1.5-fold)-155 in cardiac tissue, respectively. Conclusion: As a conclusion, it could be concluded that asthmatic condition induces systemic inflammation in cardiac tissue. On a more general note, we propose that therapeutical approaches directed to inflammatory pathway may be required to preserve cardiac injuries caused of asthma.

The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity.

Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose-dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX-induced cardiotoxicity (DICT). In an in vivo study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (Il6) and programmed cell death 1 (Pdcd1) in blood exhibited significant and positive correlations with the severity of DICT. In an in vitro study using cardiomyocyte H9c2 cells, knockdown of Il6 or Pdcd1 by small interfering RNA was revealed to enhance DOX-induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of Il6 and Pdcd1 in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for Il6 and Pdcd1 mRNA expression in DICT.

The Relationship between Serum Levels of Cardiac Enzymes and Junctional Ectopic Tachycardia (JET) after Cardiac Surgery of Congenital Heart Disease

Background In this study, we aimed to survey the relationship between serum levels of cardiac enzymes and junctional ectopic‏ tachycardia (JET) after corrective surgery of congenital heart disease (CHD). Materials and Methods: In this cohort study, 140 children with CHD who were hospitalized in intensive care unit of Shahid Modarres hospital in Tehran, Iran, were divided into case group (the JET group including 37 patients), and control group including 103 patients. These two groups were compared based on the previous studies and collected data. Results: Based on the analysis of the area under the Receiver Operating Characteristic curve, the Creatine Kinase Myocardial Band (CK-MB) level assessment can predict the occurrence of JET after the surgery (area under the curve is 0.849, 95% confidence interval is 0.786- 0.911), and the best cut-off point for it is 95.5 to predict the occurrence of JET. So, CK-MB will diagnose the occurrence of JET with 97.3% sensitivity and 67% specificity‏. In the same analysis, the troponin level assessment can predict the occurrence of JET after the surgery (area under the curve is 0.877, 95% confidence interval is 0.821- 0.933). Accordingly, the best cut-off point for the troponin is 45 to predict the occurrence of junctional ectopic‏ tachycardia which will diagnose it with 97.3% sensitivity, and 72.8% specificity‏. Conclusion There is a positive correlation between the occurrence of JET after corrective surgery of CHD and an increase in the level of CK-MB and troponin enzymes. So that the level of CK-MB above 95.5 and the level of troponin above 45 might predict the occurrence of JET in these patients with high accuracy.

Release of high-sensitive TROPonin T by implantation of an entirely subcutaneous Implantable Cardioverter-defibrillator compared to a conventional transvenous approach: the TROPIC registry.

Implantation of a subcutaneous implantable cardioverter-defibrillator (S-ICD) has become an alternative option when a conventional transvenous approach is not suitable. The myocardial damage caused by S-ICD implantation appears to be minimal despite mandatory defibrillation threshold (DFT) testing. However, there has not been a direct comparison with the traditional transvenous placement of a single-chamber ICD (VVI-ICD). The aim of this study was to determine the extent of myocardial damage by analysing the changes in serum levels of cardiac enzymes after S-ICD implantation in comparison with VVI-ICD. In 43 patients who received an S-ICD system, differences in serum levels of high-sensitive troponin T (ΔhsTnT) and creatine kinase total (ΔCK) and muscle brain fraction (ΔCK-MB) were acquired by blood sampling before and the day after implantation. The control group consisted of 43 patients from the TropShock study who had received a transvenous VVI-ICD without DFT. After S-ICD implantation and testing procedure, ΔhsTnT (0.000ng/ml, IQR - 0.003-0.002ng/ml) was significantly lower than after conventional VVI-ICD implantation (0.018ng/ml, IQR 0.004-0.032ng/ml; p < 0.001). There was no significant difference in CK (ΔCKS-ICD 85.0U/I, IQR 30.5-225.8U/I vs ΔCKVVI-ICD 69.5U/I, IQR 22.9-172.3U/I; p = 0.357), but there was a significant difference in CK-MB (ΔCK-MBS-ICD of - 0.60, IQR - 2.60-1.0 vs ΔCK-MBVVI-ICD 1.0, IQR - 1.08-3.18; p = 0.030). S-ICD implantation causes less myocardial damage than VVI-ICD implantation evidenced by ΔhsTnT and ΔCK-MB.

Curcumin suppresses doxorubicin-induced cardiomyocyte pyroptosis via a PI3K/Akt/mTOR-dependent manner.

Doxorubicin (DOX) is one of the most effective anti-neoplastic drugs although its clinical use is limited by the severe cardiotoxicity. Apoptosis and defective autophagy are believed to contribute to DOX-induced cardiotoxicity. Here we explored the effect of curcumin (Cur) on DOX-induced cardiac injury and the mechanism involved with a focus on oxidative stress, autophagy and pyroptosis. Kunming mice were challenged with DOX (3 mg·kg-1, i.p. every other day) with cohorts of mice receiving Cur at 50, 100, 200 and 400 mg·kg-1 via gavage daily. Serum levels of cardiac enzymes, such as aspartate amino transferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), and heart homogenate oxidative stress markers, such as superoxide dismutase (SOD) and malondialdehyde (MDA) were determined. Echocardiographic and cardiac contraction were examined. Apoptosis, pyroptosis, autophagy and Akt/mTOR-signalling proteins were detected using western blot or electron microscopy. Cardiac contractile properties were assessed including peak shortening, maximal velocity of shortening/relengthening (± dL/dt), time-to-PS, and time-to-90% relengthening (TR90). Superoxide levels were evaluated using DHE staining. GFP-LC3 was conducted to measure autophagosomes. Our study showed that Cur protected against cardiotoxicity manifested by a significant decrease in serum myocardial enzymes and improvement of anti-oxidative capacity. Cur inhibited autophagy and offered overt benefit for cardiomyocyte survive against DOX-induced toxicity. Cur attenuated DOX-induced cardiomyocyte pyroptosis as evidenced by NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and interleukin-18 levels. DOX impaired cardiac function (reduced fractional shortening, ejection fraction, increased plasma cTnI level and TR90, decreased PS and ± dL/dt), the effects of which were overtly reconciled by 100 mg·kg-1 but not 50 mg·kg-1 Cur. H9c2 cells exposure to DOX displayed increased intracellular reactive oxygen species (ROS) and autophagy, the effects of which were nullified by Cur. Autophagy activator rapamycin cancelled off Cur-induced protective effects. Our finding suggested that Cur rescued against DOX-induced cardiac injury probably through regulation of autophagy and pyroptosis in a mTOR-dependent manner.

Short-term remote ischemic conditioning may protect monkeys after ischemic stroke.

ObjectiveWe aimed to evaluate the safety and effectiveness of short‐term remote ischemic postconditioning (RIPC) in acute stroke monkey models.MethodsAcute stroke monkeys were allocated to four groups based on the number of limbs exposed to RIPC. RIPC was initiated by 5‐min cuff inflation/deflation cycles of the target limb(s) for 5–10 bouts. Vital signs, skin integrity, brain MRI, and serum levels of cardiac enzymes (myoglobin, creatine kinase [CK], CK‐muscle/brain [CK‐MB]), one inflammatory marker (high‐sensitivity C‐reactive protein [hsCRP], and one endothelial injury marker (von Willebrand factor [vWF]) were assessed. Spetzler scores were used to assess neurological function.ResultsNo significant differences in vital signs or local skin integrity were found. Short‐term RIPC did not reduce infarct volume under any condition at the 24th hour after stroke. However, neurological function improved in multi‐limb RIPC compared with sham and single‐limb RIPC at the 30th day follow‐up after stroke. Myoglobin, CK, and CK‐MB levels were reduced after multi‐limb RIPC, regardless of the number of bouts. Moreover, multi‐limb RIPC produced a greater diminution in CK‐MB levels, whereas two‐limb RIPC was more effective in reducing serum CK levels at the 24th hour after stroke. hsCRP increased after 5 bouts of multi‐limb RIPC before decreasing below baseline and single‐limb RIPC levels. Serum vWF was decreased at later time points after RIPC in all RIPC groups.ConclusionsStroke monkeys in hyperacute stage may benefit from short‐term RIPC; however, whether this intervention can be translated into clinical use in patients with acute ischemic stroke warrants further study.

The protective effects of compatibility of Aconiti Lateralis Radix Praeparata and Zingiberis Rhizoma on rats with heart failure by enhancing mitochondrial biogenesis via Sirt1/PGC-1α pathway

Aconiti Lateralis Radix Praeparata (“Fuzi” in Chinese) in combination with Zingiberis Rhizoma (“Ganjiang” in Chinese) is commonly applied for the treatment of heart failure for thousands of years in China. However, its therapeutic mechanism is still poorly defined. This study aimed to investigate whether the compatibility of Fuzi and Ganjiang can protect rats with acute heart failure by enhancing mitochondrial biogenesis via Sirt1/PGC-1α signaling pathway. Hemodynamic parameters, including heart rate and left ventricular maximal rate of pressure rise and decline, were recorded in rats with acute heart failure induced by Propafenone hydrochloride. The serum levels of cardiac enzymes, including creatine kinase, lactate dehydrogenase, brain natriuretic peptide and cardiac troponin T, were also determined. The gene and protein levels of Sirtuin 1 (Sirt1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and their downstream transcription factors were measured as well. The results indicated that Fuzi-Ganjiang herbal couple provided more significant benefits by restoring the left ventricular function and cardiac enzyme activities in comparison with their single use. Moreover, this herbal couple possessed a significant cardio-protection by increasing both gene and protein levels of Sirt1 and PGC-1α. In conclusion, the compatibility of Fuzi and Ganjiang had better therapeutic effect than their single use against failing heart, and the underlying mechanisms were partially through increasing mitochondrial biogenesis via Sirt1/PGC-1α pathway.

Role of ATP-Sensitive Potassium Channels in Remote Ischemic Preconditioning Induced Tissue Protection.

Remote ischemic preconditioning (RIPC) is an innovative treatment strategy that alleviates ischemia-reperfusion injury, whereby short episodes of regional ischemia and reperfusion delivered to remote organs including hind limb, kidney and intestine, and so on provide protection to the heart. The RIPC is known to reduce infarct size, serum levels of cardiac enzymes, and myocardial dysfunction in various animal species as well as in patients. There have been a large number of studies suggesting that the ATP-sensitive potassium channels (KATP channel) play a significant role as a mediator or end effector in RIPC. The present review discusses the role of KATP channels and possible mechanisms in RIPC-induced cardioprotection.

ECG changes in birth asphyxia and its correlation with Cardiac troponin-I

Introduction: Cardiac dysfunction is well known in perinatal asphyxia caused by transit myocardial ischemia. Sometimes cardiac dysfunction may be so severe that it can cause congestive cardiac failure and shock that leads to death of newborn. ECG and serum levels of cardiac enzymes can be used to demonstrate impaired myocardial function. Material and Methods: It was a case control study conducted in the department of paediatrics, Gandhi Medical College, Bhopal over a period of 12 months from January 2013 to December 2013. Forty asphyxiated full term neonates were taken as cases and 20 healthy full term neonates as controls. Forty neonates with asphyxia admitted to NICU with gestational age &gt;37 completed weeks and with birth weight &gt;2 kg taken as cases and twenty healthy full term neonates (37 completed wks) unasphyxiated weighing &gt;2 kg at birth with clear liquor and 1 min Apgar score &gt;7. Results: Myocardial dysfunction was present in 90% of the newborns with severe birth asphyxia and 40% of newborns with moderate birth asphyxia. T wave changes were seen in 80% neonates with severe asphyxia and 33% neonates with moderate asphyxia. In present study, cTn I levels in severely asphyxiated neonates were significantly higher than moderately asphyxiated neonates and control group neonates (4.6 ng/ml, range 2.1 – 7.8, and 1.8 ng/ml, range 0.2 – 4.8 ng/ml and 0.6ng/ml, range 0.2-1ng/ml respectively). Conclusion: We found a linear relationship between levels of cardiac troponin-I and birth asphyxia. Therefore cardiac troponin-I level may be useful in predicting the mortality and outcome in perinatal asphyxia.

Not Acute Myocardial Infarction in a Teenager Due to Adderall XR

The case report of Sylvester and Agarwala [4] purports to be that of a myocardial infarction in a teenager receiving methylphenidate. The electrocardiogram (ECG) shown is typical of early repolarization changes that are a normal variant and that often cause concern when a young (usually male) patient presents to the emergency room with chest pain. This presentation is, of course, also typical of acute inflammatory pericarditis. Although there is an impression that raised serum levels of cardiac enzymes are specific for myocardial infarction, this is not necessarily the case. Certainly, when the clinical picture is that of myocardial ischemia, these raised serum levels of cardiac enzymes are extremely helpful in establishing or excluding myocardial infarction. When the clinical picture is not that of myocardial ischemia, then they should not automatically be attributed to myocardial infarction, and there are many noncardiac causes [2]. The most likely cause for the reported patient’s disorder is acute pericarditis or possibly myopericarditis, although with the latter, even higher levels of cardiac enzymes might have been expected. The headache for several days before the presentation would be typical of a viral prodrome, which in itself can cause a rise in serum troponin. Viral titers performed at presentation and in the recovery phase would have been very helpful. Unless the ECG changes reversed completely when the pain subsided, the disorder also is highly unlikely to have been coronary spasm, in which the major ST elevation typically should have been coved upward. If it was myocardial infarction, then the ECG would have shown progressive changes. Although some reports have described myocardial ischemia when stimulant medication for attention deficit hyperactivity disorder (ADHD) has been used in overdose or abuse [1, 3], this case does not add to these concerns with normal dosing.

Acute Reversible Stress-Induced Cardiomyopathy Associated with Cesarean Delivery under Spinal Anesthesia

Stress-induced cardiomyopathy (SIC), also known as transient left ventricular apical ballooning or Tako-tsubo cardiomyopathy, is characterized by reversible left ventricular dysfunction, chest pain or dyspnea, ST-segment elevation, and minor elevations in serum levels of cardiac enzymes, in the absence of significant coronary artery disease.1 Although its pathogenesis is incompletely understood, intense emotional or physical stress is a well-recognized precipitant.2 We present a case of SIC with severe left ventricular dysfunction but minimal ECG changes in a young, woman who received spinal anesthesia for elective cesarean delivery. A 31-year-old healthy woman was admitted at 40 weeks gestation for elective repeat cesarean delivery. Both her previous and current pregnancies were uncomplicated. Her first cesarean delivery was performed uneventfully with epidural anesthesia. She had no family history of heart disease and appeared calm on entry into the operating room. Successful spinal anesthesia was achieved …

A case of Takotsubo cardiomyopathy mimicking an acute coronary syndrome

A 71-year-old woman presented with severe chest pain after an episode of acute emotional distress. Her serum levels of cardiac enzymes were slightly elevated and electrocardiography revealed anterior ST-segment elevations. Significant coronary stenoses were excluded. A left ventriculogram revealed apical ballooning and a hypercontractile basal segment. Serum cardiac enzyme measurements, echocardiography, coronary angiography and left ventriculography. Takotsubo cardiomyopathy. Treatment with beta-blockers, aspirin, angiotensin-converting-enzyme inhibitors, and intravenous diuretics.