Creatine Phosphokinase MB Isoenzyme Research Articles

HGF ameliorates cardiomyocyte apoptosis and inflammatory response in sepsis via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway

ObjectiveThis study aimed to analyze the impact of HGF on cardiomyocyte injury, apoptosis, and inflammatory response induced by lipopolysaccharide (LPS). MethodsEnzyme-linked immunosorbent assay (ELISA) was utilized to quantify the levels of HGF, interleukin (IL)-6, IL-10, creatine phosphokinase-isoenzyme-MB (CK-MB), and cardiac troponin I (cTnI) in the samples. qPCR and Western blotting (WB) were employed to assess the mRNA and protein expressions of HGF, IL-10, IL-6, PI3K, AKT, p-PI3K, and p-AKT. ResultsThe outcomes of the in vivo experiment revealed that serum levels of IL-6, IL-10, HGF and SOFA scores in the SC group were elevated in contrast to the non-SC group. The correlation analysis indicated a substantial and positive association among serum HGF, IL-6, and IL-10 levels and SOFA scores. Relative to IL-6, IL-10 levels, and SOFA scores, serum HGF demonstrated the highest diagnostic value for SC. Following LPS administration to stimulate H9c2 cells across various periods (0, 12, 24, 48, and 72 h), the levels of myocardial injury markers (CK-MB and cTnI) in the cell supernatants, intracellular inflammatory factors (mRNA and protein levels of IL-10 and IL-6), apoptosis and ROS levels, exhibited a gradual increase followed by a subsequent decline. Following the overexpression of HGF, there was an increase in cell viability, and a decrease in apoptosis, inflammation, oxidative stress injuries, and the protein phosphorylation expressions of PI3K and AKT. After knockdown of HGF expression, the activity of LPS-induced H9c2 cells was further reduced, leading to increased cell injury, apoptosis, inflammation, oxidative stress,and the expression levels of PI3K and Akt protein phosphorylation were further elevated. ConclusionHGF was associated with decreased LPS-induced H9c2 apoptosis and inflammation in H9c2 cells, alongside an improvement in cell viability, indicating potential cytoprotective effects. The mechanism underlying these impacts may be ascribed to the suppression of the PI3K/AKT signaling pathway.

ECG and Biomarker Profile in Patients with Acute Heart Failure: A Pilot Study.

Biomarkers, electrocardiogram (ECG) and Holter ECG are basic, accessible and feasible cardiac investigations. The combination of their results may lead to a more complex predictive model that may improve the clinical approach in acute heart failure (AHF). The main objective was to investigate which ECG parameters are correlated with the usual cardiac biomarkers (prohormone N-terminal proBNP, high-sensitive cardiac troponin I) in patients with acute heart failure, in a population from Romania. The relationship between certain ECG parameters and cardiac biomarkers may support future research on their combined prognostic value. In this prospective case-control study were included 49 patients with acute heart failure and 31 participants in the control group. For all patients we measured levels of prohormone N-terminal proBNP (NT-proBNP), high-sensitive cardiac troponin I (hs-cTnI) and MB isoenzyme of creatine phosphokinase (CK-MB) and evaluated the 12-lead ECG and 24 h Holter monitoring. Complete clinical and paraclinical evaluation was performed. NT-proBNP level was significantly higher in patients with AHF (p < 0.001). In patients with AHF, NT-proBNP correlated with cQTi (p = 0.027), pathological Q wave (p = 0.029), complex premature ventricular contractions (PVCs) (p = 0.034) and ventricular tachycardia (p = 0.048). Hs-cTnI and CK-MB were correlated with ST-segment modification (p = 0.038; p = 0.018) and hs-cTnI alone with complex PVCs (p = 0.031). The statistical relationships found between cardiac biomarkers and ECG patterns support the added value of ECG in the diagnosis of AHF. We emphasize the importance of proper ECG analysis of more subtle parameters that can easily be missed. As a non-invasive technique, ECG can be used in the outpatient setting as a warning signal, announcing the acute decompensation of HF. In addition, the information provided by the ECG complements the biomarker results, supporting the diagnosis of AHF in cases of dyspnea of uncertain etiology. Further studies are needed to confirm long-term prognosis in a multi-marker approach.

Influence of Ginsenoside Rh2 on Cardiomyocyte Pyroptosis in Rats with Acute Myocardial Infarction.

Objective This paper intends to verify through in vivo experiments whether ginsenoside Rh2 (G-Rh2) can play an anti-inflammatory role by modulating cardiomyocyte (CM) pyroptosis in rats with acute myocardial infarction (AMI), thereby alleviating myocardial injury. Methods Twenty SD rats were randomized into control, L-Rh2, M-Rh2, and H-Rh2 groups, among which the latter three groups were modeled for AMI and given an intraperitoneal injection of G-Rh2 (L-Rh2: 2 mg/kg; M-Rh2: 4 mg/kg; H-Rh2: 8 mg/kg), while the control group was only treated with thoracotomy and sodium chloride injection. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), and left ventricular end-diastolic pressure (LVEDP) were recorded by ultrasonic diagnosis. Rats were killed under anesthesia, and the morphological characteristics of ventricular tissue were observed by electron microscope. Additionally, cardiac blood and ventricular tissues were collected to quantify the contents of myocardial injury markers (creatine phosphate kinase (CK), creatine phosphokinase-MB isoenzyme (CK-MB), and lactate dehydrogenase (LDH) by ELISA, as well as the expression of pyroptosis-related genes cysteinyl aspartate specific proteinase 1 (Caspase-1), gasdermin D (GSDMD), interleukin (IL)-1β, and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) by qRT-PCR and Western blot). Results Ultrasonic examination identified lower HR, SBP, DBP, MAP, and LVSP in the three Rh2 injection groups compared with the control group (P < 0.05); and in comparison with M- and H-Rh2 groups, HR, SBP, DBP, MAP, and LVSP were all lower in L-Rh2 group, while LVEDP was higher (P < 0.05). Microscopically, CMs and organelles in the L-RH2, M-RH2, and H-RH2 groups were damaged to varying degrees compared with the control group, with those in the L-RH2 group being the most serious. CK, CK-MB, and LDH were also the highest in the L-Rh2 group and the lowest in the control group, while their levels were obviously reduced in M- and H-Rh2 groups (P < 0.05). Finally, GSDMD, IL-1β, NLRP3, and Caspase-1 were found to be reduced in the control group, while pyroptosis-related gene expression in the M-Rh2 group was improved markedly (P < 0.05). Conclusion G-Rh2 can inhibit the pathological development of AMI by relieving the focal death of CM and inhibiting the release of proinflammatory factors in the body, and the effect is significantly related to the dosage, which is expected to become a new treatment option for AMI in the future.

The disquietude of clozapine continuation during the COVID-19 pandemic.

The disquietude of clozapine continuation during the COVID-19 pandemic.

Malignant hyperthermia when dantrolene is not readily available

BackgroundMalignant hyperthermia is a rare but life-threatening pharmacogenetic muscle disorder characterized by abnormal hypermetabolic reactions and commonly triggered in susceptible individuals by volatile anesthetics or succinylcholine, or both. Unfortunately, the specific medicine dantrolene is not readily available in many countries including China. The aim of this study was to find the characteristics of malignant hyperthermia under the situation that dantrolene is not readily available.MethodsThe cases of malignant hyperthermia reported on the most commonly used databases in China from 1985 to 2020 were analyzed. The inclusion criteria were the MH episodes only related to anesthesia. The exclusion criteria were dubious MH episodes only caused by Ketamine administration or MH episodes irrelevant to anesthesia. Independent samples t-test and Pearson’s chi-squared test were applied to assess the difference between the survived and death cases.ResultsNinety-two cases of malignant hyperthermia reported on the most commonly used databases in China from 1985 to 2020 were analyzed. Median (IQR [range]) age was 18.5 (11.8–37.0 [0–70.0]) years. Compared with the survived cases, the death cases had higher maximum end-tidal partial pressure of CO2 (P = 0.033), the maximum arterial partial pressure of CO2 (P = 0.006), temperature first measured when the patient was first discovered abnormal (P = 0.012), and maximum temperature (P < 0.001). Besides, the death cases had less minimum pH (P < 0.001) and higher potassium (P < 0.001) and were more likely to have coagulation disorders (p = 0.018). Concerning treatment, cases used furosemide (P = 0.024), mannitol (P = 0.029), blood purification treatment (P = 0.017) had the advantage on the outcome. Creatine phosphokinase, myoglobin, and MB isoenzyme of creatine phosphokinase differed greatly among cases during the first week. 43 (46.7%) cases had congenital diseases. 12 (13.0%) cases were reported with abnormal laboratory test results or abnormal signs that are possibly relevant before anesthesia.ConclusionsIn countries that dantrolene is not readily available, early warning, diagnosis, and prompt effective therapies are crucial for MH patients to survive.

Clinical and echocardiographic predictors of left ventricular remodeling following anterior acute myocardial infarction

OBJECTIVES:Coronary artery disease is the primary cause of death and is responsible for a high number of hospitalizations worldwide. Ventricular remodeling is associated with worse prognosis following ST-segment elevation myocardial infarction (STEMI) and is a risk factor for ventricular dysfunction and heart failure. This study aimed to identify the predictors of ventricular remodeling following STEMI. Additionally, we evaluated the clinical, laboratory, and echocardiographic characteristics of patients with anterior wall STEMI who underwent primary percutaneous intervention in the acute phase and at 6 months after the infarction.METHODS:This prospective, observational, and longitudinal study included 50 patients with anterior wall STEMI who were admitted to the coronary care unit (CCU) of a tertiary hospital in Brazil between July 2017 and August 2018. During the CCU stay, patients were evaluated daily and underwent echocardiogram within the first three days following STEMI. After six months, the patients underwent clinical evaluation and echocardiogram according to the local protocol.RESULTS:Differences were noted between those who developed ventricular remodeling and those who did not in the mean±standard deviation levels of creatine phosphokinase MB isoenzyme (CKMB) peak (no remodeling group: 323.7±228.2 U/L; remodeling group: 522.4±201.6 U/L; p=0.008) and the median and interquartile range of E/E’ ratio (no remodeling group: 9.20 [8.50-11.25] and remodeling group: 12.60 [10.74-14.40]; p=0.004). This difference was also observed in multivariate logistic regression.CONCLUSIONS:Diastolic dysfunction and CKMB peak in the acute phase of STEMI can be predictors of ventricular remodeling following STEMI.

Effects and mechanisms of glucose-insulin-potassium on post-procedural myocardial injury after percutaneous coronary intervention.

ObjectiveTo evaluate the effects and mechanisms of glucose-insulin-potassium (GIK) on post-procedural myocardial injury (PMI) after percutaneous coronary intervention (PCI).MethodsA total of 200 non-diabetic patients with documented coronary heart disease (CHD) were divided into the Group GIK and Group G, with 100 patients in each group. Patients in Group G were given intravenous infusion of glucose solution 2 hours before PCI. As compared, patients in Group GIK were given GIK.ResultsBoth post-procedural creatine phosphokinase isoenzyme MB (CK-MB; 62.1 ± 47.8 vs. 48.8 ± 52.6 U/L, P = 0.007) and cTnI (0.68 ± 0.83 vs. 0.19 ± 0.24 ng/mL, P < 0.001) in Group GIK were significantly higher than those in Group G. In Group G, 9.0% and 4.0% of patients had post-procedural increases in CK-MB 1-3 times and > 3 times, which were significantly lower than those in Group GIK (14.0% and 7.0%, respectively; all P values < 0.01); 13.0% and 7.0% of patients had post-procedural increases in cTnI 1-3 times and > 3 times, which were also significantly lower than those in Group GIK (21.0% and 13.0%, respectively; all P < 0.001). Pre-procedural (10.2 ± 4.5 vs. 5.1 ± 6.3, P < 0.001) and post-procedural rapid blood glucose (RBG) levels (8.9 ± 3.9 vs. 5.3 ± 5.6, P < 0.001) in Group G were higher than those in Group GIK. In adjusted logistic models, usage of GIK (compared with glucose solution) remained significantly and independently associated with higher risk of post-procedural increases in both CK-MB and cTnI levels > 3 times. Furthermore, pre-procedural RBG levels < 5.0mmol/L were significantly associated with higher risk of post-procedural increases in both CK-MB and cTnI levels.ConclusionsIn non-diabetic patients with CHD, the administration of GIK may increase the risk of PMI due to hypoglycemia induced by GIK.

Point-of-Care Diagnosis of Acute Myocardial Infarction in Central Vietnam: International Exchange, Needs Assessment, and Spatial Care Paths.

Objectives were to (a) advance point-of-care (POC) education, international exchange, and culture; (b) report needs assessment survey results from Thua Thien Hue Province, Central Vietnam; (c) determine diagnostic capabilities in regional health care districts of the small-world network of Hue University Medical Center; and (d) recommend Spatial Care Paths that accelerate the care of acute myocardial infarction (AMI) patients. We organized progressively focused, intensive, and interactive lectures, workshops, and investigative teamwork over a 2-year period. We surveyed hospital staff in person to determine the status of diagnostic testing at 15 hospitals in 7 districts. Questions focused on cardiac rapid response, prediabetes/diabetes, infectious diseases, and other serious challenges, including epidemic preparedness. Educational exchange revealed a nationwide shortage of POC coordinators. Throughout the province, ambulances transfer patients primarily between hospitals, rarely picking up from homes. No helicopter rescue was available. Ambulance travel times from distant sites to referral hospitals were excessive, longer in costal and mountainous areas. Most hospitals (92.3%) used electrocardiogram and creatine phosphokinase-MB isoenzyme to diagnose AMI. Cardiac troponin I/T testing was performed only at large referral hospitals. Central Vietnam must improve rapid diagnosis and treatment of AMI patients. Early upstream POC cardiac troponin testing on Spatial Care Paths will expedite transfers directly to hospitals capable of intervening, improving outcomes following coronary occlusion. Point-of-care coordinator certification and financial support will enhance standards of care cost-effectively. Training young physicians pivots on high-value evidence-based learning when POC cardiac troponin T/cardiac troponin I biomarkers are in place for rapid decision making, especially in emergency rooms.

Prognostic Predictors of Outcome in Patients with Snake Bite, Based on Initial Findings in the Emergency Department

Purpose: This study was conducted to identify predictors of serious poisoning in patients with snake bite based on initial findings. Methods: We conducted a retrospective study of patients with snake bite who were treated at the emergency department between January 2010 and December 2016. The patients were divided into two groups according to the severity of symptoms based on the traditional snakebite severity grading scale. The mild poisoning group (MP) was classified as those who had a grade I snakebite severity during the hospital stay, and the severe poisoning group (SP) was classified as patients who had grade I at the time of admission, but progressed to grade II-IV during hospitalization. Initial clinical manifestations and laboratory findings of the two groups were compared. Results: Bite to hospital time intervals of SP were longer than those of MP (p=0.034), and the local effect score (LES) was higher in SP (p&lt;0.001). Laboratory analyses revealed that creatine phosphokinase (p=0.044), creatine phosphokinase MB isoenzyme (CK-MB, p=0.011) and serum amylase (p=0.008) were significantly higher in SP. LES, CK-MB and serum amylase were significant prognostic predictors as indicated by univariate logistic regression analysis. Multivariate analysis revealed the following two significant predictors: LES (odds ratio=3.983, p&lt;0.001) and serum amylase (odds ratio=1.020, p=0.017). Conclusion: In managing cases of snake bites, clinical manifestations and laboratory findings must be carefully evaluated. LES and serum amylase are predictive factors for severe poisoning, which is especially important to rapid determination of the intensive care of the patient.

Impact of Acute Bronchiolitis on Cardiac Functions and Serum microRNA-122 and 499

Bronchiolitis is an acute inflammatory injury of the bronchioles that is usually caused by a viral infection, most commonly Respiratory Syncytial Virus (RSV). This study aimed to verify the direct injurious effect of acute bronchiolitis on the myocardium and serum level of microRNA-122 and 499 (miR-122 and miR-499) of infected infants. Serum lactate dehydrogenase (LDH), creatine phosphokinase-isoenzyme MB (CK-MB) and cardiac troponin I (cTp I) were significantly elevated in mild to moderate group as well as severe group except cTp I which showed non-significant elevation in mild to moderate group, compared to control group. Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) was carried out to evaluate the serum level of miR-122 and miR-499. Sharp elevation in serum miR-122 was observed in severe cases, while miR-499 was statistically non-significant as compared to both normal and mild to moderate groups. The flow velocities across the pulmonary, tricuspid and mitral valves were recorded using standard echocardiographic techniques. Echocardiographic data showed significant reduction in pulmonary At/Et ratio in severe bronchiolitis group, compared to both normal and mild to moderate groups, respectively. Parallel reduction was also observed in tricuspid and mitral E/A ratios, compared to both normal and mild to moderate groups, respectively. Severe bronchiolitis causes cardiac dysfunction due to hypoxia, cardiac strain and pulmonary hypertension in addition to up-regulation of serum miRNA-122.

Ultrasmall superparamagnetic iron oxide nanoparticles acutely promote thrombosis and cardiac oxidative stress and DNA damage in mice.

BackgroundUltrasmall superparamagnetic iron oxide nanoparticles (USPIO) are being developed for several biomedical applications including drug delivery and imaging. However, little is known about their possible adverse effects on thrombosis and cardiac oxidative and DNA damage.MethodsPresently, we investigated the acute (1 h) effect of intravenously (i.v.) administered USPIO in mice (0.4, 2 and 10 μg/kg). Diesel exhaust particles (DEP; 400 μg/kg) were used as positive control.ResultsUSPIO induced a prothrombotic effect in pial arterioles and venules in vivo and increased the plasma plasminogen activator inhibitor-1 (PAI-1). Both thrombogenicity and PAI-1 concentration were increased by DEP. The direct addition of USPIO (0.008, 0.04 and 0.2 μg/ml) to untreated mouse blood dose-dependently induced in vitro platelet aggregation. USPIO caused a shortening of activated partial thromboplastin time (aPTT) and prothrombin time (PT). Similarly, DEP administration (1 μg/ml) triggered platelet aggregation in vitro in whole blood. DEP also reduced PT and aPTT. The plasma levels of creatine phosphokinase-MB isoenzyme (CK-MB), lactate dehydrogenase (LDH) and troponin-I were increased by USPIO. DEP induced a significant increase of CK-MB, LDH and troponin I levels in plasma. The cardiac levels of markers of oxidative stress including lipid peroxidation, reactive oxygen species and superoxide dismutase activity were increased by USPIO. Moreover, USPIO caused DNA damage in the heart. Likewise, DEP increased the markers of oxidative stress and induced DNA damage in the heart.ConclusionWe conclude that acute i.v. administration of USPIO caused thrombosis and cardiac oxidative stress and DNA damage. These findings provide novel insight into the pathophysiological effects of USPIO on cardiovascular homeostasis, and highlight the need for a thorough evaluation of their toxicity.

Serum dosage of CPK-MB in dogs with ST deviation by chemiluminescence

Abstract: Although frequently in humans, hypoxic and ischemic heart diseases are poorly documented in dogs, with only few reports of acute myocardial infarction (AMI) in this species. Some electrocardiographic findings might suggest myocardium hypoxia/ischemia, like ST segment elevation or depression, but there are no studies showing whether deviations in ST segment are associated to myocardial injury and serum increase of creatine phosphokinase (CPK-MB). In order to investigate possible myocardial cells injury in poor perfusion conditions, 38 dogs were studied, 20 with normal electrocardiogram and 18 with ST segment elevation or depression, recorded in lead II, at a paper speed of 50 mm/sec and N sensibility (1mV=1cm). Serum measurement of creatine phosphokinase isoenzyme MB (CPK-MB) in normal dogs (group 1) determined control values (in ng/mL), which were compared to those obtained from dogs with deviation (group 2), which allowed confirmation or not of myocardial injury. CPK-MB mean values obtained from dogs in groups 1 and 2 were 0.540ng/ml (SD±0.890)ng/mL and 0.440ng/mL (SD±1.106), respectively. At a significance level of 5%, the relation of CPK-MB with age, mass and total creatine phosphokinase (CPK-T) was not significant in groups 1 and 2. CPK-MB showed no difference, at 5% level, between groups 1 and 2. In conclusion, it is possible to use the human chemiluminescent immunometric assay kit in canine species and that hypoxia/ischemia revealed by ST segment deviation does not mean significant myocardium injury.

Metformin Attenuates Doxorubicin‐induced Cardiotoxicity In Rats

The clinical use of doxorubicin (DOX), a potent chemotherapeutic agent, is limited by its cardiotoxic side effects that are attributed to free radical generation. Recent studies have established that metformin (MET), an oral antidiabetic drug, possesses an antioxidant activity. However, whether it can protect against DOX‐induced cardiotoxicity has not been reported before. The goal of the present study was to assess the extent to which MET can prevent cardiotoxicity induced by DOX. Results of our study in a rat model of DOX‐induced cardiotoxicity show that DOX treatment caused significant increases in serum levels of lactate dehydrogenase (LDH) and creatine phosphokinase isoenzyme MB (CK‐MB), indicators of cardiac injury. In addition, DOX therapy decreased cardiac glutathione, an endogenous antioxidant; CoA‐SH, an activator in mitochondrial energy providing systems. These biochemical changes were associated with myocardial histopathological and ultrastructural deteriorations. Co‐treatment with MET eliminated all DOX‐induced increases of LDH and CK‐MB and prevented GSH, CoA‐SH and ATP depletions. MET therapy also prevented all the myocardial histopathological and ultrastructural deteriorations. These findings demonstrate, that MET successfully prevents DOX‐induced cardiotoxicity.

Glycyrrhiza glabra protects from myocardial ischemia–reperfusion injury by improving hemodynamic, biochemical, histopathological and ventricular function

Present study evaluated the cardioprotective effect of Glycyrrhiza glabra against ischemia-reperfusion injury (I-R) induced by ligation of left anterior descending coronary artery (LADCA) in rats. Ligation of LADCA for 45 min followed by 60 min of reperfusion has induced significant (p<0.05) heart dysfunction evidenced by significant (p<0.05) decrease in mean arterial pressure (MAP), heart rate (HR), contractility; (+)LVdP/dtmax and relaxation; (-)LVdP/dtmax along with increased left ventricular end diastolic pressure (LVEDP). Ligation induced I-R injury also significantly (p<0.05) decreased myocyte injury enzymes, creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH) as well as antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). Furthermore, I-R injury also induced lipid peroxidation evidenced by significant (p<0.05) increase in malondialdehyde (MDA) formation and histological perturbations concomitant to depletion of glutathione (GSH) from heart. However, pretreatment with G. glabra significantly (p<0.05) prevented the depletion of the antioxidant enzymes; SOD, CAT, GSH-Px and myocyte injury marker enzymes; CK-MB isoenzyme and LDH. Pretreatment with G. glabra also prevented GSH depletion and inhibited lipid peroxidation in heart. In addition to improving biochemical indices of myocardial function, G. glabra also significantly (p<0.05) reinstated MAP, HR, (±)LVdP/dtmax and attenuated abrupt rise in LVEDP. Histopathological preservation evidenced by reduced infiltration of cells and myonecrosis depicted the myocardial salvaging effect of G. glabra. Taken together, results of the present study clearly suggest the cardioprotective potential of G. glabra against myocardial infarction by amelioration of oxidative stress and favorable modulation of cardiac function.

Tranexamic Acid Reduces Blood Loss After Off-Pump Coronary Surgery

Bleeding and the need for allogeneic transfusions are still problems after off-pump coronary artery bypass grafting (OPCAB) surgery. We therefore evaluated the effects of an antifibrinolytic, tranexamic acid, on postoperative bleeding and transfusion requirements in patients undergoing OPCAB surgery. Two hundred thirty-one consecutive patients scheduled for elective OPCAB were enrolled in the study. Using a double-blind method, the patients were randomly assigned to receive either tranexamic acid (bolus 1 g before surgical incision followed by an infusion of 400 mg/h during surgery; n = 116) or a placebo (infusion equivalent volume of saline solution; n = 115). The primary outcome was 24-hour postoperative chest tube drainage. Allogeneic transfusion, mortality, major morbidities, and resource utilization were also recorded. In comparison with the placebo group, the patients receiving tranexamic acid had a significant reduction in chest tube drainage at 6 hours (270 ± 118 mL vs 416 ± 179 mL, P < 0.001) and 24 hours (654 ± 224 mL vs 891 ± 295 mL, P < 0.001). There was also a significant reduction in allogeneic red blood cell transfusions (47 vs 31.9%, P = 0.019) and fresh frozen plasma (29.6% vs 17.2%, P = 0.027) transfusions. There were no differences in mortality, morbidity, and resource utilization between the 2 groups. Tranexamic acid reduces postoperative chest tube drainage and the requirement for allogeneic transfusion in off-pump coronary surgery.

Peri-procedural myocardial injury during percutaneous coronary intervention: an important target for cardioprotection

Percutaneous coronary intervention (PCI) has become the predominant procedure for coronary revascularization in patients with both stable and unstable coronary artery disease (CAD). Over the past two decades, technical advances in PCI have resulted in a better and safer therapeutic procedure with minimal procedural complications. However, about 30% of patients undergoing elective PCI sustain myocardial injury arising from the procedure itself, the extent of which is significant enough to carry prognostic importance. The peri-procedural injury which accompanies PCI might therefore reduce some of the beneficial effects of coronary revascularization. The availability of more sensitive serum biomarkers of myocardial injury such as creatine phosphokinase MB isoenzyme (CK-MB), Troponin T, and Troponin I has enabled the quantification of previously undetectable myocardial injury. Peri-procedural myocardial injury (PMI) can also be visualized by cardiac magnetic resonance imaging, a technique which allows the detection and quantification of myocardial necrosis following PCI. The identification of CAD patients at greatest risk of sustaining PMI during PCI would allow targeted treatment with novel therapies capable of limiting the extent of PMI or reducing the number of patients experiencing PMI.

Effect of Piper betle on cardiac function, marker enzymes, and oxidative stress in isoproterenol-induced cardiotoxicity in rats

The present study was designed to investigate the cardioprotective potential of Piper betle (P. betle) against isoproterenol (ISP)-induced myocardial infarction in rats. Rats were randomly divided into eight groups viz. control, ISP, P. betle (75, 150, and 300 mg/kg) and P. betle (75, 150, and 300 mg/kg) + ISP treated group. P. betle leaf extract (75, 150, or 300 mg/kg) or saline was orally administered for 30 days. ISP (85 mg/kg, s.c.) was administered at an interval of 24 h on the 28th and 29th day and on day 30 the functional and biochemical parameters were measured. ISP administration showed a significant decrease in systolic, diastolic, mean arterial pressure (SAP, DAP, MAP), heart rate (HR), contractility (+LVdP/dt), and relaxation (−LVdP/dt) and increased left ventricular end-diastolic pressure (LVEDP). ISP also caused significant decrease in myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and myocyte injury marker enzymes; creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH) along with enhanced lipid peroxidation; thiobarbituric acid reacting species (TBARS) in heart. Pre-treatment with P. betle favorably modulated hemodynamic (SAP, DAP, and MAP) and ventricular function parameters (−LVdP/dt and LVEDP). P. betle pre-treatment also restored SOD, CAT, GSH, and GPx, reduced the leakage of CK-MB isoenzyme and LDH along with decreased lipid peroxidation in the heart. Taken together, the biochemical and functional parameters indicate that P. betle 150 and 300 mg/kg has a significant cardioprotective effect against ISP-induced myocardial infarction. Results of the present study suggest the cardioprotective potential of P. betle.

Frequency and Clinical Consequences Associated With Sidebranch Occlusion During Stent Implantation Using Zotarolimus-Eluting and Paclitaxel-Eluting Coronary Stents

Myocardial infarction (MI) after drug-eluting stent placement has been associated with an unfavorable late prognosis. Although the etiology of periprocedural MI is multifactorial, sidebranch occlusion may be an important contributing factor. We sought to identify the incidence of sidebranch occlusion during zotarolimus-eluting stent (ZES) and paclitaxel-eluting stent (PES) placement and to relate sidebranch occlusion to the occurrence of periprocedural MI. Angiograms were reviewed from patients randomly assigned to treatment with a ZES (597 patients; 943 sidebranches) or a PES (619 patients; 977 sidebranches). Sidebranch occlusion was defined as Thrombolysis in Myocardial Infarction flow grade 0 or 1. Sidebranch occlusion was correlated with frequency of MI, as assessed by the creatine phosphokinase MB isoenzyme. Sidebranch occlusion occurred less often after the first stent deployment in patients treated with ZES (2.2%) than in patients treated with PES (4.0%; P=0.032). A similar reduction in the frequency of sidebranch occlusion at any point during the procedure was found in patients treated with ZES (2.9% versus 4.8% in PES patients; P=0.042). Multivariable predictors of sidebranch occlusion included baseline sidebranch stenosis, complex lesion morphology, smaller baseline minimal lumen diameters, and the use of a PES. Of the 20 patients with MI within 30 days of the procedure, 30% had evidence of sidebranch occlusion during the stent procedure. Patients treated with ZES were less likely to develop sidebranch occlusion during stent placement than patients treated with PES. Less frequent sidebranch occlusion with ZES may have contributed to the lower frequency rates of periprocedural MI in this study.

Effect of tirofiban plus clopidogrel and aspirin on primary percutaneous coronary intervention via transradial approach in patients with acute myocardial infarction

Aspirin and clopidogrel can improve myocardial reperfusion and alleviate myocardial injury during percutaneous coronary intervention (PCI). Whether the addition of intravenous tirofiban during this procedure produces further benefit has not been clarified in ST segment elevation myocardial infarction (STEMI) patients. We evaluated this on STEMI patients who underwent primary PCI (p-PCI) via transradial artery approach. Consecutive patients were randomized into tirofiban group (n=72) or placebo group (n=78). Angiographic analysis included initial and final thrombolysis in myocardial infarction (TIMI) flow grade (TFG), corrected TIMI frame count (CTFC) and TIMI myocardial perfusion grade (TMPG) of the thrombotic vessel. Platelet aggregation rate (PAR), creatine phosphokinase (CPK), CPK isoenzyme MB (CPK-MB) and troponin I levels were measured and TIMI definitions were used to assess bleeding complications. Left ventricular performance parameters were investigated with equilibrium radionuclide ventriculography. Major adverse cardiac events (MACE) were followed up for 6 months. The cases of TFG 0 and 1 before PCI, TFG 0 when first crossing of guide wire were less, and the cases of TFG 3 after PCI was more in tirofiban group than those in placebo group. The final CTFC was fewer and the incidence of no reflow phenomenon was lower, as well the percentage of final TFG 3 was higher in tirofiban group than those in placebo group (all P<0.05). Mean peak CPK-MB was significantly lower, while the left ventricular performance parameters 1 week after PCI were much more improved in tirofiban group than those in the placebo group. PAR was significantly decreased shortly after tirofiban infusion. The incidence of 6-month MACE in tirofiban group was obviously lower than that in the placebo group. No statistical difference was noted between the two groups with regard to bleeding complications. Intravenous tirofiban infusion, in addition to aspirin and clopidogrel in STEMI patients with p-PCI via transradial artery access, can quickly inhibit platelet aggregation, loosen occlusive thrombus, improve myocardial reperfusion and reduce incidence of MACE with few complications of vessel access and bleeding.

Change of myocardial enzymes in patients with acute tetramine poisoning

To investigate the clinical significance of myocardial enzymes in patients with acute tetramine (TEM) poisoning. The dynamic changes of the activity of myocardial enzymes and ECG were observed in 67 patients with acute TEM poisoning as well as in 67 healthy people for medical checkup at outpatient department as the control group. Myocardial enzymes of the patients with acute TEM poisoning were increased to different extents on the first day. There was significant difference in the activity of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and CPK isoenzyme MB (CK-MB) between the patients and the healthy people in the control group (P < 0.01). There was significant difference in the myocardial enzymes at different time points among the patients with mild, middle and severe poisoning (P < 0.01). The severer the TEM poisoning was, the higher the activity of myocardial enzymes and the abnormal rate of ECG were. The activity of CPK was the earliest to rise with the highest aptitude of fluctuation and the longest time of elevation. The change of the myocardial enzymes was earlier than that of ECG. The abnormal rate of AST, CPK, CK-MB, LDH, alpha-HBDH was 86.57%, 98.51%, 94.03%, 89.55% and 79.10% respectively. The abnormal rate of ECG was 49.3% on the third day of poisoning. Measurement of myocardial enzymes was better than ECG in sensitivity. Acute tetramine poisoning can damage myocardium, which is reversible. CPK is a typical marker for the damage and can serve as one of the important clinical monitoring indices.