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Introduction: Resource limitation in developing countries may preclude access to cardiac troponin- T assay thereby necessitating reliance on clinical judgment for identification of hypoxic myocardial cellular injury. Objectives: cardiac troponin–T levels. Conclusion: Clinicians working in resource–limited health facilities should have a high index of suspicion for myocardial cellular injury when these signs are e To relate selected clinical signs with elevated serum cardiac troponin-T in asphyxiated term neonates. Methods: Asphyxia was identified by low umbilical arterial blood pH ≤ 7.20 and low five minute Apgar score ≤ 6 while controls were term, non–asphyxiated neonates. All babies were examined for heart rate, heart rhythm irregularities, peripheral pulse volume, respiratory rate, pallor, cyanosis, heart murmur and sensorium. Results: Thirty term, asphyxiated neonates and their matched controls were studied. Central cyanosis, reduced pulse volume, pallor, depressed sensorium; tachycardia and tachypnea were all associated with increased odds ratios for abnormallicited.

Background: Coronary artery bypass grafting (CABG) surgery is a common procedure for revascularization in patients with coronary artery disease. Anesthetic agents used during CABG can impact perioperative myocardial injury. Troponin-T (TnT) is a sensitive biomarker for myocardial injury. This study aims to compare the cardioprotective effects of three anesthetic agents by measuring serum levels of TnT after CABG surgery. Materials and Methods: A prospective comparative study was conducted on 150 patients undergoing elective CABG surgery. Patients were divided into three groups based on the anesthetic agent used: Group A (propofol), Group B (sevoflurane), and Group C (isoflurane). Serum TnT levels were measured at baseline (preoperatively) and at 6, 12, and 24 hours postoperatively. Demographic data, surgical details, and perioperative variables were recorded. Statistical analysis was performed using ANOVA and post-hoc Tukey's test. Results: The mean baseline serum TnT levels were comparable among the three groups (p > 0.05). At 6, 12, and 24 hours postoperatively, Group A showed significantly lower serum TnT levels compared to Group B and Group C (p < 0.05). The mean TnT levels at 24 hours postoperatively were 0.12 ng/mL in Group A, 0.18 ng/mL in Group B, and 0.20 ng/mL in Group C. Conclusion: Propofol-based anesthesia demonstrated superior cardioprotective effects compared to sevoflurane and isoflurane in patients undergoing CABG surgery, as evidenced by lower serum TnT levels postoperatively. Further studies are warranted to elucidate the underlying mechanisms of this cardioprotection and its clinical implications. [ABSTRACT FROM AUTHOR]

Background: Plasma concentrations of cardiac troponins increase in healthy individuals after strenuous training, but the response to lower exercise intensities has not been characterized. Aim: To determine whether exercise at moderate intensity significantly increases plasma cardiac troponins measured with different assays in healthy recreational athletes. Methods: Twenty‐four self‐reported healthy volunteers were instructed to complete three 60‐min bouts of treadmill running at variable intensities: High‐intensity training (HIT) including a maximal exercise test and an anaerobic threshold test followed by training at 80%–95% of maximum heart rate (HRmax), Moderate‐intensity training (MIT) at 60%–75% of HRmax, and Low‐intensity training (LIT) at 45%–55% of HRmax. Blood samples were collected before and at 2, 4, and 6 h after HIT and 4 h after MIT and LIT. Troponin I and T were measured in plasma samples with assays from Abbot, Siemens, and Roche. Results: Plasma troponins measured with all assays were significantly increased compared to baseline after HIT but not after LIT. After HIT, the fraction of all participants with one or more values above the assay‐specific 99th percentiles ranged from 13% to 61%. The biomarker criteria for acute myocardial injury were met after HIT for troponin T in 75% of female participants having no clinical evidence of coronary artery disease. Conclusion: High‐intensity, but not moderate‐ or low‐intensity, training for 60 min induced a potentially clinically significant increase in plasma cardiac troponins in healthy volunteers. Results exceeding the population 99th percentiles were most frequent with the troponin T assay. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the effect of Troponin-T levels on the prognosis of neonatal encephalopathy (NE). PATIENTS AND METHODS: The study included one hundred and eleven newborns diagnosed with NE and receiving hypothermia treatment. The cases were separated into 2 groups according to the SARNAT classification as Stage 2 or Stage 3. The groups were compared in respect of anthropometric characteristics, APGAR scores, and biochemical parameters. The cases were also separated into 3 groups according to the Troponin-T levels and were compared with respect to the clinical course. RESULTS: The serum Troponin-T (p=0.012), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (p<0.0001), and lactate levels (p=0.04) in the Sarnat Stage 3 group were statistically significantly higher than in the Sarnat stage 2 group. A significant positive correlation was determined between the Troponin-T level and the total duration of respiratory support (r=0.20, p=0.03). A significant positive correlation was determined between the ALT/AST ratio and the length of stay in hospital (r=0.29, p=0.001), duration of intubation (r=0.32, p=0.01), and total duration of respiratory support (r=0.36, p<0.001). A statistically significant difference was determined in mortality rates between the 3 subgroups of Troponin-T levels; Group 1: 2.8%, Group 2:5.4%, and Group 3: 15.8%. (p=0.04, 1²=4.74). A cut-off value of 164 ng/L for Troponin-T was determined to predict mortality with 77% sensitivity and 67% specificity (AUC=0.73, p=0.023). When the groups were compared according to Troponin-T level, a statistically significant difference was determined in respect of length of stay in hospital (p=0.03, 1²=6.95) and total duration of oxygen support (p=0.01, 1²=9.12). CONCLUSIONS: The serum Troponin-T level can be evaluated as a prognostic marker in cases followed up with a diagnosis of NE and receiving hypothermia treatment. There is a need for further prospective studies with larger samples on this subject. [ABSTRACT FROM AUTHOR]

Background Long-term prognostic implications of serial high-sensitivity troponin concentrations in subjects with suspected acute coronary syndrome are unknown. Methods and results Individuals with a first diagnosis of myocardial infarction, unstable angina, observation for suspected myocardial infarction, or chest pain from 2012 through 2019 who underwent two high-sensitivity troponin-T (hsTnT) measurements 1–7 h apart were identified through Danish national registries. Absolute and relative risks for death at days 0–30 and 31–365, stratified for whether subjects had normal or elevated hsTnT concentrations, and whether these concentrations changed by <20%, > 20 to 50%, or >50% in either direction from first to second measurement, were calculated through multivariable logistic regression with average treatment effect modeling. Of the 28 902 individuals included, 2.8% had died at 30 days, whereas 4.9% of those who had survived the first 30 days died between days 31–365. The standardized risk of death was highest among subjects with two elevated hsTnT concentrations (0–30 days: 4.3%, 31–365 days: 7.2%). In this group, mortality was significantly higher in those with a > 20 to 50% or >50% rise from first to second measurement, though only at 30 days. The risk of death was very low in subjects with two normal hsTnT concentrations (0–30 days: 0.1%, 31–365 days: 0.9%) and did not depend on relative or absolute changes between measurements. Conclusions Individuals with suspected acute coronary syndrome and two consecutively elevated hsTnT concentrations consistently had the highest risk of death. Mortality was very low in subjects with two normal hsTnT concentrations, irrespective of changes between measurements. [ABSTRACT FROM AUTHOR]

Introduction: Critically ill Covid‐19 patients are likely to develop the sequence of acute pulmonary hypertension (aPH), right ventricular strain, and eventually right ventricular failure due to currently known pathophysiology (endothelial inflammation plus thrombo‐embolism) that promotes increased pulmonary vascular resistance and pulmonary artery pressure. Furthermore, an in‐hospital trans‐thoracic echocardiography (TTE) diagnosis of aPH is associated with a substantially increased risk of early mortality. The aim of this retrospective observational follow‐up study was to explore the mortality during the 1–24‐month period following the TTE diagnosis of aPH in the intensive care unit (ICU). Methods: A previously reported cohort of 67 ICU‐treated Covid‐19 patients underwent an electronic medical chart‐based follow‐up 24 months after the ICU TTE. Apart from the influence of aPH versus non‐aPH on mortality, several TTE parameters were analyzed by the Kaplan–Meier survival plot technique (K‐M). The influence of biomarkers for heart failure (NTproBNP) and myocardial injury (Troponin‐T), taken at the time of the ICU TTE investigation, was analyzed using receiver‐operator characteristics curve (ROC) analysis. Results: The overall mortality at the 24‐month follow‐up was 61.5% and 12.8% in group aPH and group non‐aPH, respectively. An increased relative mortality risk continued to be present in aPH patients (14.3%) compared to non‐aPH patients (5.6%) during the 1–24‐month period. The easily determined parameter of a tricuspid valve regurgitation, allowing a measurement of a systolic pulmonary artery pressure (regardless of magnitude), was associated with a similar K‐M outcome as the generally accepted diagnostic criteria for aPH (systolic pulmonary artery pressure >35 mmHg). The biomarker values of NTproBNP and Troponin‐T at the time of the TTE did not result in any clinically useful ROC analysis data. Conclusion: The mortality risk was increased up to 24 months after the initial examination in ICU‐treated Covid‐19 patients with a TTE diagnosis of aPH, compared to non‐aPH patients. Certain individual TTE parameters were able to discriminate 24‐month risk of morality. [ABSTRACT FROM AUTHOR]

Introduction: Influenza and the coronavirus disease 2019 (COVID-19) are two potentially severe viral infections causing significant morbidity and mortality. The causative viruses, influenza A/B and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) can cause both pulmonary and extra-pulmonary disease, including cardiovascular involvement. The objective of this study was to determine the levels of cardiac biomarkers in hospitalized patients infected with influenza or COVID-19 and their correlation with secondary outcomes. Methods: We performed a retrospective comparative analysis of cardiac biomarkers in patients hospitalized at our department with influenza or COVID-19 by measuring high-sensitivity troponin-T (hs-TnT) and creatinine kinase (CK) in plasma. Secondary outcomes were intensive care unit (ICU) admission and all-cause in-hospital mortality. Results: We analyzed the data of 250 influenza patients and 366 COVID-19 patients. 58.6% of patients with influenza and 46.2% of patients with COVID-19 presented with increased hs-TnT levels. Patients of both groups with increased hs-TnT levels were significantly more likely to require ICU treatment or to die during their hospital stay. Compared with COVID-19, cardiac biomarkers were significantly higher in patients affected by influenza of all age groups, regardless of pre-existing cardiovascular disease. In patients aged under 65 years, no significant difference in ICU admission and mortality was detected between influenza and COVID-19, whereas significantly more COVID-19 patients 65 years or older died or required intensive care treatment. Conclusions: Our study shows that increased cardiac biomarkers are associated with higher mortality and ICU admission in both, influenza and SARS-CoV-2-infected patients. Cardiac biomarkers are higher in the influenza cohort; however, this does not translate into worse outcomes when compared with the COVID-19 cohort. [ABSTRACT FROM AUTHOR]

AimsExtracellular vesicles (EVs) were investigated as potential biomarkers associated with heart failure (HF) pathophysiology in patients undergoing elective coronary artery bypass surgery characterized by HF phenotype.Materials and methodsPatients with preoperative proxy-diagnoses of HF types i.e., preserved (HFpEF; n = 19) or reduced ejection fraction (HFrEF; n = 20) were studied and compared to patients with normal left ventricular function (n = 42). EVs in plasma samples collected from the coronary sinus, an arterial line, and from the right atrium were analyzed by flow cytometry. We studied EVs of presumed cardiomyocyte origin [EVs exposing Connexin-43 + Caveolin-3 (Con43 + Cav3) and Connexin-43 + Troponin T (Con43 + TnT)], of endothelial origin [EVs exposing VE-Cadherin (VE-Cad)] and EVs exposing inflammatory markers [myeloperoxidase (MPO) or pentraxin3 (PTX3)].ResultsMedian concentrations of EVs exposing Con43 + TnT and Con43 + Cav3 were approximately five to six times higher in coronary sinus compared to radial artery indicative of cardiac release. Patients with HFrEF had high trans-coronary gradients of both Con43 + TnT and Con43 + Cav3 EVs, whereas HFpEF had elevated gradients of Con43 + Cav3 EVs but lower gradients of Con43 + TnT. Coronary sinus concentrations of both Con43 + TnT and Con43 + Cav3 correlated significantly with echocardiographic and laboratory measures of HF. MPO-EV concentrations were around two times higher in the right atrium compared to the coronary sinus, and slightly higher in HFpEF than in HFrEF. EV concentrations of endothelial origin (VE-Cad) were similar in all three patient groups.ConclusionCon43 + TnT and Con43 + Cav3 EVs are released over the heart indicating cardiomyocyte origin. In HFrEF the EV release profile is indicative of myocardial injury and myocardial stress with elevated trans-coronary gradients of both Con43 + TnT and Con43 + Cav3 EVs, whereas in HFpEF the profile indicates myocardial stress with less myocardial injury.

Background: Patients with chronic obstructive pulmonary disease (COPD) often have cardiovascular comorbidities. Patients of COPD with cardiovascular complications tend to have more symptoms and a higher mortality than do patients with COPD alone. There are several cardiac biomarkers such as Troponin-T, creatine phosphokinase-MB (CPK-MB), and N-terminal pro-brain natriuretic peptide (NT-proBNP) which can be used to detect cardiac dysfunction in patients of COPD. Retrospective studies suggest that plasma levels of NT-proBNP and cardiac Troponin-T are often elevated in patients with acute exacerbations of COPD and are associated with increased mortality. Aims and Objectives: In this study, we assessed the presence of cardiac dysfunction in patients presenting with acute exacerbation of COPD (AECOPD) by using cardiac biomarkers proBNP, Troponin-T, and CPK-MB. Patients were followed up for 30 days to know the relationship between cardiac dysfunction and outcome in terms of repeated admissions, intensive care units (ICU) admissions, and/or mortality. Methodology: Ninety patients of AECOPD were enrolled in our study. A detailed history was taken and physical examination performed in these patients. All patients in the study were subjected to hematological and biochemical investigations. ProBNP, Troponin-T, and CPK-MB were measured within 48 h of admission as measure of cardiac dysfunction; and outcome was assessed in terms of mortality, ICU admission, and repeated admissions within 30 days of admission. Results: Among the study population, 77.77% had at least one deranged cardiac biomarker, and 18.88% of populations had all the three biomarkers of cardiac dysfunction deranged. 24 out of the 90 participants required ventilatory support in the form of noninvasive or invasive ventilation. 7.14% of the study population had repeated admissions, 24.28% had ICU admissions and 11.43% had mortality. All of them had deranged cardiac biomarkers. There was a significant association between deranged proBNP and ICU admission and mortality (P = 0.0151 and 0.0217, respectively). COPD was more prevalent in the age group of 50-70 years and in males. ProBNP levels were significantly elevated in patients who required ventilatory support (P = 0.003). Conclusions: Cardiac dysfunction is common during exacerbations of COPD and portends a poor prognosis. Cardiac dysfunction was more prevalent in the elderly. Patients with deranged cardiac biomarkers had a greater number of ICU admissions, repeated hospital admissions, and a higher mortality. In the follow-up, elevated proBNP was found to be a strong marker for predicting ICU admission, mortality, and repeated admissions. [ABSTRACT FROM AUTHOR]

Background and Objectives: Cardioplegia is one of the most significant components used to protect the myocardium during cardiac surgery. There is a paucity of evidence regarding the utilization of whole-blood Del Nido cardioplegia (WB-DNC) on clinical outcomes in coronary artery bypass grafting (CABG). The purpose of this retrospective cross-sectional study is to compare the effectiveness of diluted (blood to crystalloid; 1:4) Del Nido cardioplegia (DNC) with WB-DNC in patients who underwent elective CABG in a tertiary care hospital in Lahore-Pakistan. Materials and Methods: This was a retrospective descriptive study conducted at the Department of Cardiovascular Surgery, King Edward Medical University, Lahore. The medical database of all consecutive patients admitted from January 2018 to March 2020 and who fulfilled the inclusion criteria were reviewed. Results: Out of 471 patients admitted during the study period, 450 underwent various elective cardiac surgeries. Out of 450, 321 patients (71.33%) were operated on for CABG. Only 234/321 (72.89%) CABG patients fulfilled our inclusion criteria; 120 (51.28%) patients received WB-DNC, while 114 (48.71%) patients were administered with DNC. The former group presented with better clinical outcomes compared with the latter in terms of lesser requirements of inotropic support, low degree of hemodilution, shorter in-hospital stay, improved renal function, and cost-effectiveness. Peak values of serum Troponin-T (Trop-T), creatine kinase-myocardial band (CK-MB) release, and activated clotting time (ACT) were also lower in the WB-DNC group compared with the DNC group. Conclusions: The WB-DNC conferred better myocardial protection, improved early clinical outcomes, and also proved to be economical for patients undergoing elective CABG compared with classical crystalloid cardioplegia solution. [ABSTRACT FROM AUTHOR]

Introduction: Influenza and the coronavirus disease 2019 (COVID-19) are two potentially severe viral infections causing significant morbidity and mortality. The causative viruses, influenza A/B and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) can cause both pulmonary and extra-pulmonary disease, including cardiovascular involvement. The objective of this study was to determine the levels of cardiac biomarkers in hospitalized patients infected with influenza or COVID-19 and their correlation with secondary outcomes. Methods: We performed a retrospective comparative analysis of cardiac biomarkers in patients hospitalized at our department with influenza or COVID-19 by measuring high-sensitivity troponin-T (hs-TnT) and creatinine kinase (CK) in plasma. Secondary outcomes were intensive care unit (ICU) admission and all-cause in-hospital mortality. Results: We analyzed the data of 250 influenza patients and 366 COVID-19 patients. 58.6% of patients with influenza and 46.2% of patients with COVID-19 presented with increased hs-TnT levels. Patients of both groups with increased hs-TnT levels were significantly more likely to require ICU treatment or to die during their hospital stay. Compared with COVID-19, cardiac biomarkers were significantly higher in patients affected by influenza of all age groups, regardless of pre-existing cardiovascular disease. In patients aged under 65 years, no significant difference in ICU admission and mortality was detected between influenza and COVID-19, whereas significantly more COVID-19 patients 65 years or older died or required intensive care treatment. Conclusions: Our study shows that increased cardiac biomarkers are associated with higher mortality and ICU admission in both, influenza and SARS-CoV-2-infected patients. Cardiac biomarkers are higher in the influenza cohort; however, this does not translate into worse outcomes when compared with the COVID-19 cohort.

Background: Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide. Nimodipine is a calcium (Ca2+) channel blocker as well as a PDE1 inhibitor and primarily used in subarachnoid haemorrhage (SAH) due to its blood-brain barrier crossing property. Nimodipine and vinpocetine inhibit the degradation of phosphodiester bond which increases cGMP and cAMP levels causing vasodilation. Material and methods: We have divided rats randomly into Group I - Vehicle control; Group II - Toxic control (ISO 85 mg/kg, i.p.); Group III, IV and V - Nimodipine (5, 10 and 15 mg/kg, i.p. respectively) with ISO; Group VI- Nimodipine (15 mg/kg) alone; Group VII – Nimodipine + Vinpocetine (10 mg/kg + 10 mg/kg) with ISO; Group VIII - Nimodipine + Vinpocetine (10 mg/kg + 10 mg/kg) alone; Group IX- Diltiazem (25 mg/kg, p.o) with ISO; Group X- Diltiazem (25 mg/kg) alone and Group XI- Vinpocetine (10 mg/kg, p.o.) with ISO for 7 days. After 24 h of the last dose, haemodynamics were assessed then animals were sacrificed and biochemical, histopathological and ultrastructural changes were measured. Results: Treatment with ISO significantly deviated the haemodynamic parameters (HR, SAP, DAP and MAP), biochemical parameters (CK-MB, LDH, SGOT, cGMP and Troponin-T) and antioxidant markers (TBARS, SOD, CAT, GSH, GPx, GST and GR). Haemotoxylin and eosin staining of the cardiac tissue and ultrastructural study also indicated significant myocardial damage. Pretreatment with nimodipine (10 and 15 mg/kg, i.p), vinpocetine (10 mg/kg, p.o) and their combination significantly restored the antioxidant status, haemodynamic profile, cellular architecture and ultrastructural changes in the heart. Conclusion: Nimodipine and vinpocetine both showed cardioprotection when given alone. However, their combination showed better restoration in terms of oxidative stress, cardiac membrane damage, haemodynamics, histopathology and ultrastructural changes.

The main aim of this study was to evaluate the effect of remote ischaemic preconditioning (RIPC) on preventing the leakage of cardiac damage biomarkers in patients undergoing vascular surgery. This is a randomised, sham-controlled, double-blinded, single-centre study. Patients undergoing open abdominal aortic aneurysm repair, surgical lower limb revascularisation surgery or carotid endarterectomy were recruited non-consecutively. The RIPC protocol consisting of 4 cycles of 5 minutes of ischaemia, followed by 5 minutes of reperfusion, was applied. A RIPC or a sham procedure was performed noninvasively along with preparation for anaesthesia. High sensitivity troponin T level was measured preoperatively and 2, 8 and 24 hours after surgery and pro b-type natriuretic peptide was measured preoperatively and 24 hours after surgery. There was significantly higher leakage of high sensitivity troponin T (peak change median 2 ng/L, IQR 0.9–6.2 ng/L vs 0.6 ng/L, IQR 0.7–2.1 ng/L, p =.0002) and pro b-type natriuretic peptide (change median 144 pg/mL, IQR 17–318 pg/mL vs 51 pg/mL, IQR 12–196 pg/mL, p =.02) in the sham group compared to the RIPC group. RIPC reduces the leakage of high sensitivity troponin T and pro b-type natriuretic peptide. Therefore, it may offer cardioprotection in patients undergoing non-cardiac vascular surgery. The clinical significance of RIPC has to be evaluated in larger studies excluding the factors known to influence its effect. [ABSTRACT FROM AUTHOR]

Background: In perinatal asphyxia, hypoxia often leads to myocardial ischaemia. Few studies have assessed the degree of myocardial dysfunction in severely asphyxiated term neonates. Aim: To assess the extent of myocardial damage in newborns with severe perinatal asphyxia. Methods: A case–control study was conducted in asphyxiated newborns with hypoxic ischaemic encephalopathy (HIE) and in controls who were term non-asphyxiated newborns. Total (T) creatinine kinase (CK), CK-MB, troponin-T and 12-lead electrocardiography (ECG) and echocardiography were performed in both groups within 24–48 h after birth. The proportions of asphyxiated neonates with myocardial dysfunction and its relationship between severity of HIE and immediate outcome was compared. Results: Five of 23 asphyxiated neonates developed stage I, 10 stage II and eight stage III HIE. Serum levels of CK-T and CK-MB were raised in all 23 cases and troponin-T was raised in 13 (56.5%) HIE cases. ECG was abnormal in all cases and echocardiography in three (13%). Left ventricular ejection fraction (LVEF) and right ventricular ejection fraction (RVEF) were significantly decreased in all asphyxiated neonates. Eight (35%) patients died. Enzyme levels were higher and ECG and echocardiography abnormalities were common in infants with more severe HIE (p <0.05). Mean serum levels of CK-T and MB (p <0.001) and troponin-T (p =0.002) were higher in non-survivors. Mean LVEF and RVEF values were higher in survivors (p <0.001). All the controls had normal enzyme levels and echocardiography. ECG was abnormal in one control. Conclusion: Cardiac enzymes, ECG and echocardiography changes were associated with increasing severity of HIE and mortality. [ABSTRACT FROM AUTHOR]

Background and Objectives: Cardioplegia is one of the most significant components used to protect the myocardium during cardiac surgery. There is a paucity of evidence regarding the utilization of whole-blood Del Nido cardioplegia (WB-DNC) on clinical outcomes in coronary artery bypass grafting (CABG). The purpose of this retrospective cross-sectional study is to compare the effectiveness of diluted (blood to crystalloid; 1:4) Del Nido cardioplegia (DNC) with WB-DNC in patients who underwent elective CABG in a tertiary care hospital in Lahore-Pakistan. Materials and Methods: This was a retrospective descriptive study conducted at the Department of Cardiovascular Surgery, King Edward Medical University, Lahore. The medical database of all consecutive patients admitted from January 2018 to March 2020 and who fulfilled the inclusion criteria were reviewed. Results: Out of 471 patients admitted during the study period, 450 underwent various elective cardiac surgeries. Out of 450, 321 patients (71.33%) were operated on for CABG. Only 234/321 (72.89%) CABG patients fulfilled our inclusion criteria; 120 (51.28%) patients received WB-DNC, while 114 (48.71%) patients were administered with DNC. The former group presented with better clinical outcomes compared with the latter in terms of lesser requirements of inotropic support, low degree of hemodilution, shorter in-hospital stay, improved renal function, and cost-effectiveness. Peak values of serum Troponin-T (Trop-T), creatine kinase-myocardial band (CK-MB) release, and activated clotting time (ACT) were also lower in the WB-DNC group compared with the DNC group. Conclusions: The WB-DNC conferred better myocardial protection, improved early clinical outcomes, and also proved to be economical for patients undergoing elective CABG compared with classical crystalloid cardioplegia solution.

MicroRNAs (miRNAs) are small noncoding endogenous RNAs, typically 21–23 nucleotides long, that regulate gene expression, usually post-transcriptionally, by binding to the 3′-UTR of target mRNA, thus blocking translation. The expression of several miRNAs is significantly altered during cardiac hypertrophy, myocardial ischemia, fibrosis, heart failure, and other cardiac myopathies. Recent studies have implicated miRNA-9 (miR-9) in myocardial hypertrophy. However, a detailed mechanism remains obscure. In this study, we have addressed the roles of miR-9 in muscle development and function using a genetically tractable model system, the indirect flight muscles (IFMs) of Drosophila melanogaster. Bioinformatics analysis identified 135 potential miR-9a targets, of which 27 genes were associated with Drosophila muscle development. Troponin-T (TnT) was identified as major structural gene target of miR-9a. We show that flies overexpressing miR-9a in the IFMs have abnormal wing position and are flightless. These flies also exhibit a loss of muscle integrity and sarcomeric organization causing an abnormal muscle condition known as “hypercontraction.” Additionally, miR-9a overexpression resulted in the reduction of TnT protein levels while transcript levels were unaffected. Furthermore, muscle abnormalities associated with miR-9a overexpression were completely rescued by overexpression of TnT transgenes which lacked the miR-9a binding site. These findings indicate that miR-9a interacts with the 3′-UTR of the TnT mRNA and downregulates the TnT protein levels by translational repression. The reduction in TnT levels leads to a cooperative downregulation of other thin filament structural proteins. Our findings have implications for understanding the cellular pathophysiology of cardiomyopathies associated with miR-9 overexpression.

This study was designed to determine the effects of µ/m‐calpain on the degradation of cytoskeletal proteins in pectoralis major. Four chickens were slaughtered and the breasts were removed and stored for 12 hr at 4 °C. Each sample was divided into three groups and respectively immersed in control reagent, calpain inhibitor, and caspase inhibitor at 4 °C. The samples were used to evaluate troponin‐T and desmin degradation, calpain activity, and myofibril ultrastructure at 12 hr, day 1, day 3, and day 7. Casein zymography revealed that µ‐calpain could not be detected in all samples after 12 hr postmortem. The calpain inhibitor inhibited µ/m‐calpain activity and reduced troponin‐T and desmin degradation during 7 day postmortem. The caspase inhibitor inhibited µ/m‐calpain activity and, troponin‐T and desmin degradation before day 3 postmortem. The findings suggest that, µ/m‐calpain had an effect on cytoskeletal protein degradation after 12 hr postmortem. [ABSTRACT FROM AUTHOR]

Introduction: Metabolic syndrome (MetS) and high-sensitivity cardiac troponin T (hs-TnT) are associated with higher risk for cardiovascular diseases (CVD). Our aim was to assess the relation between hs-TnT elevation and MetS in a general population sample. Materials and methods: Individuals participating in an annual health survey program between 2010 and 2016 were included in the study. Blood samples including hs-TnT levels were collected. The study population was divided into three groups based on hs-TnT levels – undetectable (<5 ng/L), intermediate (5–14 ng/L) and elevated (>14 ng/L). Results: A total of 5994 subjects were included in the study, the mean age was 48.5 and 4336 (72%) were males. Compared with subjects with undetectable hs-TnT the prevalence of MetS was higher in those with detectable and elevated levels – 392 (10%) vs. 270 (15%) and 51 (33%), respectively (p < 0.001). In a multivariate model adjusted for age, gender and multiple co-morbidities, the number of MetS components and presence of MetS were significantly associated with an increased risk for detectable hs-TnT levels (OR = 1.02 {for each component}; 95% CI [1.00–1.05], p = 0.04) and (OR = 1.13; 95% CI [1.07–1.2], p < 0.001) respectively. Only the waist, glucose and hypertension components of the MetS were significantly associated with elevated troponin. Conclusions: The MetS and its distinct components have a cumulative impact on hs-TnT levels in apparently healthy subjects. [ABSTRACT FROM AUTHOR]

Abstract Background Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is characterized by biphasic seizures and impaired consciousness. Takotsubo cardiomyopathy (TTC), which is typically triggered by psychological or physical stress, is characterized by transient myocardial dysfunction affecting the left ventricular apex. Recent reports have suggested that seizures can also trigger TTC. However, no cases of TTC accompanied by AESD have been reported. Patient A previously healthy 4-year-old girl was brought to a hospital with first-time febrile generalized tonic-clonic convulsions, which lasted approximately 40 min. After the seizure resolved, she was intubated due to respiratory deterioration. On the next day, her cardiac function deteriorated, and echocardiography revealed systolic apical ballooning of the left ventricle accompanied by hyperkinesis of the basal wall, which are typical in patients with TTC. Her condition gradually improved, and catecholamine support was tapered. However, 6 days after admission, she experienced a cluster of brief convulsions. Ten days after admission, head MRI revealed lesions with reduced diffusion throughout the cortex, except in the occipital lobe, as well as perirolandic sparing. Follow-up MRI 35 days after onset revealed whole-brain atrophy, following which she developed severe cognitive dysfunction. Conclusions Our patient developed TTC accompanied by features of AESD. Our findings may thus provide insight into the development of TTC and prompt further studies regarding the relationship between prolonged seizures and TTC. [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • Biofunctionalization of DNA aptamer against cardiac marker protein Troponin-T on ZnO channel surface. • Characterization of biofunctionalized surface using XPS and AFM techniques. • A novel approach (KPFM) to understand the efficacy of biomolecular interaction between cardiac Troponin-T and its corresponding aptamer. • Fabrication and characterization of ZnO-TFT as a sensor device for Troponin-T detection. Abstract In this work, we have demonstrated the use of DNA aptamer as a selective bio recognizable entity towards the qualitative detection of cardiac Troponin-T (cTnT), a clinically important cardiac marker protein. Prior to this, the ZnO thin film surface as an active semiconducting channel material was first biofunctionalized with DNA aptamer by using standard biotin-streptavidin chemistry. Biofunctionalization was further confirmed by analyzing the ZnO surface with atomic force microscope (AFM) and X- ray photoelectron spectroscopy (XPS) techniques. In order to understand the efficacy of biomolecular interaction between cardiac Troponin-T (cTnT) and its corresponding aptamer, Kelvin Probe Force Microscopy (KPFM) technique was performed to monitor the effective contact potential difference. Further, to realize the essential technological importance of this methodology as a sensor platform, a thin-film transistor (TFT) micro device was fabricated using ZnO as a channel material and characterized. These fabricated devices were further used to demonstrate the qualitative detection of cardiac Troponin-T protein by employing aptamer-mediated biofunctionalization of ZnO TFT. [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • Isoproterenol caused oxidative stress and myocardial damage as evident by increase in different biochemical parameters. • ISO also disturbed the haemodynamics and the cellular architecture of heart. • Vinpocetine and nimodipine successfully reversed the oxidative stress, restored cellular architecture and cGMP level thereby showed cardioprotection. Abstract Background Myocardial infarction (MI) remains a major cause of morbidity and mortality worldwide. Nimodipine is a calcium (Ca2+) channel blocker as well as a PDE1 inhibitor and primarily used in subarachnoid haemorrhage (SAH) due to its blood-brain barrier crossing property. Nimodipine and vinpocetine inhibit the degradation of phosphodiester bond which increases cGMP and cAMP levels causing vasodilation. Material and methods We have divided rats randomly into Group I - Vehicle control; Group II - Toxic control (ISO 85 mg/kg, i.p.); Group III, IV and V - Nimodipine (5, 10 and 15 mg/kg, i.p. respectively) with ISO; Group VI- Nimodipine (15 mg/kg) alone; Group VII – Nimodipine + Vinpocetine (10 mg/kg + 10 mg/kg) with ISO; Group VIII - Nimodipine + Vinpocetine (10 mg/kg + 10 mg/kg) alone; Group IX- Diltiazem (25 mg/kg, p.o) with ISO; Group X- Diltiazem (25 mg/kg) alone and Group XI- Vinpocetine (10 mg/kg, p.o.) with ISO for 7 days. After 24 h of the last dose, haemodynamics were assessed then animals were sacrificed and biochemical, histopathological and ultrastructural changes were measured. Results Treatment with ISO significantly deviated the haemodynamic parameters (HR, SAP, DAP and MAP), biochemical parameters (CK-MB, LDH, SGOT, cGMP and Troponin-T) and antioxidant markers (TBARS, SOD, CAT, GSH, GPx, GST and GR). Haemotoxylin and eosin staining of the cardiac tissue and ultrastructural study also indicated significant myocardial damage. Pretreatment with nimodipine (10 and 15 mg/kg, i.p), vinpocetine (10 mg/kg, p.o) and their combination significantly restored the antioxidant status, haemodynamic profile, cellular architecture and ultrastructural changes in the heart. Conclusion Nimodipine and vinpocetine both showed cardioprotection when given alone. However, their combination showed better restoration in terms of oxidative stress, cardiac membrane damage, haemodynamics, histopathology and ultrastructural changes. [ABSTRACT FROM AUTHOR]

Soluble ST2 is a novel cardiac biomarker that reflects cardiac injury and the response to treatment. Previous studies showed that ST2 has less confounding and more specific than NT-proBNP. ACCF/AHA has proposed 2013 Guidelines for the Management of Heart Failure that includes ST2 in the recommendations. In the research proposal, we will assess the clinical role of serum ST2 level in cardiac non-coronary valve surgical patients. We will recruit 70 patients who undergo cardiac non-coronary valve operations. Serum levels of ST2 and NT-proBNP and troponin-T will be measured at preoperative baseline, postoperative 24 hours, and postoperative 5 to 10 days in the routine blood sampling. The endpoints include hospital mortality, all-cause mortality, unexpected ICU return, MACE, time to extubation, and total length of stay. We will also collect various preoperative, operative, and postoperative variables, such as EuroScore-II. Their relationships will be analyzed. We expect to demonstrate the superior role of ST2 to NT-proBNP and other variables in risk stratification and outcome prediction and assessment in our cohort.

Introduction: High sensitive C-reactive protein (HS-CRP) is very sensitive acute phase reactant of inflammation. It is hypothesized that a relationship exists between HS-CRP and acute coronary artery disease (CAD). Materials and Methods: Consecutive sampling of 100 patients were done who presented with acute attack of CAD. In all these patients, Serum analysis for cardiac markers such as troponin-T and creatine phosphokinase-MB (CPK-MB) and serum analysis for quantitative estimation of HS-CRP were done along with few other parameters. Results: In our study, HS-CRP was raised in 90% of patients, along with CPK-MB and troponin-T and as an acute phase reactant, it showed parallel rise in total leukocyte count and absolute neutrophil count. The correlation scatter graphs were plotted, which were found to be statistically significant, (P < 0.05). Conclusion: HS-CRP as an acute phase reactant correlates with other acute phase reactants such as total leukocyte count and absolute neutrophil count and also the rise in HS-CRP value in patients of acute CAD correlates with CPK-MB and troponin-T, so that it can be used as a marker for diagnostic purpose in these patients.

Selective COX-2 inhibitors are most widely used analgesic and anti-inflammatory drugs; however, its maximal use is highly associated with various serious abnormal cardiovascular events. Beraprost sodium (BPS), prostacyclin analogue has been shown to vasodilatory, antiplatelates, anti-inflmmatory, and antioxidant activity. The objective of the present study was to evaluate the effect of BPS on celecoxib cardiotoxicity in rats. Toxicity was induced in male Albino rats (250-280 g) by celecoxib (100 mg/kg/day). BPS (30 µg/kg/day) was administered alone and in combination with celecoxib for 14 days and various biochemicals, hemodynamic, left ventricular, biochemical, and histopathological parameters were studied. Cardiotoxicity of celecoxib was revealed by a significant increase in serum lactate dehydrogenase (LDH), troponin-T (Tn-T), tumor necrosis factor-α (TNF- α), creatine kinase-MB (CK-MB) and systolic blood pressure (SBP), left ventricular end diastolic pressure (LVEDP), LV (dp/dt)max, and LV (dp/dt)min as well as tissue thiobarbituric acid reactive substance (TBARS) and a significant decrease in tissue reduced glutathione (GSH). However, treatment with BPS reversed these alteration in LDH, Tn-T, TNF-α, CK-MB, SBP, LVEDP, LV (dp/dt)max, LV (dp/dt)min, TBARS and GSH levels. The histopathological study in cardiac left ventricle revealed protection of myocardium as manifested reduction of fibrosis by abolition of collagen deposition when celecoxib was combined with beraprost sodium. It could be concluded that beraprost sodium may prove a useful adjunct in patients being prescribed celecoxib. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are small noncoding endogenous RNAs, typically 21-23 nucleotides long, that regulate gene expression, usually post-transcriptionally, by binding to the 39-UTR of target mRNA, thus blocking translation. The expression of several miRNAs is significantly altered during cardiac hypertrophy, myocardial ischemia, fibrosis, heart failure, and other cardiac myopathies. Recent studies have implicated miRNA-9 (miR-9) in myocardial hypertrophy. However, a detailed mechanism remains obscure. In this study, we have addressed the roles of miR-9 in muscle development and function using a genetically tractable model system, the indirect flight muscles (IFMs) of Drosophila melanogaster. Bioinformatics analysis identified 135 potential miR-9a targets, of which 27 genes were associated with Drosophila muscle development. Troponin-T (TnT) was identified as major structural gene target of miR-9a. We show that flies overexpressing miR-9a in the IFMs have abnormal wing position and are flightless. These flies also exhibit a loss of muscle integrity and sarcomeric organization causing an abnormal muscle condition known as "hypercontraction." Additionally, miR-9a overexpression resulted in the reduction of TnT protein levels while transcript levels were unaffected. Furthermore, muscle abnormalities associated with miR-9a overexpression were completely rescued by overexpression of TnT transgenes which lacked the miR-9a binding site. These findings indicate that miR-9a interacts with the 39-UTR of the TnT mRNA and downregulates the TnT protein levels by translational repression. The reduction in TnT levels leads to a cooperative downregulation of other thin filament structural proteins. Our findings have implications for understanding the cellular pathophysiology of cardiomyopathies associated with miR-9 overexpression. [ABSTRACT FROM AUTHOR]

BACKGROUND: Troponin-T is a commonly used cardiac biomarker, which could be useful in perinatal asphyxia. We aimed to analyze troponin-T concentrations in asphyxiated neonates and to correlate the concentrations with clinical outcomes. METHODS: Data were collected from electronic medical records of neonates diagnosed with perinatal asphyxia over a period of four years. RESULTS: There were 63 neonates with moderate to severe encephalopathy, in whom serial troponin-T concentrations had been done on days 1, 3, and 7. 53 (84%) asphyxiated infants had troponin-T concentration >100 pg/ml at 2-4 h of life. The difference in troponin-T concentrations between moderate and severe encephalopathy was not statistically significant (173 vs. 263 pg/ml, p value 0.40). The difference in the concentrations at 72 hours between cooled and non-cooled neonates was not significant (48.5 vs. 62.5 pg/ml, p value 0.22). Troponin-T concentration was significantly higher in babies with hypotensive shock and hepatic injury, but not acute kidney injury. There was no significant correlation between troponin-T and the extent of resuscitation needed. Troponin-T concentration on day 1 of lifewas significantly higher in babies who died than who survived (407 vs. 168 pg/ml, p value 0.03). ROC curve for troponin-T to predict mortality had an area under the curve (AUC) of 0.803; the best cut-off value (190 pg/ml) had 82% sensitivity and 80% specificity. CONCLUSION: There was no significant difference in troponin-T concentrations between cooled and non-cooled neonates. Troponin-T concentration had a good predictive accuracy for mortality before discharge. [ABSTRACT FROM AUTHOR]

Background: The TRAPID-AMI trial study (High-Sensitivity Troponin-T Assay for Rapid Rule-Out of Acute Myocardial Infarction) evaluated high-sensitivity cardiac troponin-T (hs-cTnT) in a 1-hour acute myocardial infarction (AMI) exclusion algorithm. Our study objective was to evaluate the prognostic utility of a modified HEART score (m-HS) within this trial.Methods and Results: Twelve centers evaluated 1282 patients in the emergency department for possible AMI from 2011 to 2013. Measurements of hs-cTnT (99th percentile, 14 ng/L) were performed at 0, 1, 2, and 4 to 14 hours. Evaluation for major adverse cardiac events (MACEs) occurred at 30 days (death or AMI). Low-risk patients had an m-HS≤3 and had either hs-cTnT<14 ng/L over serial testing or had AMI excluded by the 1-hour protocol. By the 1-hour protocol, 777 (60%) patients had an AMI excluded. Of those 777 patients, 515 (66.3%) patients had an m-HS≤3, with 1 (0.2%) patient having a MACE, and 262 (33.7%) patients had an m-HS≥4, with 6 (2.3%) patients having MACEs (P=0.007). Over 4 to 14 hours, 661 patients had a hs-cTnT<14 ng/L. Of those 661 patients, 413 (62.5%) patients had an m-HS≤3, with 1 (0.2%) patient having a MACE, and 248 (37.5%) patients had an m-HS≥4, with 5 (2.0%) patients having MACEs (P=0.03).Conclusions: Serial testing of hs-cTnT over 1 hour along with application of an m-HS identified a low-risk population that might be able to be directly discharged from the emergency department. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Cardiovascular diseases are prevalent in asymptomatic chronic hemodialysis patients. New cardiac biomarkers are required for early diagnosis of cardiovascular diseases. In our study, we aimed to investigate associations of troponin-T (Tn-T), heart type fatty acid binding protein (H-FABP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels with clinical, echocardiographic and laboratory parameters of asymptomatic hemodialysis patients. MATERIAL and METHODS: A total of 60 hemodialysis patients who were asymptomatic for cardiovascular diseases and 62 age- and sex-matched healthy subjects were enrolled. Demographic features were recorded, and Tn-T, H-FABP, and NT-proBNP were measured. Clinical, biochemical and echocardiographic evaluations were performed. RESULTS: Tn-T, H-FABP, NT-proBNP levels were significantly higher in hemodialysis patients (p<0.05). There was no association between cardiac biomarkers and left ventricular hypertrophy or ejection fraction (p>0.05). However, NT-proBNP level >12914 pg/mL was associated with left ventricular hypertrophy. H-FABP was higher in the presence of pulmonary hypertension and tricuspid regurgitation (p=0.025). NT-proBNP was negatively correlated with C-reactive protein (r=-41, p<0.01) and albumin (r=-0.29, p<0.05). NT-proBNP was significantly higher in hypertensive hemodialysis patients (p=0.038). CONCLUSION: Tn-T, H-FABP and NT-proBNP levels are higher in asymptomatic HD patients. Nonetheless, there are no strong correlations between the biomarkers and cardiac abnormalities and cut-off values for cardiac abnormalities should be determined in such these patients. [ABSTRACT FROM AUTHOR]

The diagnosis of acute myocardial infarction (AMI), especially within the first hours after onset of ischemia, poses a challenge to the forensic pathologist. During this time, the infarction is generally not visible macroscopically nor with routine histology. Whilst cardiac Troponin T (cTnT) is a well-established biomarker for AMI clinically, its use as a postmortem diagnostic tool is less conclusive, warranting further investigation. The aim of this study was to investigate the sensitivity and specificity of cTnT as a postmortem diagnostic marker of AMI and the impact of postmortem interval (PMI) and cardiopulmonary resuscitation (CPR) on cTnT-concentrations. Samples from 64 subjects, 15 AMI cases and 49 controls, were collected at the Department of Forensic Medicine in Stockholm and analyzed for cTnT: one femoral blood sample was taken at arrival of the body to the morgue, and again during autopsy. Pericardial fluid (PCF) was only collected during autopsy. Sensitivity and specificity for serum cTnT were calculated to be 86.7 %/67.3 % and for pericardial fluid 86.7 %/44.9 %. cTnT samples taken during autopsy were generally higher than samples taken upon arrival to the morgue. A CPR-dependent elevation in serum cTnT was noted (P = .005). With a cut off at 56 n/L, serum cTnT can be used to rule out AMI. The postmortem interval and CPR must be taken into consideration when interpreting postmortem cTnT. [ABSTRACT FROM AUTHOR]

Introduction: The aim of the study was to assess whether a cardiac troponin T (cTnT) level 1 ng/ml or below threshold is safe and to evaluate mid-term follow-up results in stable patients with non-ST-segment elevation after acute myocardial infarction.Material and Methods: Among cTnT positive patients who presented to the emergency unit with chest pain and received coronary angiography, 100 patients who underwent isolated coronary artery bypass grafting (CABG) constituted the study group (group 1). The same number of patients (n = 100) who were cTnT negative and underwent an isolated CABG operation under elective conditions were selected as the control group (group 2).Results: Among preoperative criteria, group 1 had significantly higher smoking rates (74% vs. 41%, p = 0.0001), and significantly lower ejection fraction values (47.1 ±8.25, 54.69 ±8.73, p = 0.0001). There were no significant differences between the groups with respect to operative parameters. Postoperative follow-up periods were significantly longer in group 1 (23.25 ±14 vs. 17.55 ±7.95 months, p = 0.001). Average waiting time for cTnT to drop below the 1 ng/ml threshold value was 5.73 ±2.95 (1-12) days. Intra-aortic balloon pump use in Groups 1 and 2 was 3% and 1%, respectively. There were no hospital mortalities in either group. Mortality rates at mid term were 6% in both groups.Conclusions: This study compared two groups positive and negative for preoperative cTnT. The findings show that it is safe to wait until cTnT levels decrease to the 1 ng/ml threshold value in cTnT positive patients having a stable course. This waiting period is not very long, which is significant with respect to potential complications. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the cardioprotective effect of hydroxytyrosol (HT) against isoproterenol-induced myocardial infarction in rats. Male rats were randomly divided into four groups, control, isoproterenol (Isop) and pretreated animals with HT in two different doses (2 and 5 mg/kg) orally for 7 days and intoxicated with isoproterenol (Isop + HT1) and (Isop + HT2) groups. Myocardial infarction in rats was induced subcutaneously by isoproterenol (100 mg/kg, s.c.) at an interval of 24 h on 6th and 7th day. On 8th day, electrocardiographic (ECG) pattern, gravimetric and biochemical parameters were assessed. Isoproterenol exhibited changes in ECG pattern, including significant ST-segment elevation and increase in the serum troponin-T level by 317 % as compared to control rats. Moreover, cardiac injury markers (creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase) underwent a notable rise in serum of infarcted animals. Else, a disturbance in lipids profile and significant increase in lipase and angiotensin-converting enzyme (ACE) activities and heart weight ratio were observed in isoproterenol group. However, pre- and co-treatment with HT (2 and 5 mg/kg) improved the myocardium injury, restored the hemodynamic function and inhibited the ACE activity that prevent cardiac hypertrophy and remodeling. Overall, these findings demonstrated that HT exerted a potent cardioprotective effect against isoproterenol-induced myocardial infarction. [ABSTRACT FROM AUTHOR]

The article presents a study that determined the effect of omentin and apelin in adults with and without Type 2 diabetes mellitus (T2DM) or cardiovascular disease (CVD). The results reveal that obese patients with T2DM or CVD affect inflammation or anti-inflammation levels, that low omentin with high apelin are linked in the increase of metabolic risk factors, and that omentin and apelin are good biomarkers for determining metabolic risk factors.

Objective: Acute rheumatic fever (ARF) is an endemic disease observed in children of developing countries. The purpose of this study was to test if it was possible to identify myocardial involvement in cases with rheumatic carditis by the measurement of serum cardiac TnT. Methods: 30 patients diagnosed as ARF underwent echocardiography and their cardiac troponin T (cTnT) serum levels were measured. Patients were divided into group 1: Arthritis alone, group 2: carditis, and group 3 carditis with congestive heart failure (CHF). Results: cTnT serum levels were normal in all except one patient with in group 3. Two patients in carditis (group 2) and three patients in CHF (group 3) had dilation in left ventricular end diastolic diameter. Conclusions: Normal cTnT levels in our patient group suggests that inflammation rather than myocardial necrosis is predominant in ARF carditis.

Introduction: High sensitive C-reactive protein (HS-CRP) is very sensitive acute phase reactant of inflammation. It is hypothesized that a relationship exists between HS-CRP and acute coronary artery disease (CAD). Materials and Methods: Consecutive sampling of 100 patients were done who presented with acute attack of CAD. In all these patients, Serum analysis for cardiac markers such as troponin-T and creatine phosphokinase- MB (CPK-MB) and serum analysis for quantitative estimation of HS-CRP were done along with few other parameters. Results: In our study, HS-CRP was raised in 90% of patients, along with CPK-MB and troponin-T and as an acute phase reactant, it showed parallel rise in total leukocyte count and absolute neutrophil count. The correlation scatter graphs were plotted, which were found to be statistically significant, (P < 0.05). Conclusion: HSCRP as an acute phase reactant correlates with other acute phase reactants such as total leukocyte count and absolute neutrophil count and also the rise in HS-CRP value in patients of acute CAD correlates with CPK-MB and troponin-T, so that it can be used as a marker for diagnostic purpose in these patients. [ABSTRACT FROM AUTHOR]

Objective: Myocardial infarction remains the major cause of global death due to cardiovascular diseases. This study aimed to assess the protective role of oleuropein in attenuating the cardiac remodeling in isoproterenol-induced myocardial infarction in rats. Methods and results: Male Wistar rats were randomly divided into four groups, control, isoproterenol (Isop) and pretreated animals with oleuropein at two different doses (20 and 40 mg/kg) orally for 7 days and intoxicated with isoproterenol (Isop+Oleu20) and (Isop+Oleu40) groups. The subcutaneous injection of isoproterenol (100 mg/kg body weight) to untreated rats for two consecutive days showed significant increases in ST-segment elevation, heart weight index and alteration in the ECG pattern and hemodynamic function. Else, serum levels of cardiac troponin-T, creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) underwent a notable rise in serum of Isop group by (345, 82, 73 and 106%, respectively) as compared to normal rats. Isoproterenol-induced myocardial injury was evidenced by alteration in serum lipids profile and increased activities of pancreatic lipase by 94% and angiotensin-converting enzyme (ACE) by 78% which reflects the occurrence of cardiac remodeling process. The histopathological findings of the infarcted group showed myocardium necrosis and cells inflammatory infiltration. However, the treatment with oleuropein gave a good protection of the myocardium by decreasing cardiac injury markers specially troponin-T, restoring hemodynamic parameters and attenuating cardiac remodeling process through inhibition of ACE activity. Conclusion: Oleuropein offers high preventive effects from cardiac remodeling process in rats with acute myocardial infarction. [ABSTRACT FROM AUTHOR]

Background The estimation of postmortem interval (PMI) is of paramount importance for the police in their investigation when arriving at the scene of a questionable death. The aim of present study is to evaluate the effect of elapsed time on cardiac Troponin-T degradation and its association with PMI in cases of death due to electrocution. Methods Cardiac tissue samples were collected from medico-legal autopsies, after informed consent from the relatives. The cases included were the subjects of electrocution without any prior history of disease who died in the hospital and their exact time of death was known. The analysis involves extraction of the protein at room temperature for different time periods (∼5, 26, 50, 84, 132, 157, 180, 205 and 230 Hrs), separation by SDS-PAGE and visualization by Western blot using cTnT specific monoclonal antibodies. Results The results specify a characteristic banding pattern amongst human cadavers (n = 5), a pseudo-linear relationship between percent cTnT degraded and the time since death (R 2 = 0.87, p = 0.0001) was observed. The area of the bands within a lane was quantified by scanning and digitizing the image using Gel Doc (Universal Hood II). Conclusions The post-mortem Troponin-T fragmentation observed in this study reveals a sequential, time-dependent process with the potential for use as a predictor of PMI in cases of electrocution. [ABSTRACT FROM AUTHOR]

In this study, the effect of pulsed electric field (PEF) treatment and ageing on the quality of beef M. longissimus lumborum (LL) and M. semimembranosus (SM) muscles was evaluated, including the tenderness, water loss and post-mortem proteolysis. Muscles were obtained from 12 steers (6 steers for each muscle), removed from the carcasses 4 hour postmortem and were treated with pulsed electric field within 2 h. Six different pulsed electric field intensities (voltages of 5 and 10 kV × frequencies of 20, 50 and 90 Hz) plus a control were applied to each muscle to determine the optimum treatment conditions. Beef LL was found to get tougher with increasing treatment frequency whereas beef SM muscle was found to have up to 21.6% reduction in the shear force with pulsed electric field treatment. Post-mortem proteolysis showed an increase in both troponin and desmin degradation in beef LL treated with low intensity PEF treatment (20 Hz) compared to non-treated control samples. [ABSTRACT FROM AUTHOR]

Background After the death of an organism, intracellular enzymes cause protein to degrade into smaller fragments as the time passes, if these fragments can be isolated and visualized, and if the fragmentation is proved to be measurable and quantifiable, it can be a good sign of the post-mortem interval (PMI). The aim of this study is to evaluate the effect of PMI on Troponin-T protein degradation in cardiac tissues of cadavers through quantitative analysis of Troponin-T degradation by easily electrophoretic method and its association with PMI in case of deaths due to burn. Methods An efficient extraction protocol to analyze the banding pattern of cTnT in post-mortem tissue was developed. The analysis involves extraction of the protein (at different PMI (~ 7.30, 18.20, 30.30, 41.20, 41.40, 54.30..................88.40 h), from the heart muscles of cadavers (burn cases), separation by denaturing gel electrophoresis (SDS-PAGE) and visualization by Western blot using cTnT specific monoclonal antibodies. Results The results specify a characteristic banding pattern amongst human cadavers (n = 9), a pseudo-linear relationship between percent cTnT degraded and the time since death (r = 0.87, p = 0.0001). The area of the bands within a lane was quantified by scanning and digitizing the image using commonly available scanners. Conclusions The present research used a simple, easy, applicable and highly informative electrophoresis method that make it an ideal for the busy forensic laboratory. The post-mortem Troponin-T fragmentation observed in this study reveals a sequential, time-dependent process with the potential for use as a predictor of PMI in cases of burning. This result shows a potential for use as a future applied method of evaluating time since death. [ABSTRACT FROM AUTHOR]

The effects of pulsed electric field (PEF) and ageing (3, 7, 14 and 21 days) on the shear force, protein profile, and post-mortem proteolysis of beef loins ( M. Longissimus lumborum , LL) and topsides ( M. Semimembranosus , SM) w ere investigated using a range of pulsed electric field treatments [voltages (5 and 10 kV) and frequencies (20, 50, and 90 Hz)]. PEF treatment decreased the shear force of beef LL and SM muscles by up to 19%. The reduction in the shear force in the LL was not affected by the treatment intensity whereas the reduction in the SM was dependent on PEF frequency. PEF treated beef loins showed increased proteolysis, both early post-mortem and during subsequent post-mortem storage reflected by increased degradation of troponin-T and desmin. The most prominent troponin-T degradation was found in samples treated with 5 kV–90 Hz, 10 kV–20 Hz at day 3 and day 7 post-treatment in addition to 10 kV–50 Hz in subsequent post-treatment times. The degradation of desmin in PEF treated beef loins increased with ageing time. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of the present review is to summarize the current knowledge on PH in relation to COPD and ILD from a clinical perspective with emphasis on diagnosis, biomarkers, prevalence, impact, treatment, and practical implications. PH in COPD and ILD is associated with a poor prognosis, and is considered one of the most frequent types of PH. However, the prevalence of PH among patients with COPD and ILD is not clear. The diagnosis of PH in chronic lung disease is often established by echocardiographic screening, but definitive diagnosis requires right heart catheterization, which is not systematically performed in clinical practice. Given the large number of patients with chronic lung disease, biomarkers to preclude or increase suspicion of PH are needed. NT-proBNP may be used as a rule-out test, but biomarkers with a high specificity for PH are still required. It is not known whether specific treatment with existent drugs effective in pulmonary arterial hypertension (PAH) is beneficial in lung disease related PH. Studies investigating existing PAH drugs in animal models of lung disease related PH have indicated a positive effect, and so have case reports and open label studies. However, treatment with systemically administered pulmonary vasodilators implies the risk of worsening the ventilation–perfusion mismatch in patients with lung disease. Inhaled vasodilators may be better suited for PH in lung disease, but new treatment modalities are also required. [Copyright &y& Elsevier]

Objective: We tried to identify the influence on the fetus infected with parvovirus B19 (PB19) and retrospectively analyze the severity of fetal infection. Methods: Twenty pregnant women who developed maternal PB19 infection were included in this study. A total of 20 amniotic fluid samples were collected for measurement of PB19-DNA, erythropoietin (Epo) and troponin-T (TnT). Results: Of the 5 fetuses with hydrops, 2 were rescued by fetal therapy. Significant differences between groups were found for Epo and TnT: Epo 107.1 ± 45.3 mU/ml and TnT 0.040 ± 0.028 ng/ml (mean ± standard deviation) for the symptomatic fetus group; and Epo 18.9 ± 13.7 mU/ml and TnT 0.008 ± 0.014 ng/ml for the asymptomatic fetus group ( p = 0.043 for both variables). Setting Epo ≥50 mU/ml as the predictor of disease onset resulted in an Odds ratio of 56.0, with a 95 % confidence interval of 7.68-1,108.76. Conclusion: The study has determined an amniotic Epo level of ≥50 mU/ml as a factor of the influence on the fetus infected with PB19. The measurement of amniotic Epo level combined with amniotic TnT level is effective for determining the severity of fetal hypoxia. [ABSTRACT FROM AUTHOR]

We reported marked differences in the myosin heavy and light chain (MHC and MLC) isoform composition of fast and slow fibers between the global and orbital layers of dog extraocular muscles. Many dog extraocular fibers, especially orbital fibers, have MHC and MLC isoform patterns that are distinct from those in limb skeletal muscles. Additional observations suggested possible differences in the tropomyosin (Tm) and troponin T (TnT) isoform composition of global and orbital fibers. Therefore, we tested, using SDS-PAGE and immunoblotting, whether differences in Tm and TnT isoform expression do, in fact, exist between global and orbital layers of dog and rat EOMs and to compare expression patterns among identified fast and slow single fibers from both muscle layers. The Tm isoforms expressed in global fast and slow fibers are the same as in limb fast (α-Tm and β-Tm) and slow (γ-Tm and β-Tm) fibers, respectively. Orbital slow orbital fibers, on the other hand, each co-express all three sarcomeric Tm isoforms (α, β and γ). The results indicate that fast global and orbital fibers express only fast isoforms of TnT, but the relative amounts of the individual isoforms are different from those in limb fast muscle fibers and an abundant fast TnT isoform in the orbital layer was not detected in fast limb muscles. Slow fibers in both layers express slow TnT isoforms and the relative amounts also differ from those in limb slow fibers. Unexpectedly, significant amounts of cardiac TnT isoforms were also detected in slow fibers, especially in the orbital layer in both species. TnI and TnC isoform patterns are the same as in fast and slow fibers in limb muscles. These results expand the understanding of the elaborate diversity in contractile protein isoform expression in mammalian extraocular muscle fibers and suggest that major differences in calcium-activation properties exist among these fibers, based upon Tm and TnT isoform expression patterns. [ABSTRACT FROM AUTHOR]

Summary: Background: Pulmonary hypertension (PH) is an important complication to interstitial lung disease (ILD). The aim of the present study was to investigate the relation of NT-proBNP, fibrin D-dimer, troponin-T, uric acid and exhaled nitric oxide (NO) to the presence of PH and mortality in ILD. Methods: In a previously described cohort of 212 ILD patients of whom 29 had PH, levels of the above mentioned biomarkers were analyzed as routine tests. Results: A value of NT-proBNP below 95 ng/l had a negative predictive value for PH of 99% (95% CI: 94–100). Values of troponin-T were higher in patients with PH (median (inter quartile range) = 9 (9–20) vs. 9(9–10) ng/l), and the odds ratio (OR) for PH was increased in patients with abnormal levels of uric acid (OR (95% CI) = 3.1(1.1–8.8)). NT-proBNP and troponin-T values above the 50th percentile, and uric acid and fibrin D-dimer values above the 90th percentile were each associated with increased mortality. Conclusions: A value of NT-proBNP below 95 ng/l may be used as a rule-out test for PH in ILD, while an abnormal value of uric acid is a risk factor for PH. NT-proBNP, troponin-T, uric acid and fibrin D-dimer have prognostic value in ILD patients, while exhaled levels of NO do not seem to predict PH or mortality. [ABSTRACT FROM AUTHOR]

Abstract: In order to study the effect of high-pressure (HP) treatment and two different methods of brine addition (important for lysosomal membrane destabilisation) on lysosomal enzymes activity and protein degradation, pork semitendinosus muscle was brine enhanced by injection or tumbling, and HP treated at 600MPa following storage at 2°C for up to 8weeks. In this report a novel protocol for SDS gelatin zymography was established, and an increase of cathepsin B and L activity after HP treatment was shown followed by a decrease during storage. No calpain activity was detected following HP treatment. HP treatment was shown to induce a decrease in protein solubility in both myofibrillar and sarcoplasmic fractions. LC–MS analysis of these fractions showed changes in the peptide pattern during storage. Western blot analysis showed that troponin-T was indeed degraded during storage after HP treatment. The results therefore suggest that HP treatment induced an increase in cathepsin activity, which subsequently affected the myofibrillar protein degradation pattern in pork meat. [Copyright &y& Elsevier]

Abstract: The anti lipid peroxidative and antioxidant effects of ellagic acid against isoproterenol-induced myocardial infarcted rats were reported previously. This study was designed to evaluate the protective effects of ellagic acid on the levels of cardiac troponin-T, lysosomal enzymes, and membrane bound ATPases along with the role of pro inflammatory cytokine. Male albino Wistar rats were pretreated with ellagic acid (7.5 and 15mg/kg body weight) daily for a period of 10days. After the pretreatment period isoproterenol (100mg/kg) was subcutaneously injected to rats twice at an interval of 24h. The protective effects of pretreatment with ellagic acid were measured by biochemical analysis and reverse transcriptase polymerase chain reaction. Evidence of myocardial infarction in isoproterenol induced rats included significant increase in the serum level of cardiac troponin-T and decreased levels of creatine kinase and lactate dehydrogenase in heart tissue homogenate .The pretreatment with ellagic acid restored the levels of cardiac markers in the serum and heart tissue homogenates. The activities of lysosomal enzymes (β-d-glucuronidase, β-N-acetyl glucosaminidase, β-galactosidase, cathepsin-d and acid phosphatase) were increased significantly in the serum and heart tissue of isoproterenol-induced rats. The activity of Na+/K+ATPase declined while the activities of Ca2+ATPase and Mg2+ATPase were increased significantly in the heart of isoproterenol-induced rats. Pretreatment with ellagic acid restored the activities of lysosomal enzymes and membrane bound ATPases. The higher expressions of pro-inflammatory cytokines such as interleukin-1β, interleukin-6 and tumour necrosis factor-α in the isoproterenol-induced rats were controlled by the pretreatment with ellagic acid. Our results imply that oral pretreatment with ellagic acid protects the heart lysosomal membrane against isoproterenol-induced cardiac damage. The observed effects might be due to the free radical scavenging, membrane stabilizing and anti-inflammatory properties of ellagic acid. [Copyright &y& Elsevier]

Muscle shortening and postmortem proteolysis both influence beef tenderness, but their interacting effects on tenderness are relatively unknown. Inherent myofibril structure and the extent of overlap between myosin and actin filaments are hypothesized to affect the availability of substrates for degradation by calpains. The objective of this study was to determine the influence of sarcomere length on the extent of calpain-induced proteolysis of bovine myofibrils in vitro. Bovine semitendinosus muscles were excised within 20 mm postmortem and dissected into strips, which were stretched and attached to applicator sticks or allowed slack to generate samples with different sarcomere lengths upon rigor completion. Samples were allowed to undergo rigor in a neutral pH buffer containing a protease inhibitor. Myofibrils were isolated and incubated at room temperature with excess exogenous μ-calpain at a ratio of 1:800 (wt/wt; enzyme:myofibrillar protein) at pH 6.8 for 0, 2, 60, 1,440, or 2,880 mm. Purified troponin was subjected to the same digestion conditions. Proteolysis of troponin T (TnT) was monitored using SDS-PAGE and Western blotting. Sarcomere length was greater (P < 0.0001) in stretched versus shortened samples (2.99 μm ± 0.03 vs. 2.12 ± 0.03 pm, respectively, means ± SE). Western blots for both stretched and shortened samples exhibited bands corresponding to intact TnT and TnT fragments. The abundance of intact TnT decreased (P < 0.0001) with incubation time across both treatments. At 1,440 and 2,880 min, less (P < 0.05) intact TnT was detected in samples with long sarcomeres. These data indicate proteolysis of TnT occurs to a greater extent in samples with longer sarcomeres, possibly due to easier access of proteases to their targeted substrates. Degradation patterns of TnT were qualitatively similar between myofibrils and purified troponin after incubation with μ-calpain. Therefore, it is unlikely that the mechanism by which proteolysis is limited in short sarcomeres involves an actomyosin-mediated interference of TnT. [ABSTRACT FROM AUTHOR]

The interaction between sarcomere length and postmortem proteolysis as related to meat tenderness is not clear. The extent of thick and thin filament overlap alters actomyosin binding and may alter substrate availability during aging-induced tenderization. The objective of this study was to determine the influence of sarcomere length on proteolytic degradation in beef. Strips from bovine semitendinosus were either stretched 40% and restrained or allowed to shorten unrestrained in an ice bath. After rigor completion, 0.6-cm cross sections were fabricated and were randomly assigned to 2, 4, 7, or 10 d of aging treatments. Myofibrils were isolated for sarcomere length determination. Samples were collected and frozen for shear force analysis, and muscle proteins were extracted for SDS-PAGE and Western blotting analyses to determine troponin T (TnT) proteolysis. Sarcomere length was greater (P < 0.01) in stretched muscle samples compared with shortened samples (2.57 vs. 1.43 μm, respectively). Correspondingly, shear force values were greater (P < 0.05) in shortened samples than stretched samples. Western blots revealed the presence of 3 major intact TnT bands that diminished with time postmortem and 4 bands (TnT degradation products) that accumulated during postmortem storage. Quantification of intact TnT showed increased (P < 0.05) proteolysis at 4 and 7 d postmortem in samples with long sarcomeres. By 10 d, only traces of the greatest molecular weight intact TnT band were evident in both shortened and stretched samples, suggesting this TnT band may be more susceptible to proteolysis than other intact TnT bands. Degradation products of TnT appeared earlier postmortem in samples with long sarcomeres. The 30- kDa TnT fragment appeared after 7 d of postmortem storage in samples with long sarcomeres but not until 10 d in muscle containing short sarcomeres. Collectively, these data show that postmortem TnT proteolysis is sarcomere length-dependent and suggest that thick and thin filament overlap may influence the postmortem aging process in beef. [ABSTRACT FROM AUTHOR]

Abstract: In the present study cDNA clones representing two slow skeletal muscle troponin T genes (sTnT1sb and sTnT2sb) in the sea bream (Sparus auratus), an important aquaculture species, were isolated and characterised. A third, intronless, TnT gene (iTnTsb), which is an apparent orthologue of a previously described zebrafish TnT, was also isolated. In adult sea bream sTnT expression was restricted to red muscle and, using northern blotting, a single low abundance transcript was identified for sTnT1sb (1260 nucleotides) and a single high abundance transcript was identified for sTnT2sb (1000 nucleotides). In contrast, iTnTsb is predominantly expressed in adult fast muscle. All three TnT genes are also expressed during larval development. Phylogenetic analysis of sea bream sTnT proteins to identify maximum parsimony showed that iTnTsb, sTnT1sb and sTnT2sb each cluster in independent groups. sTnT1sb clustered with other vertebrate sTnTs, while sTnT2 clustered with a group of fish specific sequences (from Fugu rubripes, Oryzia latipes and Salmo trutta). The teleost sTnT2 and iTnT each constitute new, apparently teleost specific, TnT groups. Analysis of the corresponding Fugu scaffold indicates that sTnT2sb is encoded by a gene with twelve exons. The two sTnT cDNAs isolated in sea bream probably arose by duplication of an ancestral gene, and iTnT by reverse transcription. It remains to be established if the encoded proteins have different structural and mechanistic roles in fish muscle. [Copyright &y& Elsevier]