Increased cTnI Concentrations Research Articles

Pharmacological Mechanisms of Periplocae Cortex Against Congestive Heart Failure Based on Network Pharmacology and Experimental Evaluation

Background Periplocae cortex is a well-known Traditional Chinese Medicine with abundant effects, including the treatment of chronic congestive heart failure (CHF). However, the principal components and mechanisms have not been fully elucidated. This study aims to analyze the active ingredients and potential mechanisms of the periplocae cortex in CHF treatment. Methods TCMSP, GeneCards, and Comparative Toxicogenomics databases were used to mine the active ingredients and potential targets of the periplocae cortex. Cytoscape 3.9.1 software was employed to construct the “periplocae cortex-active ingredients-potential targets” and protein–protein interaction network. The DAVID 6.8 database was used for Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the predicted targets. The protective effects of β-sitosterol (BSS) were detected in doxorubicin (Dox)-induced H9c2 cells using MTT assay, while the regulatory pathways of BSS were examined using various assays, including real-time quantitative PCR and Western blot. The cardiac troponin I (cTn-I) concentration was also measured. Results A total of 13 active ingredients were identified, and 33 targets of CHF were predicted. Network analysis highlighted BSS as the key active ingredient, interacting with 29 targets. GO and KEGG analyses indicated significant involvement of these targets in calcium and apoptosis signaling pathways. Experimental findings demonstrated that BSS enhanced cell viability, reduced intracellular calcium ion concentration, and inhibited caspase 3 activity in Dox-induced H9c2 cells. BSS significantly altered the expression of CHRM1, CASP3, and CASP9 genes ( P < .05), and increased CHRM2 expression. Additionally, BSS significantly increased cTn-I concentration. Notably, suppression of calcium and apoptosis signaling pathways partially mitigated BSS's effects on cell viability and cTn-I concentration. Conclusion Through network pharmacology and experimental verification, establishes BSS as a key active ingredient in the periplocae cortex for CHF treatment. BSS appears to modulate calcium and apoptosis signaling pathways, thereby exerting therapeutic effects in the treatment of CHF.

Copeptin for the differentiation of type 1 versus type 2 myocardial infarction or myocardial injury

BackgroundThe rapid and reliable differentiation of myocardial infarction (MI) due to atherothrombosis (T1MI) from MI due to supply-demand mismatch (T2MI) or acute myocardial injury is of major clinical relevance due to very different treatments, but still a major unmet clinical need. This study aimed to investigate whether copeptin, a stress hormone produced in the hypothalamus, helps to differentiate between T1MI versus T2MI or injury. MethodsIn a retrospective analysis, 1271 unselected consecutive patients presenting with symptoms suggestive of MI to the emergency department were evaluated. Patients diagnosed with ST-elevation MI were excluded. All patients with elevated cardiac troponin I (cTnI) concentration possibly indicating MI were classified into T1MI, T2MI, or acute myocardial injury using detailed clinical assessment and coronary imaging. Copeptin plasma concentration was measured in a blinded fashion. A multicenter diagnostic study with central adjudication of the final diagnosis served as external validation cohort (n = 1390). ResultsAmong 1161 patients, 154 patients had increased cTnI concentration. Of these, 78 patients (51%) were classified as T1MI and 76 (49%) as T2MI or myocardial injury. Patients with T2MI or myocardial injury had significantly higher copeptin plasma concentration between patients versus T1MI (21,4 pmol/l versus 8,1 pmol/l, p = 0,001). A multivariable regression analysis revealed that higher concentrations of copeptin and C-reactive protein, higher heart rate at presentation and lower frequency of smoking remained significantly associated with T2MI and myocardial injury. Findings were largely confirmed in the external validation cohort. ConclusionIn patients without ST-segment elevation, copeptin concentration was higher in T2MI and myocardial Injury versus T1MI and may help in their differential diagnosis.

Effect of racing on cardiac troponin I concentration and associations with cardiac rhythm disturbances in Standardbred racehorses

Introduction/ObjectivesAccumulating evidence indicates intense exercise can be associated with myocardial damage. Investigating the impact of maximal effort on myocardium and exploring possible association of injury with rhythm disturbance requires a high-sensitivity cardiac troponin assay. The objectives of this study were: (1) to determine the effect of racing on serum cardiac troponin I (cTnI) in Standardbred horses using a high-sensitivity assay; (2) to determine the 99th percentile of cTnI in healthy horses and investigate the effect of demographic variables on cTnI prevailing pre-race in Standardbred horses using a validated high-sensitivity assay and a contemporary assay, and; (3) to explore associations between exercise-associated arrhythmia and cTnI concentration. AnimalsRacehorses (n = 145). Materials and methods≤ 2 h pre-race, cTnI concentrations were measured in 158 race starts. Electrocardiogram (ECG) monitoring was applied during racing and race recovery and screened for complex ventricular arrhythmia. Associations between cTnI prevailing before racing concentration, age, sex, and gait were investigated. Demographic and performance variables were evaluated for associations with cTnI concentration post-race and rhythm disturbance. ResultsIncidence of arrhythmia was 11.6% (16 horses). A significant increase in median (interquartile range) cTnI concentration of 1.36 (0.49–2.81) ng/L was found post-race (p < 0.0001). Serum cardiac troponin I (cTnI) concentration prevailing pre-race was positively associated with increasing age, and gait. Serum cardiac troponin I prevailing post-race was positively associated with concentration prevailing pre-race. Interaction between arrhythmia and finishing distanced revealed horses finishing distanced and experiencing arrhythmia displayed higher cTnI release than with the presence of either alone. ConclusionsRacing increased cTnI concentration. Horses finishing distanced and also exhibiting arrhythmia may be experiencing myocardial compromise.

Ambulatory electrocardiography and serum cardiac troponin I measurement in 21 dogs envenomated by the European adder (Vipera berus).

BackgroundEnvenomation by the European adder (Vipera berus) is common in dogs in Europe. Cardiac arrhythmias occur but clinical studies of envenomated dogs are limited.ObjectivesTo describe arrhythmias in dogs within 48 hours of envenomation, and investigate associations between arrhythmia grade, serum troponin I (cTnI), and snakebite severity score (SS score).AnimalsTwenty‐one client‐owned dogs bitten by V berus.MethodsProspective cohort study of envenomated dogs. Ambulatory electrocardiograms were recorded from presentation to 48 hours after snakebite, and arrhythmias graded 0 to 3 based on frequency and severity. Serum cTnI was measured at presentation, 12 hours, 24 hours, 36 hours, and 14 days after bite. An SS score of 1 to 3 was recorded at admission and based on clinical examination.ResultsAll dogs survived. Twelve dogs (57%) developed arrhythmias, all of which were ventricular in origin. Severe complex ventricular arrhythmias (VAs) were observed in 6 dogs (29%). Eighty‐one percent of dogs (n = 17) had increased cTnI concentrations at 1 or more time points. Dogs that developed arrhythmias had significantly higher concentrations of cTnI at 12 hours (1.67 [0.04‐32.68] versus 0.03 [0.01‐0.052]; P = .002), 24 hours (1.88 [0.2‐14.23] versus 0.06 [0.01‐2.06]; P = .009), and 36 hours (3.7 [0.02‐16.62] versus 0.06 [0.01‐1.33]; P = .006) after bite compared to those that did not. Contingency table analysis showed that SS score was not significantly associated with arrhythmia grade (P = .9).Conclusions and Clinical ImportanceMyocardial cell injury, reflected by increased cTnI concentrations and VAs, is common after V berus envenomation in dogs. Prolonged electrocardiography monitoring is advised, particularly where cTnI is increased.

Prognostic importance of serum troponin concentration in patients with an implanted cardioverter‑defibrillator admitted to the emergency department due to electric shock.

High-energy implantable cardioverter-defibrillator (ICD) therapy may increase serum troponin (cTnI) concentration. Aims: We aimed to assess an impact of cTnI concentration after ICD high-energy therapy on mortality. A total of 150 patients aged 64.2 +/- 12.8 years admitted to the Emergency Departments (EDs) due to at least one electrical shock during the last 24 hours with measured serum cTnI concentration at admission were included. Age, gender, comorbidities, shocks' numbers, therapy appropriateness, serum creatinine concentration, and left ventricular ejection fraction were noted for the retrospective analysis. Survival was obtained using the personal identification numbers (PESEL), on November 2018 until death or a period of three years had elapsed (1057 days). cTnI concentration was increased in 92 (61.3%) patients. The mortality rate was related to age - HR: 1.04, 95% CI: 1.01-1.08, p = 0.026; increased cTnI concentration - HR: 2.88, 95% CI: 1.30-6.37, p = 0.009; diabetes - HR: 2.19, 95% CI: 1.09-4.39, p = 0.027; ischemic heart disease - HR: 2.96, 95% CI: 1.11-7.87, p = 0.030, serum creatinine concentration - HR: 2.17, 95% CI: 1.18-4.00, p = 0.013; LVEF (HR 0.95, 95% CI: 0.91-0.99, p = 0.009), and previous or current CABG or PCI (HR: 0.38, 95% CI: 0.15-0.96, p = 0.040 and HR: 0.29, 95% CI: 0.13-0.65, p = 0.003, respectively). Increased mortality rate in patients with ICD shocks is multifactorial. Increased cTnI concentration at ED admission, but not the number of ICD shocks, is an independent marker of higher long-term mortality.

Diagnostic utility of cardiac troponin I in cats with hypertrophic cardiomyopathy.

BackgroundCardiac troponin I (cTnI) is useful for assessing hypertrophic cardiomyopathy (HCM) in cats.ObjectiveTo measure plasma cTnI concentrations in healthy cats and evaluate the clinical utility of cTnI in determining the severity of HCM.AnimalsClinically healthy cats (n = 88) and cats with HCM (n = 93).MethodsMulticenter prospective study. Cats with HCM, including hypertrophic obstructive cardiomyopathy at various stages, were diagnosed using echocardiography. Plasma cTnI concentrations were analyzed by a commercial laboratory. Receiver‐operating characteristic curve analysis was used to evaluate the accuracy of plasma cTnI concentrations to detect HCM.ResultsThe median cTnI concentration was 0.027 ng/mL (interquartile range, 0.012‐0.048 ng/mL) in healthy cats. Concentrations were significantly higher in diseased cats than in healthy controls, and concentrations were significantly higher in cats with heart failure than in asymptomatic cats. A plasma cTnI concentration of 0.163 ng/mL had a sensitivity of 62.0% and specificity of 100% when used to distinguish normal cats from asymptomatic HCM cats without left atrial dilatation. A cutoff of 0.234 ng/mL had high sensitivity (95.0%) and specificity (77.8%) for assessing heart failure. The areas under the receiver‐operating characteristic curves were 0.85 and 0.93, respectively.Conclusions and Clinical ImportanceIncreased cTnI concentrations reflect the severity of HCM. If other causes of cardiac injury are ruled out, plasma cTnI concentration may be useful for predicting the severity of HCM in cats.

Incidence of Undetectable, Measurable, and Increased Cardiac Troponin I Concentrations Above the 99th Percentile Using a High-Sensitivity vs a Contemporary Assay in Patients Presenting to the Emergency Department.

We compared the incidence of undetectable [below the limit of detection (LoD)], measurable (LoD to 99th percentile), and increased cardiac troponin I (cTnI) concentrations above the 99th percentile between Abbott high-sensitivity cTnI (hs-cTnI) and contemporary cTnI assays in a US emergency department population. Patients (n = 2100) presenting to the emergency department who had serial cTnI (0, 3, 6, 9 h) measurements ordered on clinical indication were enrolled. Contemporary cTnI [Abbott Architect used clinically; 99th percentile: 0.030 μg/L (30 ng/L)] and hs-cTnI [Abbott investigational; sex-specific 99th percentiles: female (F) 16 ng/L, male (M) 34 ng/L] assays simultaneously measured fresh EDTA plasma. The hs-cTnI assay measured fewer undetectable cTnI concentrations compared to the contemporary cTnI assay across baseline (F: 31% vs 47%, M: 22% vs 40%) and serial (F: 21% vs 46%; M: 19% vs 54%) measurements. Conversely, the proportion of measurable cTnI concentrations was higher using hs-cTnI compared to contemporary cTnI assay across both baseline (F: 46% vs 31%; M: 60% vs 33%) and serial (F: 48% vs 28%; M: 83% vs 40%) measurements. The overall proportion of patients with increased cTnI concentrations above the 99th percentile was not significantly different between the contemporary (31%) and hs-cTnI (26%) assays (P = 0.09). In patients presenting to the emergency department, the use of the Abbott hs-cTnI assay provides clinicians with more numeric cTnI concentrations. This occurs via a shift from results below the LoD to those between the LoD and the 99th percentile and does not increase in the number of cTnI concentrations above the 99th percentile.

Serum cardiac troponin I concentrations in dogs with systemic inflammatory response syndrome.

BackgroundMyocardial injury can be detected by cardiac troponin I (cTnI) concentration, which appears to be a predictor of short‐term death in critically ill patients. It is unknown if the best prognostic indicator of short‐term survival is cTnI measurement at admission or at later time points.Hypothesis/ObjectivesMeasuring cTnI with a high‐sensitivity (HS) test at different time points after admission may be a better short‐term prognostic indicator than a single cTnI measurement at admission in dogs with systemic inflammatory response syndrome (SIRS).AnimalsProspective, observational clinical study of 60 dogs with SIRS.MethodsCardiac troponin I concentration was measured in 133 serum samples, collected at days 1, 2, 3, and 5. Additionally, the acute patient physiologic and laboratory evaluation (APPLE) fast score was evaluated at admission. Prognostic capabilities of cTnI measurement and APPLE fast score for 28‐day mortality were assessed by receiver operating characteristic curve analysis.ResultsForty‐one dogs with SIRS that survived 28 days had significantly lower serum cTnI concentrations at admission (median, 0.09 ng/mL; P = .004) and at the peak time point (median, 0.23 ng/mL; P = .01) compared to 19 nonsurvivors (median at admission, 0.63 ng/mL; median at peak, 1.22 ng/mL). Area under the curve to predict survival, using cTnI was similar at admission (0.732) and at peak (0.708), and was 0.754 for the APPLE fast score.Conclusions and Clinical ImportanceIncreased cTnI concentration in dogs with SIRS is associated with poor outcome. Daily follow‐up measurement of cTnI concentration provides no additional prognostic information for short‐term mortality.

Elevated serum concentration of cardiac troponin I in a Dorcas gazelle (Gazella dorcas) with mitral vegetation

A 15-month-old male Dorcas gazelle (Gazella dorcas), with a history of weight loss, anorexia, fever, and lethargy of 2 weeks’ duration was examined. The gazelle showed several symptoms of illness including fever, lethargy, and tachycardia. The serum cardiac troponin I (cTnI) was as high as 2.18 ng/ml then dropped to 0.09 ng/ml after treatment. Transthoracic echocardiography revealed 1.02 × 1.37 cm irregular vegetation located on the left atrioventricular valve compatible with mitral endocarditis. This is the first report showing mitral vegetation in a gazelle associated with increased cTnI concentration and its recovery.

Preliminary Investigation of Cardiac Troponin I Concentration in Cows with Common Production Diseases

Increased cTnI concentrations are associated with adverse outcomes in humans and animals. Limited information is available on the prognostic value of cTnI in cows. To measure cTnI in cows with noncardiac diseases and evaluate the association of cTnI concentration with adverse outcomes such as death or early removal from the herd. Thirty control and 53 diseased cows. Serum cTnI concentrations were determined with a point-of-care immunoassay. Cows were diagnosed ante- or postmortem with metritis (n = 6), mastitis (n = 4), peritonitis (n = 6), LDA (n = 14), LDA and metritis (n = 4), pneumonia (n = 6), dystocia requiring cesarean section (n = 5), and downer cow syndrome (n = 8). Animal survival was determined for up to 2 months after presentation. The immunoassay showed reliability for the detection of bovine cTnI. Cows with LDA and metritis (P < .05), peritonitis (P < .05), LDA (P < .001), dystocia requiring cesarean section (P < .01), and downer cow syndrome (P < .001) had higher cTnI concentrations than control cows. The odds of a negative outcome (death or culling) for cows with cTnI concentrations of ≥ 0.05, ≥ 0.1, ≥ 0.2, and ≥ 0.5 ng/mL were 2.4, 2.9, 4.8, and 6.2, respectively. Cows with noncardiac diseases may have some degree of myocardial injury. The magnitude of cTnI increased may assist clinicians in evaluating the risk of an adverse outcome and help guide decision-making regarding treatment and prognosis.

Utility of cardiac biomarkers during adulticide treatment of heartworm disease (Dirofilaria immitis) in dogs

Heartworm disease (Dirofilaria immitis) is a parasitic disease of dogs and other carnivores, characterized by the presence of adult worms in the pulmonary arteries and right ventricle, leading to pulmonary hypertension which may progress to congestive heart failure. Cardiac biomarkers are biological parameters that can be objectively measured as indicators of pathological processes, or to assess the response to therapeutic interventions. To evaluate the myocardial damage during the adulticide treatment in 15 heartworm-infected dogs with ivermectin, doxycycline and melarsomine, measurements of cardiac troponin I (cTnI), myoglobin, MB isoenzyme of creatine kinase (CK-MB) and aspartate aminotransferase (AST) were carried out on days 0, 60 and afterwards weekly on days 67, 75, 82, 91, 106, 113 and 120. Dogs were divided by low parasite burden (n=9) and high parasite burden (n=6). On day 0, dogs with high worm burden showed increased cTnI concentrations (3.62±4.78ng/ml) while dogs with low worm burden had concentrations similar to those of healthy dogs (0.78±0.22ng/ml), CK-MB concentrations were increased only in dogs with high parasite burden as well (54.4±54.2U/l) and 26.6% (4/15) of the dogs showed pathological concentrations of myoglobin. On day 91, most dogs showed pathological concentrations of myoglobin, CK-MB and AST, probably due to the myositis associated to the intramuscular injection of melarsomine. The rest of the measurements made in the study, the biomarkers concentrations were within normal values, except for cTnI in dogs with high parasite burden, which remained above reference concentrations for healthy dogs during all the study. The evaluation of cardiac biomarkers seems to be a helpful test in the assessment of the myocardium in dogs with heartworm disease during the adulticide treatment.

Serum cardiac troponin I concentrations in dogs with leishmaniasis: correlation with age and clinicopathologic abnormalities

There is anecdotal evidence of myocardial injury in dogs with leishmaniasis due to generalized vasculitis and myocarditis. The aims of this study were to evaluate serum concentration of cardiac troponin I (cTnI) as an indicator of myocardial injury in dogs with leishmaniasis and to assess the relationship between cTnI concentration and age, serum antibody titer, and a variety of blood analytes. In this retrospective study, serum cTnI concentration was measured in dogs with leishmaniasis and in age-matched healthy dogs. Diagnosis was based on clinical signs and moderate-to-high seropositivity for Leishmania as measured by ELISA. Correlations between cTnI concentration and ELISA seropositivity, PCV, concentrations of serum creatinine, total protein, albumin, and globulin, albumin:globulin ratio (A/G), and urine protein:creatinine ratio (UPC) were investigated. The Mann-Whitney test was used to compare analytes between dogs with normal and increased (> 0.06 μg/L) cTnI concentration and to compare cTnI concentrations between dogs with and without anemia, azotemia, and proteinuria. In dogs with leishmaniasis (n = 40), median cTnI concentration was higher than in control dogs (n = 11) (P = .011). Sixteen dogs (40%) with leishmaniasis had increased cTnI concentration; cTnI was moderately to weakly correlated with decreased albumin concentration, decreased A/G, increased UPC, decreased PCV, positive Leishmania titer, and increased age. Dogs with leishmaniasis had significantly higher total protein and globulin concentrations and lower PCV, albumin concentration, and A/G than control dogs. Hematologic and biochemical analytes did not differ significantly between dogs with cTnI concentration within the reference interval and those with increased concentrations. Concentration of cTnI was higher in proteinuric dogs compared with nonproteinuric dogs (P = .017). A proportion of dogs with leishmaniasis have increased serum cTnI concentration, indicative of some degree of cardiac injury. Additional studies are needed to investigate the relationship between leishmaniasis and possible myocardial injury.

Raised serum cardiac troponin I concentrations predict hospital mortality in intensive care unit patients

Recent work suggests that increased plasma concentrations of cardiac troponin I (cTnI) are common in critically ill patients and are associated with poor outcome. We measured the frequency of increased plasma cTnI concentrations during patients' stay in a mixed medical/surgical intensive care unit (ICU) and compared our findings with hospital mortality. Basic details, organ support, and hospital mortality were recorded for all patients treated in ICU during a 6 month period. cTnI concentrations were sampled daily for all patients, using 0.04 µg litre(-1) as the upper limit of normal, and 0.12 µg litre(-1) as an additional stratification point. Of 663 patients, 54% were male, with a mean (sd) age of 60 (18) yr, 65% were surgical patients, and the median Acute Physiology and Chronic Ill Health II (APACHE II) score was 15 (inter-quartile range 12-20). Increased cTnI concentrations were found in 345 patients (52%) while in ICU. One hundred and twenty patients (18%) died in hospital. cTnI concentration >0.04 µg litre(-1) was associated with reduced odds of hospital survival, independent of age, medical admission, unplanned admission, APACHE II score, mechanical ventilation, and haemofiltration (adjusted odds ratio 0.25, 95% confidence interval 0.08-0.75, P=0.014). Stratification by the degree of cTnI increase revealed an incremental trend towards a lower odds of hospital survival, including for patients with 'minor' elevations of cTnI (0.05-0.12 µg litre(-1)). Increased serum cTnI concentrations during ICU stay independently predicts hospital mortality, even when the threshold is low. We found a trend towards an association between 'minor' elevations in cTnI and higher in-hospital mortality.

Serum cardiac troponin I concentrations in naturally occurring myelosuppressive and non-myelosuppressive canine monocytic ehrlichiosis

The aim of this study was to determine whether serum cardiac troponin I (cTnI) concentration measured on admission was associated with the clinical severity of canine monocytic ehrlichiosis and was predictive of clinical outcome (death or survival) in dogs naturally infected with Ehrlichia canis. Serum cTnI concentration was compared among 22 dogs with non-myelosuppressive ehrlichiosis (NME), 22 dogs with myelosuppressive ehrlichiosis (ME) and 10 healthy dogs. Unlike healthy dogs, 45.5% NME and 59.1% ME dogs had increased cTnI concentrations. There was no difference in the frequency of cTnI increase or mean cTnI concentrations between the NME and ME groups, whereas mean cTnI concentration was significantly lower in healthy dogs. No association was established between cTnI concentration on admission and clinical outcome.

Acute and Long‐Term Cardiomyopathy and Delayed Neurotoxicity after Accidental Lasalocid Poisoning in Horses

Horses are extremely susceptible to ionophore intoxication. Although numerous reports are available regarding monensin, little is known about lasalocid toxicity. To describe accidental lasalocid poisoning on a farm in Belgium. Eighty-one horses, of which 14 demonstrated clinical signs from day 0-21 after being fed a new concentrate batch. One horse died on day 20 and another on day 27. The most severe cases (n=7), admitted to the clinic on day 29-46, underwent cardiac examination and blood biochemical analysis, including determination of plasma cardiac troponin I (cTnI) at admission and during follow-up. On day 57-70, cardiac examination, cTnI determination or both were undertaken on 72 remaining horses. Short-term effects of lasalocid intoxication included inappetance, lethargy, sweating, and muscular weakness. All 7 horses admitted to the clinic demonstrated signs of myocardial degeneration such as increased cTnI, dysrhythmia and reduced myocardial contractility. Four horses developed ataxia on day 40-50. Five horses died or were euthanized on day 30-370, 2 horses recovered fully and returned to previous athletic use. None of the 72 remaining horses exhibited clinical signs between day 57-70, but 34 had dysrhythmia and 13 had increased cTnI concentrations. After a period of rest, all horses returned to their previous work. Lasalocid was detected in hepatic tissue of 2 necropsied horses. Lasalocid intoxication induced myocardial and neurological damage. Although uncommon, this should be included as differential diagnosis for unexplained inappetance, signs of depression, cardiomyopathy, and ataxia in horses.

Effects of Inula Britannica on myocardial caspase-3 and cytochrome C expression following overtraining-induced acute myocardial injury in rats

Objective To investigate the effects of Inula Britannica on myocardial caspase-3 and cytochrome c ( cyt c) following overtraining-induced acute myocardial injury in rats.Methods Forty-eight male Wistar rats weighing 200-220 g were randomly divided into 3 groups:group control (group C,n =8) ; group exhausting swim (group E,n =24) and group Inula Britannica (group IB,n =16).The animal model of overtraining-indnced acute myocardial injury was developed by exhausting swim.The animals were forced to swim until they were exhausted.The animals sank to the bottom and no righting reflex or escape response was elicited when they were taken out of water in groups E and IB.In group IB oral Inula Britannica 25 ml/kg was given 24 h and immediately before overtraining.Blood samples were taken from inferior vena cava immediately and at 6,24 h after overtraining in group E and at 6,24 h after overtraining in group IB for determination of serum cardiac troponin I (cTnI) concentration (by ELISA).The animals were sacrificed after blood sampling and myocardial specimens were obtained for microscopic examination and determination of caspase-3 and cyt c expression (by immuno-histochemistry).Results Overtraining significantly increased serum cTnI concentration and up-regulated myocardial caspase-3 and cyt c expression in group E as compared with group C.Oral Inula Britannica significantly attenuated overtraining-induced increase in serum cTnI concentration and myocardial caspase-3 and cyt c expression in group IB as compared with group E.Conclusion Inula Britannica can reduce overtraining-induced acute myocardial injury by down-regulating caspase-3 and cyt c expression. Key words: Inula; Hyperkinesis; Cardiomyopathies; Cytochromes c; Caspase 3

Circulating Troponin As Measured by a Sensitive Assay for Cardiovascular Risk Assessment in Primary Prevention

Measuring circulating cardiac troponin using novel sensitive assays has revealed that even minute elevations are associated with increased mortality in patients with coronary artery disease or even in the general population. Less well defined, however, is the incremental value of measuring circulating cardiac troponin I (cTnI) by a sensitive assay for risk assessment in primary prevention. We measured circulating concentrations of cTnI, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity C-reactive protein (hsCRP) in 5388 individuals free of known cardiovascular disease recruited into the DETECT study, a prospective longitudinal population-based cohort study. We determined the prognostic implications for incident major adverse cardiovascular events (MACE) during 5 years of follow-up. Circulating cTnI was detectable in 19% of the subjects. Increased cTnI concentrations were associated with established risk factors for atherosclerosis and demonstrated a graded relationship with all-cause mortality and incident MACE during 5-year follow-up. A single measurement of cTnI significantly improved risk prediction over established risk factors, and also added prognostic information, when adjusted for serum concentrations of NT-proBNP and hsCRP. Minute increases in cTnI are associated with increased mortality and incident MACE in a large primary prevention cohort and, thus, identify contributors to cardiovascular risk not fully captured by traditional risk factor assessment.

Effects of sevoflurane wash-in during cardiopulmonary bypass on myocardial injury in patients undergoing coronary artery bypass grafting

Objective To investigate the effects of sevoflurane wash-in during cardiopulmonary bypass (CPB) on myocardial injury in patients undergoing coronary artery bypass grafting(CABG).Methods Forty ASA Ⅱ or Ⅲ patients aged 50-64 yr,weighing 53-90 kg undergoing scheduled for CABG under CPB were randomly divided into 2 groups (n =20): control group (group C) and sevoflurane group(group S).Anesthesia was maintained with propofol 3-5 mg·kg-1 ·h-1 and sufentanil 0.5-1.0 μg·kg-1 ·h-1 in both groups.Sevoflurane 1％-2％ was washed into extracorporeal circuit during CPB in group S.Blood samples were taken from central vein after the induction of anesthesia (T0,baseline) and at 6,12 and 24 h (T1-3) after operation for determination of plasma cardiac troponin I(cTnI) concentration and creatine kinase-MB (CK-MB) activity.Myocardial specimens were obtained from right auricle before aortic cross-clamping and at the end of CPB for ultrastructure examination.The severity of mitochondria injury was assessment and scored (0 =normal,4 =impaired inner mitochondrial membrane integrity).Results CPB significantly increased plasma cTnI concentration at T1-3 as compared with the baseline values at T0 before CPB.Plasma cTnI concentration was significantly lower at T2 and T3 in group S than in group C.Mitochondrial injury index was significantly lower at the end of CPB in group S than in group C.There was no significant difference in plasma CK-MB activity between the 2 groups.Conclusion Wash-in of sevoflurane during CPB can attenuate myocardial injury in patients undergoing CABG. Key words: Anesthetics, inhalation; Myocardial reperfusion injury; Cardiopulmonary bypass; Coronary artery bypass graft

Serial Cardiac Troponin Concentrations as Marker of Cardiac Toxicity in Children With Status Asthmaticus Treated With Intravenous Terbutaline

The study's objectives were to evaluate serial troponin concentrations as a marker of cardiac toxicity in children receiving intravenous terbutaline for status asthmaticus and to study if troponin concentrations are affected by severity of asthma and risk factors for severe asthma. This was a prospective observational study in 20 consecutive patients who were admitted to a tertiary care pediatric intensive care unit for status asthmaticus and received intravenous terbutaline. Cardiac troponin I (cTnI) concentrations were measured half an hour before the bolus of intravenous terbutaline, 4 hours after terbutaline, and then every 24 hours until discontinuation of the continuous terbutaline infusion. Ten patients had cTnI concentrations greater than 0.03 ng/mL. Maximum cTnI concentrations were recorded after the terbutaline bolus in 6 patients, during terbutaline infusion in 3 patients, and before terbutaline use in 1 patient. Three of these 10 (3/10) patients showed increased cTnI concentrations before the terbutaline bolus. One patient had a significant elevation in cTnI concentration (peak level of 3.79 ng/mL) with electrocardiogram (ECG) changes of myocardial injury that normalized upon discontinuation of terbutaline. All other patients with elevated cTnI concentrations had normal ECG findings. Elevated cTnI concentrations were observed in 50% of patients treated with intravenous terbutaline for status asthmaticus. Clinically significant cardiotoxicity was not observed except in 1 patient in whom the abnormal ECG findings normalized upon discontinuation of terbutaline. There was no statistically significant difference in asthma severity or in the risk factors for severe asthma in children with and without elevation of cTnI concentrations.

Cardiac troponin-I concentrations in dogs with bradyarrhythmias before and after artificial pacing

Objectives To quantify cardiac troponin-I (cTnI) concentration in dogs with symptomatic bradyarrhythmias before and after artificial pacing and to correlate cTnI concentration with diagnosis, echocardiographic parameters, serology, and outcome. Animals, materials and methods Medical records from the University of Pennsylvania from 2006 to 2009 were reviewed, and 14 dogs with cTnI assay results before and after pacemaker were identified. The ECG diagnosis included complete atrioventricular block (AVB), sick sinus syndrome, 2nd degree AVB, and atrial standstill. Serology, presence of premature beats, echocardiographic measurements, and pacing modality were recorded. Results Mean cTnI concentration was elevated both pre- and post-pacing, and was significantly higher pre-pacing vs. post-pacing. Post-pacing cTnI concentration in 9 of 14 dogs (64%) remained above the reference range. Four dogs yielded high serum titers for Bartonella spp. Four dogs with markedly increased cTnI concentration had progressive left ventricular enlargement and myocardial failure as compared to pre-pacing examination. Conclusions Elevated cTnI concentration suggests that cardiac injury persists after artificial pacing in dogs with bradyarrhythmias. Myocarditis secondary to Bartonella spp. or other causes may be an important cause of AVB in dogs. Prospective studies investigating the correlation of cTnI to potential etiology and development of post-pacing LV dysfunction and outcome are needed.