Serum Levels Of troponin-T Research Articles

Troponin-T value as a prognostic marker in neonates diagnosed with neonatal encephalopathy and receiving hypothermia treatment.

The aim of this study was to investigate the effect of Troponin-T levels on the prognosis of neonatal encephalopathy (NE). 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. 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, χ²=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, χ²=6.95) and total duration of oxygen support (p=0.01, χ²=9.12). 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.

Training vs. racing: A comparison of arrhythmias and the repeatability of findings in Thoroughbred Chuckwagon racehorses

Arrhythmias are commonly reported in exercising horses, however due to regulatory constraints electrocardiograms (ECGs) are acquired during training but not competition, raising questions about the repeatability of findings. The aims were (1) compare training and competition arrhythmias and (2) describe the repeatability of arrhythmias during maximal-intensity exercise. A convenience sample of 52 healthy Thoroughbreds (aged 8.7 ± 2.5 years) competing in the World Professional Chuckwagon Association were obtained, totaling 152 training or competition ECGs (2–7 ECGs/horse). Speed, heart rate (HR) and arrhythmias (supraventricular premature complex, SVPC; ventricular premature complex, VPC) were examined. Pre- and post-recovery (approximately 6 min) blood samples measured lactate and high-sensitivity troponin-T. Training and competition arrythmias were compared (Friedman’s test) and reliability of repeated ECGs assessed (intraclass correlation; P < 0.05). Training vs. competition: Forty horses had clean tracing from training and competition (n = 80 ECGs); the number and type of arrhythmias were not different. In training, VPCs were present in 7/40 horses (median [interquartile range, IQR]/ECG; range; 0 [0,0]; 0–4) and 9/40 horses (0 [0,0]; 0–5) in active-recovery. In competition, VPCs were present in 7/40 horses (0 [0,0]; 0–8) and 8/40 horses (0 [0,0]; 0–5) in active-recovery. Arrhythmias were primarily single premature complexes. Training and competition speed, HR, lactate and troponin-T did not differ however, sampling was too early for peak serum Troponin-T levels. Repeatability: total arrhythmias between serial ECGs did not differ. The reliability to detect SVPCs and VPCs was poor to moderate, and poor, respectively. Overall, the total number of arrhythmias was repeatable, but the reliability of arrhythmia type was poor to moderate.

Cancer Therapy-Related Cardiac Dysfunction in Patients Treated with a Combination of an Immune Checkpoint Inhibitor and Doxorubicin.

Simple SummaryImmune checkpoint inhibitors (ICIs) have demonstrated promising efficacy against various types of cancer. Although ICIs exhibit strong anti-cancer effects, they can cause adverse cardiac events. However, only a few case reports have focused on whether ICIs and cardiotoxic agents increase the risk of cancer therapy-related cardiac dysfunction (CTRCD). Therefore, we evaluated cardiac dysfunction in patients with sarcoma who were receiving doxorubicin with or without ICI using echocardiography and left ventricular global longitudinal strain (LVGLS). This study shows that ICIs may increase the risk of CTRCD when used concomitantly with cardiotoxic agents. Furthermore, the serum troponin-T level was significantly elevated in patients receiving doxorubicin with ICIs. Therefore, CTRCD should be monitored in patients who are being treated with ICIs by cardiac biomarkers and echocardiography including myocardial strain.Backgrounds: There are scarce data on whether immune checkpoint inhibitors (ICIs) increase the risk of cardiac dysfunction when used with cardiotoxic agents. Thus, we evaluated cardiac dysfunction in patients with sarcoma receiving doxorubicin with or without ICI using echocardiography and left ventricular global longitudinal strain (LVGLS). Methods: A total of 95 patients were included in this study. Echocardiography and LVGLS were evaluated at baseline and follow-up (at 3 and 6 months of chemotherapy) and compared with the doxorubicin (Dox; n = 73) and concomitant ICI with doxorubicin (Dox-ICI; n = 22) groups. Cancer therapy-related cardiac dysfunction (CTRCD) was defined as a left ventricular ejection fraction (LVEF) drop of >10% and LVEF of <50% (definite CTRCD), LVEF drop of >10%, LVEF of ≥50%, and LVGLS relative reduction of >15% (probable CTRCD) at six months. Results: There were no significant differences in age, cumulative dose of doxorubicin, and cardiovascular risk factors between the two groups. At baseline, the LVEF was similar in the Dox and Dox-ICI groups (p = 0.493). In the Dox group, LVEF decreased to 59 ± 6% (Δ −7 ± 1.3%, p < 0.001) and LVGLS decreased from −17.3 ± 3.2% to −15.4 ± 3.2% (Δ −10.1 ± −1.9%, p < 0.001) at six months. In the Dox-ICI group, LVEF decreased to 55 ± 9% (Δ −9 ± 2.1%, p < 0.001), along with a significant decrease in LVGLS (from −18.6 ± 1.9% to −15.3 ± 3.6%, Δ −12.4 ± −2.4%, p < 0.001). Over a median follow-up of 192 days, there were no cases with clinical manifestations of fulminant myocarditis. In the Dox group, definite and probable CTRCD were observed in seven (10.1%) and five (7.4%) patients, respectively. In the Dox-ICI group, definite and probable CTRCD were observed in four (19%) and four (19%) patients, respectively. The total number of patients who developed CTRCD was significantly higher in the Dox-ICI group than in the Dox group (38.1% vs. 17.4%, p = 0.042). Serum troponin-T level was significantly higher in the Dox-ICI group than in the Dox group (53.3 vs. 27.5 pg/mL, p = 0.023). Conclusions: ICIs may increase the risk of CTRCD when used with cardiotoxic agents. CTRCD should be monitored in patients treated with ICIs by cardiac biomarkers and echocardiography, including LV-GLS.

Clinical implications of troponin-T elevations following TAVR

Abstract Funding Acknowledgements Type of funding sources: None. Background Baseline and post-procedural elevations in serum troponin-T levels are associated with increased morbidity and mortality following transcatheter aortic valve replacement (TAVR). However, the prognostic impact of change in serum troponin-T level following TAVR remains unknown. Methods Among the patients with severe aortic stenosis who underwent TAVR, those with baseline serum troponin-T level ≥51.5 ng/L were excluded. The impact of increases in serum troponin-T level to an abnormally high range (≥51.5 ng/L) following TAVR on 2-year cardiovascular death or heart failure readmissions was investigated. Results Among 189 included patients (median 86 years old, 28% men), serum troponin-T level increased in 79 patients following TAVR. An increase in serum troponin-T was associated with a higher rate of 30-day adverse events, predominantly due to pacemaker implantation for complete atrio-ventricular block, and a higher 2-year cumulative incidence of the primary endpoint (hazard ratio 3.97, 95% confidence interval 1.51-10.4, p = 0.005) adjusted for the use of balloon-expandable valve and post-TAVR pacemaker implantation (Figure 1). Conclusion Post-procedural increase in serum troponin-T level was associated with adverse clinical outcomes following TAVR. Abstract Figure. Cumulative incidence of endpoint

The Value of Admission Serological Indicators for Predicting 28-Day Mortality in Intensive Care Patients With Acute Heart Failure: Construction and Validation of a Nomogram.

Background: Acute heart failure (AHF) is a severe clinical syndrome characterized as rapid onset or worsening of symptoms of chronic heart failure (CHF). Risk stratification for patients with AHF in the intensive care unit (ICU) may help clinicians to predict the 28-day mortality risk in this subpopulation and further raise the quality of care.Methods: We retrospectively reviewed and analyzed the demographic characteristics and serological indicators of patients with AHF in the Medical Information Mart for Intensive Care III (MIMIC III) (version 1.4) between June 2001 and October 2012 and our medical center between January 2019 and April 2021. The chi-squared test and the Fisher's exact test were used for comparison of qualitative variables among the AHF death group and non-death group. The clinical variables were selected by using the least absolute shrinkage and selection operator (LASSO) regression. A clinical nomogram for predicting the 28-day mortality was constructed based on the multivariate Cox proportional hazard regression analysis and further validated by the internal and external cohorts.Results: Age > 65 years [hazard ratio (HR) = 2.47], the high Sequential Organ Failure Assessment (SOFA) score (≥3 and ≤8, HR = 2.21; ≥9 and ≤20, HR = 3.29), lactic acid (Lac) (>2 mmol/l, HR = 1.40), bicarbonate () (>28 mmol/l, HR = 1.59), blood urea nitrogen (BUN) (>21 mg/dl, HR = 1.75), albumin (<3.5 g/dl, HR = 2.02), troponin T (TnT) (>0.04 ng/ml, HR = 4.02), and creatine kinase-MB (CK-MB) (>5 ng/ml, HR = 1.64) were the independent risk factors for predicting 28-day mortality of intensive care patients with AHF (p < 0.05). The novel nomogram was developed and validated with a promising C-index of 0.814 (95% CI: 0.754–0.882), 0.820 (95% CI: 0.721–0.897), and 0.828 (95% CI: 0.743–0.917), respectively.Conclusion: This study provides a new insight in early predicting the risk of 28-day mortality in intensive care patients with AHF. The age, the SOFA score, and serum TnT level are the leading three predictors in evaluating the short-term outcome of intensive care patients with AHF. Based on the nomogram, clinicians could better stratify patients with AHF at high risk and make adequate treatment plans.

Clinical implications of troponin-T elevations following TAVR: Troponin Increase Following TAVR

BackgroundBaseline and post-procedural elevations in serum troponin-T levels are associated with increased morbidity and mortality following transcatheter aortic valve replacement (TAVR). However, the prognostic impact of change in serum troponin-T level following TAVR remains unknown. MethodsAmong the patients with severe aortic stenosis who underwent TAVR, those with baseline serum troponin-T level ≥51.5 ng/L were excluded. The impact of increases in serum troponin-T level to an abnormally high range (≥51.5 ng/L) following TAVR on 2-year cardiovascular death or heart failure readmissions was investigated. ResultsAmong 189 included patients (median 86 years old, 28% men), serum troponin-T level increased in 79 patients following TAVR. An increase in serum troponin-T was associated with a higher rate of 30-day adverse events, predominantly due to pacemaker implantation for complete atrio-ventricular block, and a higher 2-year cumulative incidence of the primary endpoint (hazard ratio 5.24, 95% confidence interval 1.64-16.8, p = 0.005) adjusted for the potential confounders. ConclusionPost-procedural increase in serum troponin-T level was associated with adverse clinical outcomes following TAVR.

Electrocardiographic changes in young patients with spontaneous pneumothorax: A retrospective study.

Primary spontaneous pneumothorax (PSP) commonly occurs in adolescents. PSP symptoms can mimic cardiac event. We aimed to examine electrocardiography (ECG) changes that accompanied PSP in relation to side and size of pneumothorax.A retrospectively reviewed 57 adolescents presented with PSP and underwent a cardiac evaluation.Overall, 49 patients (86%) were male, median age of 16 years. Of these, 1 patient had a known mitral valve prolapse. In 56 patients the initial episode of PSP was unilateral (16 left sided and 40 right sided), and 1 was bilateral. The main initial symptom was chest pain or dyspnea and chest pain 66.6% and 33.3% respectively. Small pneumothorax was right and left sided in 1and 8 patients respectively, medium right (n = 8) medium left (n = 22), large right (n = 7) and large left (n = 10). One additional patient had medium bilateral pneumothorax. ECG findings were abnormal in 12 patients (21%) and included ST elevation in 5 patients, inverted T wave in 2 patients, incomplete right bundle branch block in 2 patients, poor R wave progression, left axis deviation and low QRS voltage in 1 patient each. Only 2 patients had abnormal echocardiography findings, MPV (n = 1) and minimal mitral and tricuspid regurgitation (n = 1). Serum troponin-T levels were normal in all patients.ECG changes were found in 21% among pediatric patients with PSP. No correlation was observed between ECG changes and side/size of pneumothorax. It is important to rule out pneumothorax among children presented with chest pain, dyspnea and ECG changes.

RNA-sequencing-based transcriptome analysis of cantharidin-induced myocardial injury.

The cardiotoxicity of cantharidin has been well characterized, but the understanding of the underlying mechanism(s) is incomplete. To more fully understand the differentially expressed genes (DEGs) in cantharidin-induced myocardial injury, Sprague-Dawley rats were exposed to cantharidin (1.34 mg/kg or 2.67 mg/kg) for 24 h and then the heart was sampled for pathologic changes analysis and RNA-sequencing-based transcriptomic profiling. In addition, serum troponin T (TN-T) levels were also tested using the enzyme-linked immunosorbent assay method. The results showed that cantharidin could cause myocardial damage and elevated serum TN-T levels. The genes with a fold change ≥2 were considered as DEGs and we found 38 DEGs that were mainly enriched in eight pathways revealed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The cellular component of gene ontology analysis showed that the DEGs were mostly enriched in the extracellular matrix. In conclusion, our present study demonstrated that cantharidin induces myocardial injury by multiple modulatory mechanisms, which provide new insights for further study of the pathophysiologic mechanism of cantharidin-induced myocardial injury.

Study of the Clinical, Electrocardiographic and Biochemical Spectrum of Cardiovascular Complications in Patients With Aneurysmal Subarachnoid Hemorrhage − An Initial Experience at a Tertiary Centre in India

Objectives: Aneurysmal subarachnoid hemorrhage (SAH) is an extremely fatal condition with mortality as high as 45%. Apart from the intra-cranial causes, there are cardiovascular events, which add to the morbidity and mortality. These can manifest with deranged cardiac biomarkers. However, quantitative assessment of these biochemical markers and its correlation with prognosis has not been adequately studied. We tried to analyse the spectrum and outcome of cardiovascular complications in patients with aneurysmal SAH and whether elevated levels of serum biochemical markers have any association with the prognosis. Study Design: Prospective observational study. Materials and Method: We included patients of all grades of aneurysmal SAH with ictus less than 48 hours at the time of admission. The patient’s serum biochemical marker levels [troponin T (TnT), total creatine phosphokinase (CPK), cardiac-specific creatine phosphokinase (CPK − MB), brain natriuretic peptide (BNP) and C reactive protein (CRP)] were measured for 6 consecutive days from the day of admission (Day 0). Patient also underwent 12 lead Electrocardiography (ECG) and two dimensional echocardiography (2D Echo) on Day 0, Day 1 and Day 5. Statistical Analysis: Data analysis was performed by using Statistical Package for Social Sciences (SPSS) version 20:0. Chi-square test and Fisher’s exact test were used to find the association between diagnosis and various data variables associated with diagnosis. P value less than 0.05 was considered as significant. Data was graphically depicted with the help of box plots. Receiver Operating Characteristic (ROC) curves were plotted for TnT, CPK and BNP. Results: Twenty five patients were enrolled in the study. Out of the five serum biochemical markers studied, TnT, CPK and BNP were statistically associated with outcome. Serum TnT levels on day 4; serum CPK levels on day 3 and day 4; and serum BNP levels on day 3, day 4 and day 5 were statistically significant. BNP was the serum biochemical marker which had the strongest statistical association with outcome. ECG abnormalities were observed in 76% of the cases. Prolonged corrected QT (QTc) interval was the most common abnormal ECG finding among the patients who died. One patient developed 3rd degree heart block and another patient developed left ventricular dysfunction with an ejection fraction of 40% on 2D Echo following aneurysmal SAH. Conclusion: Cardiovascular complications are common in patients with aneurysmal SAH. Serum quantitative levels of TnT, CPK and BNP can be incorporated in the battery of routine blood tests in SAH patients for predicting outcome.

Acute canagliflozin treatment protects against in vivo myocardial ischemia\u2013reperfusion injury in non-diabetic male rats and enhances endothelium-dependent vasorelaxation

BackgroundThe sodium–glucose cotransporter-2 (SGLT2) inhibitor canagliflozin has been shown to reduce major cardiovascular events in type 2 diabetic patients, with a pronounced decrease in hospitalization for heart failure (HF) especially in those with HF at baseline. These might indicate a potent direct cardioprotective effect, which is currently incompletely understood. We sought to characterize the cardiovascular effects of acute canagliflozin treatment in healthy and infarcted rat hearts.MethodsNon-diabetic male rats were subjected to sham operation or coronary artery occlusion for 30 min, followed by 120 min reperfusion in vivo. Vehicle or canagliflozin (3 µg/kg bodyweight) was administered as an intravenous bolus 5 min after the onset of ischemia. Rats underwent either infarct size determination with serum troponin-T measurement, or functional assessment using left ventricular (LV) pressure–volume analysis. Protein, mRNA expressions, and 4-hydroxynonenal (HNE) content of myocardial samples from sham-operated and infarcted rats were investigated. In vitro organ bath experiments with aortic rings from healthy rats were performed to characterize a possible effect of canagliflozin on vascular function.ResultsAcute treatment with canagliflozin significantly reduced myocardial infarct size compared to vehicle (42.5 ± 2.9% vs. 59.3 ± 4.2%, P = 0.006), as well as serum troponin-T levels. Canagliflozin therapy alleviated LV systolic and diastolic dysfunction following myocardial ischemia–reperfusion injury (IRI), and preserved LV mechanoenergetics. Western blot analysis revealed an increased phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and endothelial nitric-oxide synthase (eNOS), which were not disease-specific effects. Canagliflozin elevated the phosphorylation of Akt only in infarcted hearts. Furthermore, canagliflozin reduced the expression of apoptotic markers (Bax/Bcl-2 ratio) and that of genes related to myocardial nitro-oxidative stress. In addition, treated hearts showed significantly lower HNE positivity. Organ bath experiments with aortic rings revealed that preincubation with canagliflozin significantly enhanced endothelium-dependent vasodilation in vitro, which might explain the slight LV afterload reducing effect of canagliflozin in healthy rats in vivo.ConclusionsAcute intravenous administration of canagliflozin after the onset of ischemia protects against myocardial IRI. The medication enhances endothelium dependent vasodilation independently of antidiabetic action. These findings might further contribute to our understanding of the cardiovascular protective effects of canagliflozin reported in clinical trials.

Inhibition of inducible nitric oxide synthase (iNOS) by simvastatin attenuates cardiac hypertrophy in rats.

The left ventricular hypertrophy (LVH) occurs in response to the haemodynamic overload in some physiological and pathological conditions. This study was designed to investigate the possible cardioprotective effect of simvastatin (SIM) treatment against isoproterenol (ISO)-induced LVH and the probable underlying mechanism in adult male Wistar rats. Animals were allocated into four groups. Rats of control group received normal saline orally for 30 days and intraperitoneally for the last 7 days. Rats of SIM group received SIM orally (10 mg/kg/day in saline) for 30 days. Rats of ISO group received normal saline orally for 30 days and ISO intraperitoneally (5 mg/kg) for the last 7 days to induce LVH. Rats of ISO/SIM group received SIM for 30 days and ISO intraperitoneally for the last 7 days. At the end of the experiment, all animals were sacrificed by cervical decapitation under anaesthesia. Truncal blood was collected and serum was separated and used for biochemical assay. The heart was dissected and processed for histological and immunohistochemical studies. The results of the present study confirmed the ISO-induced myocardial lesions including significant increase of heart weight (HW), heart weight/body weight (HW/BW) ratio, LVH, interstitial myocardial fibrosis (increased collagen types I and III), inflammatory cellular infiltration, necrosis of cardiomyocytes, and increased expression of inducible nitric oxide synthase (iNOS) and thioredoxin in cardiomyocytes. These changes were accompanied by significant increase in serum levels of troponin-T, creatine phosphokinase-MB (CPK-MB), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Co-administration of SIM to ISO-injected rats significantly reduced all these cardiac changes and serum biochemical markers in addition to marked depletion of iNOS and thioredoxin expression in cardiomyocytes. It is concluded that SIM co-administration attenuated ISO-induced cardiac lesions including LVH by inhibiting iNOS expression in cardiomyocytes.

Protective Effect of Hydroxytyrosol Against Cardiac Remodeling After Isoproterenol-Induced Myocardial Infarction in Rat.

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 5mg/kg) orally for 7days and intoxicated with isoproterenol (Isop+HT1) and (Isop+HT2) groups. Myocardial infarction in rats was induced subcutaneously by isoproterenol (100mg/kg, s.c.) at an interval of 24h 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 5mg/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.

Successful Percutaneous Coil Embolization of a Large and Tortuous Coronary Artery to Pulmonary Artery Fistula

We herein report the case of a 73-year-old woman with a large and tortuous coronary artery to pulmonary artery fistula treated with percutaneous coil embolization. The patient was hospitalized due to unstable angina with an elevated serum troponin-T level. Coronary angiography revealed no significant atherosclerotic stenosis, with a large and tortuous coronary artery to pulmonary artery fistula originating from the proximal portion of the left anterior descending artery. We successfully performed percutaneous coil embolization of the fistula. In this case, 320-slice multidetector computed tomography played a pivotal role in the diagnosis and percutaneous intervention.

Myocardial alterations and clinical implications associated with recovery of cardiac function in dilated cardiomyopathy with obesity

BackgroundObesity is associated with an increased risk of heart failure (HF) but the relationship between changes in cardiac function and the specific pathological features of dilated cardiomyopathy (DCM) with obesity, remains unknown. MethodsEndomyocardial biopsies from the left ventricle (LV) were obtained from 50 patients with DCM, at the first-onset of decompensated HF. Thirty patients were obese (obese-group: body mass index >30kg/m2) and 20 were non-obese (lean-group). Clinical data were acquired at the admission, after one month and one year. ResultsThe obese-group had higher systolic blood pressure (142.8±33.9 vs 113.6±18.7mmHg; p<0.001) and serum troponin-T level (0.049±0.07 vs 0.020±0.03ng/mL; p=0.022) than the lean-group. LV ejection fraction (LVEF) was not significantly different between groups, but after one year the obese-group had an improved LVEF (57.0±11.4 vs 44.3±17.1; p=0.003). Light microscopy revealed that the obese-group had larger cardiomyocytes (17.2±1.7 vs 16.4±1.4μm; p=0.033) and less myofilament lysis (37 vs 75%; p=0.008) with a higher density of lipid droplets (1.93±0.8 vs 0.94±0.7 /μm2; p<0.001). Multivariate regression analysis revealed that independent predictors of LVEF improvement after 12months were diuretics use, nuclear diameter, and absence of myofilament lysis (p=0.024, 0.012 and 0.028, respectively). ConclusionsCardiac function in most patients with DCM with obesity is reversible and myocardial structural changes are trivial even at the ultrastructural level.

Cardioprotection with forsythoside B in rat myocardial ischemia-reperfusion injury: Relation to inflammation response

The present study was undertaken to examine the effect of forsythoside B (FB) on rat myocardial ischemia-reperfusion (I/R) model and elucidate the potential mechanism. Left ventricular systolic pressure (LVSP) and +/-dp/dt(max) were detected. Blood samples were collected to determine serum levels of troponin T (Tn-T), TNF-alpha and IL-6. Hearts were harvested to assess histopathological change and infarct size, determine content of MDA, myeloperoxidase (MPO), SOD and GPx activities, analyze expression of high-mobility group box 1 (HMGB1), phosphor-I kappaB-alpha and phosphor-nuclear factor kappaB (NF-kappaB) in ischemic myocardial tissue by Western blot. Compared with control group, rats treatment with FB showed a significant recovery in myocardial function with improvement of LVSP and +/-dp/dt(max). The myocardial infarct volume, serum levels of Tn-T, TNF-alpha and IL-6, content of MDA and MPO activity in myocardial tissue were all reduced, protein expression of HMGB1, phosphor-I kappaB-alpha and phosphor-NF-kappaB were down-regulated, while attenuated the decrease of SOD and GPx activities. Besides, the infiltration of polymorph nuclear leukocytes (PMNs) and histopathological damages in myocardium were decreased in FB treated groups. These findings suggested that FB rescued cardiac function from I/R injury by limiting inflammation response and its antioxidant properties.

Elevated B-Type Natriuretic Peptide and Cardiac Troponin T Increased Cardiovascular and All-cause Mortality Risk in Hemodialysis Patients 10-Year Prospective Study

Background: It has been established that elevated plasma B-type natriuretic peptide (BNP) and serum cardiac troponin T (TnT) levels were associated with future cardiovascular (CV) events. The aim of the present study was to determine whether combination of BNP and TnT could predict mortality in hemodialysis (HD) patients. Methods: Plasma BNP and serum TnT were measured consecutively in 500 outer HD patients. These patients were divided into quartiles according to plasma BNP levels; Quartile 1 (Q1): < 145 ng/L, Q2: 145-266 ng/L, Q3: 267-628 ng/L, and Q4: > 628 ng/L, and serum TnT levels; Quartile 1 (Q1): < 0.04 ng/mL, Q2: 0.04-0.07 ng/mL, Q3: 0.07-0.13 ng/mL, and Q4: > 0.13ng/mL.

Contribution of Renal Function Impairment to Unexplained Troponin T Elevations in Congestive Heart Failure

Background. Patients with severe congestive heart failure (CHF) often have unexplained elevations in serum concentrations of troponin T (TnT), and it is proposed that this is due to cardiac TnT release because of underlying cardiac disease. We investigated whether impaired renal function is an additional underlying phenomenon contributing to increased TnT levels in patients with CHF. Methods. Sixty-two patients with nonischemic CHF, New York Heart Association (NYHA) class III–IV, with normal coronary angiogram and normal serum creatinine were included in the study. Baseline glomerular filtration rate (GFR) was calculated using the Cockcroft Gault equation. Results. Although mean creatinine level was normal (0.92 ± 0.17 mg/dL), mean GFR was low (56 ± 16 mL/min) in the cohort. Elevated (≥0.02 >g/L) TnT was measured in 33 patients (53%). Compared with patients with normal (<0.02 >g/L) TnT levels, patients with elevated TnT had significantly higher NYHA class (p = 0.02), longer duration of disease (p = 0.02), lower GFR (p = 0.0001), and lower LVEF (p = 0.0001). There were significant associations between TnT levels and duration of disease (r = 0.29, p = 0.01), creatinine (r = 0.30, p = 0.01), GFR (r = −0.55, p < 0.0001), and LVEF (r = −0.39, p = 0.001). Independence of these associations was evaluated in multiple linear regression analysis, and serum TnT was independently and negatively associated only with GFR (p = 0.005). Conclusions. Renal function (GFR) correlated significantly and more strongly than cardiac function (LVEF) with the serum TnT levels in patients with CHF. This supports our hypothesis that impaired renal function causes the accumulation of troponin and is very likely the cause of unexplained elevations of serum TnT in patients severe CHF.

Newborn piglets exposed to hypoxia after nicotine or saline pretreatment: Long-term effects on brain and heart

Objective. We wished to assess the effect of global hypoxia and the effect of nicotine pretreatment on the brain and heart of newborn pigs. Hypothesising that nicotine might give a better outcome because of its anti-apoptotic and anti-inflammatory effects.Methods. Twenty-two anaesthetised piglets were randomised to pretreatment with saline or nicotine (130 μg/kg/h) before 45 min global hypoxia. They were observed for 27 h. The brain and heart were assessed with histopathological methods. Serum for Troponin t (TnT) analyses was collected at baseline and at the end of the experiment.Results. There were no significant differences between the groups. At the end of hypoxia, BE was −14.8 ± 4.9 mmol/l and MABP was 25 ± 9 mmHg. Seven animals had autolysis of the cerebrum/cerebellum, their BE after hypoxia was −19 ± 1.8 mmol/l and MABP 23 ± 3 mmHg. The remaining 15 animals had a BE of −13 ± 4.7mmol/l (p = 0.0004) and a MABP of 26 ± 11 mmHg (ns). Eleven animals presented myocardial damage. A significant increase in TnT occurred in both groups. TnT increase and myocardial damage correlated (p = 0.001; r = 0.67). Animals with severe increase in TnT presented severe brain damage.Conclusions. Severe increase in serum TnT levels was linked to severe cerebral damage. Nicotine pretreatment had no impact on cerebral or cardiac histopathology.

The effect of metoprolol on perioperative outcome in coronary patients undergoing nonvascular abdominal surgery

Study Objective To analyze the clinical effectiveness of the β-1-aderenergic blocker, metoprolol. Design Prospective, observational, clinical study. Setting Operating room and intensive care unit of a tertiary-care teaching hospital. Patients 111 ASA physical status II, III, and IV consecutive patients who were scheduled for open abdominal nonvascular surgery. Interventions Patients were divided into two stratification groups: 83 (74.8%) of 111 received metoprolol, and 28 (25.2%) of 111 were controls. Within 24 to 96 hours, the drug was used parenterally in a dose of 5, 10, and 15 mg per 24 hours. Metoprolol cardioprotection was applied during the whole perioperative period, in the form of tablets in a dose of 25, 50, and 100 mg per 24 hours until the 30th postoperative day. Measurements During surgery, and in the first 72 postoperative hours, patients were monitored by continuous ST-T segment monitoring. A 12-lead electrocardiogram was attached immediately after surgery; on postoperative days 1, 2, and 7; and one day before discharge from the hospital. Serum troponin-T level was controlled 6, 24, and 96 hours after surgery. Main Results Postoperative mortality of cardiac etiology after 30 days of surgery was 1.2% (1/83) in the metoprolol group versus 7.1% (2/28) in the nonmetoprolol group ( P < 0.05). The causes of death in these three patients were acute myocardial infarction, congestive heart failure, and malignant arrhythmias. Conclusions Perioperative cardioprotection significantly reduced mortality until postoperative day 30 in patients having open abdominal nonvascular surgery with general anesthesia.

Association between cardiac troponin T elevation and angioscopic morphology of culprit lesion in patients with non–ST-segment elevation acute coronary syndrome

It is well known that cardiac troponin T (TnT) elevation on admission indicates a high-risk subgroup among patients with non-ST-segment elevation acute coronary syndrome (NSEACS). Although the mechanism of TnT elevation is speculated to be the microthromboembolism from unstable plaques, it has not been clarified. The aim of this study is to clarify the association between the serum TnT elevation and the angioscopically evaluated morphology of culprit lesion in the patients with NSEACS. Among 113 patients with NSEACS who had significant coronary stenosis, 62 patients with successful angioscopic examination were prospectively and consecutively enrolled from October 2001 to August 2002. Patients were divided into 2 groups according to the serum TnT level measured before percutaneous coronary intervention: TnT-positive or TnT-negative group. Thrombus and plaque color at culprit lesion were evaluated by angioscopy and were compared between the groups. Plaque color was determined as yellow or white, and thrombus as none, small, or large. Three different definitions for TnT-positive (> or =0.1, > or =0.03, and > or =0.01 ng/mL) were used and the sensitivity and specificity for detecting thrombus was compared. Prevalence of thrombus, large thrombus, and yellow plaque were all higher in TnT-positive than in TnT-negative group for 3 different cutoff values of TnT. Angiographic slow-flow occurred more frequently after percutaneous coronary intervention in TnT-positive than in TnT-negative group for 3 different cutoff values of TnT. Sensitivity/specificity of detecting large thrombus were 33%/100%, 44%/91%, and 56%/83% when TnT-positive was defined as TnT > or = 0.1, > or =0.03, and > or =0.01 ng/mL, respectively. Serum TnT level was significantly associated with the prevalence of thrombus and yellow plaque at the culprit lesions of NSEACS. Troponin T, when positive was defined as > or =0.01 ng/mL, still have a high specificity for detecting intracoronary thrombus.