Troponin I Values Research Articles

Type 2 myocardial infarction and myocardial injury: eligibility for novel medical therapy to derisk clinical trials

BackgroundPatients with type 2 myocardial infarction (T2MI) and other mechanisms of nonthrombotic myocardial injury have an unmet therapeutic need. Eligibility for novel medical therapy is generally uncertain.MethodsWe predefined colchicine, eplerenone...

Validation of the Ottawa Troponin Pathway

BackgroundThe Ottawa Troponin Pathway (OTP) was developed to improve Non-ST elevation myocardial infarction (NSTEMI) diagnosis accuracy using 3-h serial conventional troponin I (TnI) measurements. We sought to validate the OTP in patients with TnI values >99th percentile upper reference limit (>45 ng/L). MethodsWe conducted a health records review in adult patients with NSTEMI symptoms with at least two serial TnI and at least one >45 ng/L at two emergency departments (EDs). We collected baseline characteristics, ED management and disposition. 30-day outcomes included death due to cardiac ischemia, an unknown cause, or NSTEMI. Results635 patients were included, and 107 patients were diagnosed with NSTEMI within 30-days. 217 patients had at least one TnI value >45 ng/L but <100 ng/L, of whom 4 patients were diagnosed with NSTEMI. 418 patients had at least one TnI value ≥100 ng/L, and 103 were diagnosed with NSTEMI. The OTP accurately identified all 107 patients with NSTEMI: sensitivity and specificity was 100% (95% CI 96.6%–100%) and 32.2% (95% CI 28.2%–36.4) respectively. ConclusionsThe OTP is validated among patients with TnI values above the 99th percentile with symptoms concerning for ACS. Using OTP will allow for early referral and discharge home and improve ED crowding. REB Number20180393-01H.

Initially elevated troponin I in rapid atrial fibrillation should lead to coronary angiography

Abstract Funding Acknowledgements Type of funding sources: None. Background In patients admitted to the emergency department (ED) with rapid atrial fibrillation (AF), the decision to undergo coronary angiography is usually due to elevated cardiac biomarkers. However, a study evaluating the rentability of this approach has never been done. Purpose Evaluate the predictors of a positive coronary angiography performed in patients with rapid AF and elevated cardiac biomarkers. Methods We retrospectively studied patients admitted to the ED between January 2016 and December 2018 with rapid AF who have undergone coronary angiography. We analysed symptoms, risk factors, initial value, peak value and curve of troponin I (TnI) and ST-T segment abnormalities. We evaluated the presence of significant coronary artery stenosis with the need of revascularization at coronary angiography and we used logistic regression to assess the predictors of a positive result. Results From 2265 patients admitted to the ED with rapid AF, 46 patients, 60.9% (28) male, median age 73 (IQR 14.75) years, were submitted to coronary angiography. Significant coronary artery stenosis was present in 24 (52.2%) patients. Regarding cardiovascular risk factors, 39 (85.6%) patients had hypertension, 15 (32.6%) had type 2 diabetes mellitus, 36 (78.3%) had dyslipidaemia, 25 (54.3%) were obese or overweight and 12 (26.1%) had a previous history of CAD. Twenty-eight (60.9%) patients presented with chest pain and 27 (58.7%) had ST-T segment abnormalities. Of note, in 17 (37.0%) cases high-sensitivity TnI was measured. In univariable analysis, ST-T segment abnormalities, the presence of typical TnI curve and an elevated initial TnI predicted the presence of significant CAD in coronary angiography. In multivariable analysis, an initial TnI value above the upper reference limit (URL) was the only independent predictor of significant CAD in coronary angiography. Conclusion In this group of patients with rapid AF an initial elevated TnI was the only independent predictor of the presence of significant CAD. Therefore, maybe it would be advisable to perform coronary angiography in these patients. Without CADWith CADUnivariate analysisOR (95% CI), p-valueMultivariate analysisOR (95% CI), p-valueAge in years, median (IQR)69 (15)77.5 (17)1.045 (0.988-1.106), 0.1270.967 (0.882-1.062), 0.484Type 2 diabetes mellitus, n (%)5 (23.8)10 (41.7)2.286 (0.629-8.313), 0.2095.865 (0.566-60.806), 0.138ST-T segment abnormalities, n (%)8 (36.4)19 (79.2%)6.650 (1.788-24.730), 0.0055.338 (0.491-58.063), 0.169Typical TnI curve, n (%)10 (52.6)20 (90.9)9.000 (1.628-49.756), 0.01217.900 (0.475-674.480), 0.119Elevated initial TnI, n (%)10 (45.5)18 (75.0)3.600 (1.033-12.542), 0.04415.167 (1.363-168.778), 0.027Peak TnI elevation &amp;gt;2 times URL, n (%)11 (50.0)18 (75.0)3.000 (0.863-10.428), 0.0840.169 (0.005-5.298), 0.312

Diagnostic Utility of Creatine Kinase in Patients Presenting to the Emergency Department with Chest Pain

Introduction: Creatine Kinase (CK) is routinely performed in some emergency departments (ED) for Non-ST-elevation myocardial infarction (NSTEMI) workup. Its diagnostic utility is not well understood. The objectives of this study were to assess the value of CK in NSTEMI diagnosis in the troponin era and the association between the highest CK/Troponin values and ejection fraction (EF) during NSTEMI follow-up. &#x0D; &#x0D; Methods: A prospective cohort study conducted at the two EDs of The Ottawa Hospital from March 2014 to March 2016 enrolled adults (≥18 years) for whom troponin I (TnI) and CK were ordered for NSTEMI symptoms. We excluded those with ST-Elevation Myocardial Infarction (STEMI). The primary outcome was a NSTEMI within 30 days. We used descriptive statistics and report test diagnostic characteristics with 95% confidence intervals (CI). We compared the highest median CK/Troponin values using Wilcoxon test.&#x0D; &#x0D; Results: Of the 2,153 patients enrolled, 99 (4.6%) suffered a NSTEMI. The sensitivity and specificity were: CK (cutoff &gt;250U/L) 31.3% (95%CI 22.2, 40.5) and 91.1% (95%CI 89.9, 92.4) respectively; TnI (cutoff &gt;0.045µg/L) 98.0% (95%CI 95.2, 100) and 86.2% (95%CI 84.7, 87.7) respectively. The median CK values were not significantly different between those with normal (n=267) and abnormal EF (n=55) on follow-up (107 U/L and 118 U/L respectively; p=0.31), whereas the median TnI values were significantly different (0.02 µg/L and 0.1 µg/L respectively; p&lt;0.0001).&#x0D; &#x0D; Conclusions: CK measurements do not provide any value in the ED work-up of NSTEMI and is not associated with EF on follow-up. Discontinuing routine CK measurements would improve resource utilization.

Early Serum Biomarkers for Intensive Care Unit Treatment within the First 24 Hours in Patients with Intracerebral Hemorrhage.

The prognostic significance of serum biomarkers in patients with intracerebral hemorrhage (ICH) is not well investigated concerning inhospital mortality (IHM) and cardiopulmonary events within the first 24 hours of intensive care unit (ICU) treatment. The influence of troponin I (TNI) value and cortisol value (CV) on cardiopulmonary events within the first 24 hours of ICU treatment was reported in subarachnoid hemorrhage patients, but not in ICH patients up to now. The aim of this study was to investigate the role of early serum biomarkers on IHM and TNI value and CV on cardiopulmonary events within the first 24 hours of ICU treatment. A total of 329 patients with spontaneous ICH were retrospectively analyzed. Blood samples were taken on admission to measure serum biomarkers. The TNI value and CV were defined as biomarkers for cardiopulmonary stress. Demographic data, cardiopulmonary parameters, including norepinephrine application rate (NAR) in microgram per kilogram per minute and inspiratory oxygen fraction (FiO2) within the first 24 hours, and treatment regime were analyzed concerning their impact on ICU treatment and in hospital outcome. Binary logistic analysis was used to identify independent prognostic factors for IHM. Patients with initially nonelevated CVs required higher NAR (p = 0.01) and FiO2 (p = 0.046) within the first 24 hours of ICU treatment. Lower cholinesterase level (p = 0.004), higher NAR (p = 0.002), advanced age (p < 0.0001), larger ICH volume (p < 0.0001), presence of intraventricular hemorrhage (p = 0.007) and hydrocephalus (p = 0.009), raised level of C-reactive protein (p = 0.024), serum lactate (p = 0.003), and blood glucose (p = 0.05) on admission were significantly associated with IHM. In a multivariate model, age (odds ratio [OR]: 1.055; 95% confidence interval [CI]: 1.026-1.085; p < 0.0001), ICH volume (OR: 1.016; CI: 1.008-1.025; p < 0.0001), and Glasgow Coma Scale (GCS) score (OR: 0.680; CI: 0.605-0.764; p < 0.0001) on admission as well as requiring NAR (OR: 1.171; CI: 1.026-1.337; p = 0.02) and FiO2 (OR: 0.951; CI: 0.921-0.983, p = 0.003) within the first 24 hours were independent predictors of IHM. Higher levels of C-reactive protein, serum lactate, blood glucose, and lower cholinesterase level on admission were significantly associated with IHM. Patients with initially nonelevated CVs required higher NAR and FiO2 within the first 24 hours of ICU treatment. Furthermore, requiring an NAR > 0.5 µg/kg/min or an FiO2 > 0.21 were identified as additional independent predictors for IHM. These results could be helpful to improve ICU treatment in ICH patients.

PSXI-35 Evaluation of biomarkers N-terminal pro-B-type natriuretic peptide and troponin-I in healthy Labrador retrievers and Labrador retrievers with subclinical dilated cardiomyopathy

Abstract Cardiovascular disease in dogs may have minimal outward signs in the beginning stages, but early detection and intervention are vital to help affected dogs live longer and have better quality of life. N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin-I are two biomarkers that show promise for detection of cardiovascular disease at a research level, but a deeper understanding is necessary to bring them into the forefront for diagnostic purposes. The aim of this research was to present values of NT-proBNP and troponin-I in healthy Labrador retrievers and in Labrador retrievers with subclinical dilated cardiomyopathy (subDCM). 55 intact Labrador retrievers (27m/28f) were selected based on good clinical health, with no prior evidence of cardiovascular disease. All dogs were maintained on the same standard kennel diet prior to testing. Each dog had plasma collected for NT-proBNP analysis (Cardiopet; Idexx) and serum collected for troponin-I analysis (Immulite; UC Davis Vet Lab). Each dog then had an echocardiogram performed by an experienced sonographer which was reviewed by a boarded veterinary cardiologist. Out of 55 adult Labrador retrievers, 46 (24m/22f) were classified as normal and 9 (3m/6f) were classified as having occult subDCM. Normal Labrador retrievers had a significantly lower mean NT-proBNP of 695 ± 432 pmol/L compared to subDCM Labrador retrievers with a mean of 1144 ± 546 pmol/L (P = 0.009). Normal Labrador retrievers had a lower mean troponin-I of 0.07 ± 0.04ng/mL compared to subDCM Labrador retrievers with a mean of 0.1 ± 0.07ng/mL, trending towards significance (P = 0.08). In summary, healthy Labrador retrievers had significantly lower NT-proBNP compared to Labrador retrievers affected with subclinical dilated cardiomyopathy.

Abstract 17331: Elevated Troponin Levels Predict Major Adverse Cardiovascular Outcomes and Mortality in COVID-19 Patients

Introduction: Measurement of cardiac biomarkers such as troponin-I (TnI) are useful in assessing for the presence of cardiovascular events. Chest pain is often not a presenting complaint of COVID-19 patients, yet there have been many cases of patients experiencing possible cardiovascular complications. We sought to examine the value of elevated TnI in predicting the occurrence of major adverse cardiovascular events (MACE) and mortality in COVID-19 patients Methods: A retrospective review was performed on 225 hospitalized patients that tested positive for COVID-19 between March and May 2020 at our quaternary care hospital. Baseline characteristics and clinical outcomes of their disease course were identified. During the chart review, we documented the admission and peak TnI levels available in the medical record, and noted the occurrence of MACE (a composite of myocardial infarction, stroke, pulmonary embolism, deep venous thrombosis, or shock requiring vasopressor support) or death. Data were analyzed using Pearson’s chi square test and logistic regression to adjust for age. Results: Of the 225 hospitalized patients, only 31(14.83%) complained of chest pain on admission. Among patients with elevated TnI, 49.15% had MACE/ Mortality, compared to 21% with non-elevated TnI. Patients with elevated TnI were nearly 4 times more likely to have MACE/Mortality than patients with non-elevated TnI (p = 0.0001; OR = 3.97; 95% CI [1.88, 8.41]). They were also 3.63 times more likely to have MACE alone (p &lt; 0.0001; OR = 3.63; 95% CI [1.70, 7.79]). Median peak TnI values were higher in patients who had a MACE compared to those who did not (0.0275 ng/mL [IQR 0.012-0.152] vs 0.012 ng/mL [IQR 0.012-0.152], p &lt;0.05). For every one-unit increase in peak TnI levels, the age-adjusted odds of having MACE increased by a factor of 4468.37 (95% CI [9.07 2200316.00]; p = 0.008). Conclusions: Based on our data, elevated troponin-I levels predict the occurrence of MACE in patients who are hospitalized with COVID-19. Furthermore, there is an association between elevated troponin-I and eventual MACE, mortality, or both. This suggests that checking troponin-I levels in COVID-19 patients holds prognostic value, irrespective of the presence of chest pain as a presenting complaint.

Abstract 15975: Association of Maximum Troponin Levels With Myocardial Infarction Diagnosis and Higher Mortality

Introduction: Cardiac troponin I (TnI) is a sensitive and specific marker of acute myocardial infarction (AMI). However, a wide range of non-AMI conditions can also cause significant elevations in cardiac troponins. Given the deleterious impact of misdiagnosis, the ability to risk stratify patients who present with an elevated troponin is paramount. Hypothesis: We hypothesized that maximum TnI would be more predictive of mortality and the diagnosis of AMI than the initial or change in TnI. Methods: Records of 30,173 patients from a nine-hospital system in Texas were reviewed over a 24-month period 2016-2018. Data were collected on patients &gt; 40 years of age and included international classification of disease (ICD-10) diagnoses, TnI, demographic data (age, sex, race, smoking status, chronic medical conditions), death during hospitalization, and readmission within 30 days. Results: Notable finding include TnI as a significant predictor of death with odds of death increased by 0.9% (1.009, 95% CI 1.004-1.013) for initial, and 0.7% (1.007, 95% CI 1.005-1.009) for delta and maximum TnI. An ROC curve demonstrated a statistically significant predictive ability of death for the maximum TnI level (0.6782, 95% CI (0.6576, 0.6989)) when compared to the initial and change in TnI. We analyzed the initial TnI as a significant predictor of AMI demonstrating the odds of AMI increased by 7.4% as initial TnI values increased (1.074, 95% CI 1.063-1.085), and 3.1% for delta and maximum TnI (1.031, 95% CI 1.028-1.034). A separate ROC curve demonstrated that the maximum TnI level 0.9401, 95% CI (0.9353, 0.9449) showed a statistically significant predictive ability to predict an AMI compared to initial change in TnI. Conclusions: Regardless of TnI level, a detectable TnI results in an increased risk of in-hospital mortality. Our study demonstrates that the maximum TnI level is a more sensitive and specific predictor of mortality when compared to delta or initial TnI. Similarly, the maximum TnI is the most predictive of an AMI versus other causes of TnI elevation. Further studies are needed to correlate TnI levels and clinical manifestations, which may be helpful in redefining AMI to better distinguish AMI from non-AMI diagnoses.

Abstract 16000: Patient Characteristics and Outcomes Associated With Troponin Testing

Introduction: Troponin I (TnI) is a principal biomarker in diagnosing acute myocardial infarction (AMI). However, large numbers of hospitalized patients are tested for TnI in whom AMI is unlikely or not expected. Hypothesis: We hypothesized the baseline comorbidities of those undergoing troponin testing differ from those not tested and that troponin testing is associated with outcomes. Methods: In total, 54,039 inpatient admissions from a 9-hospital system in Texas were reviewed over a 24-month period (2017-2018). Data were collected on primary international classification of disease (ICD-10) diagnoses, TnI, risk factors, and death during hospitalization or readmission within 30 days. Odds ratios were calculated for all patients adjusted for demographic differences in the population. Bivariate analysis was performed on the baseline risk factors for both troponin testing and troponin positivity. Results: TnI testing occurred in 30,173/54,039 (55.8%) individual hospital admissions. Of those, 19.9% had at least one elevated TnI value &gt;99th% (0.1 ng/ml). Tested patients were older (70.1 [IQR 59.5, 80.9] vs 63.7 [IQR 53.4, 73.1] years), more likely to be male (14,497/30,173 (48.1%) vs 10,845/23,866 (45.4%)) and had a greater burden of cardiovascular disease and risk factors including: gender, race, smoking, hypertension, hyperlipidemia, type 2 diabetes mellitus, coronary artery disease, chronic kidney disease, chronic obstructive pulmonary disease, prior cerebrovascular accident, and prior AMI. Troponin testing was associated with death during hospitalization (OR 3.11, 95% CI 2.63, 3.71, p&lt;0.0001), and an elevated troponin was found to be associated with mortality (OR 4.06, 95% CI 3.49, 4.72, p&lt;0.0001). Conclusions: Troponin testing is associated with death during index hospitalization. Troponin values &gt;99th% were associated only with increased mortality. This data suggest that selection plays a role in identifying patients at risk for in-hospital death.

Cardiac Troponin I Predicts Elevated B-type Natriuretic Peptide in Patients Treated with Anthracycline-Containing Chemotherapy

Background: Anthracycline is used to treat various types of cancer; however, cardiotoxicity negatively affects patient prognosis. Objectives: The aim of the present study was to investigate serial changes in levels of cardiac troponin I (TnI) and B-type natriuretic peptide (BNP) in patients treated with anthracycline-containing therapy. Methods: 91 consecutive cancer patients planned for anthracycline treatment were enrolled and followed up for 12 months. All patients underwent echocardiography and blood sampling at baseline, 3, 6, and 12 months. Results: The patients were divided into two groups based on their TnI level during the follow-up period: the elevated TnI group (TnI ≥0.03 ng/mL; n = 37) and the normal TnI group (n = 54). In the elevated TnI group, the TnI levels increased at 3 and 6 months, but they returned to within normal range at 12 months after anthracycline administration. Unlike TnI, the BNP levels began to increase after 6 months, and remained increased at 12 months. The occurrence of cancer therapeutics-related cardiac dysfunction was higher in the elevated TnI group than in the normal TnI group. When we set the cut-off value of TnI at 0.029 ng/mL, sensitivity and specificity to predict an elevated BNP level of more than 100 pg/mL were 90 and 63%, respectively. Multivariate logistic regression analysis revealed that elevated TnI was an independent predictor of elevated BNP levels. Conclusion: Elevated TnI was an independent predictor for the development of BNP increase. The different characteristics of TnI and BNP should be considered when managing patients treated with anthracycline-containing therapy.

The impact of hyperglycaemia on PKM2-mediated NLRP3 inflammasome/stress granule signalling in macrophages and its correlation with plaque vulnerability: an in vivo and in vitro study

BackgroundThe mechanism of pyruvate kinase M2 (PKM2)-mediated inflammatory signalling in macrophages when plaques rupture and the impact of hyperglycaemia on the signalling are unclear. The present study aimed to explore the impact of hyperglycaemia on PKM2-mediated NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome/stress granule signalling in macrophages and its correlation with plaque vulnerability in vivo and in vitro. MethodsFrom July to December 2019, 80 patients with coronary heart disease (CHD) were divided into acute ST-segment elevation myocardial infarction (STEMI) (n = 57) (DM-STEMI, n = 21; non-DM-STEMI, n = 36) and stable CHD (SCHD) groups (n = 23). Circulating mononuclear cells were isolated. The value of peak troponin I (TnI), the Global Registry of Acute Coronary Events (GRACE) risk score, and the expression levels of the related markers were quantified and compared. In vitro studies on the THP-1 cells were also performed. ResultsThe DM-STEMI group had a higher value of peak TnI and a higher GRACE risk score than the non-DM-STEMI group (p < 0.05). The highest expression levels of PKM2, NLRP3, interleukin (IL)-1β, and IL-18 and the lowest expression level of GTPase activating protein (SH3 domain)-binding protein 1 (G3BP1) (a stress granule marker protein) were observed in the DM-STEMI group, and they were followed by the non-DM-STEMI group and the SCHD group (p < 0.05). In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression. ConclusionHyperglycaemia might increase the activation of PKM2-mediated NLRP3 inflammasome/stress granule signalling and increase plaque vulnerability, associating it with worse prognosis. PKM2 may be a novel prognostic indicator and a new target for the treatment of patients with CHD and DM.

Does the Platelet Index Have a Guiding Role in the Association of Cancer and Pulmonary Thromboembolism?

Introduction: The diagnostic value of the D-dimer test varies with variable platelet numbers and functions in patients suffering from cancer and concomitant pulmonary thromboembolism (PTE). This requires easy and reliable evaluation tests. In this study, we aimed to investigate the hypothesis that platelet functions may be more guiding in the prediction and diagnosis of PTE rather than the number of platelets in cancer pa- tients. Methods: The clinical, laboratory and radiological findings of all patients diagnosed with PTE were retrieved, retrospectively. Comparisons were performed between “can- cer-free” and “cancer” patients. The patients were also evaluated according to their active and remission status. Results: The data of 232 patients with PTE were reviewed. 172 patients were cancer- free and 60 were diagnosed with cancer. The mean values of D-dimer, mean platelet volume (MPV) and platelet distribution width (PDW) were found to be significantly higher in patients with cancer (P=0.015, P=0.026, and P=0.023; respectively). On the other hand, mean platelet counts were significantly higher in patients without cancer (P=0.05). It was also observed that the mean values of D-dimer, Troponin-I, MPV, and PDW were found to be significantly higher in patients with active cancer (P=0.05, P=0.044, P=0.05, and P=0.042; respectively). However, the mean platelet counts were significantly higher in patients with cancer who were in remission (P=0.05). Conclusions: The morphological characteristics of the platelets are more determinant than the number of platelets in cancer patients with PTE. Platelet indexes such as MPV and PDW may be useful in the prediction, diagnosis, and follow-up of PTE in patients with cancer.

Exercise-Induced Muscle Damage and Cardiac Stress During a Marathon Could be Associated with Dietary Intake During the Week Before the Race

Adequate food intake is important prior to endurance running competitions to facilitate adequate exercise intensity. However, no investigations have examined whether dietary intake could prevent exercise-induced muscle damage (EIMD) and cardiac stress (EICS). Thus, this study’s objective was to determine the associations between EIMD, EICS and endurance athlete diets one week before a marathon race. Sixty-nine male runners participated in this study. Food intake during the week prior to the race was collected through a seven-day weighed food record. Dietary intake on race day was also recorded. At the end of the marathon, blood samples were drawn to determine serum creatine kinase (CK) and myoglobin, and muscle–brain isoform creatine kinase (CK-MB), prohormone of brain natriuretic peptide (NT-proBNP), cardiac troponin I (TNI), and cardiac troponin T (TNT) concentration as markers of EIMD and EICS, respectively. To determine the association between these variables, a stepwise regression analysis was carried out. The dependent variable was defined as EIMD or EICS and the independent variables were defined as the number of servings within each different food group. Results showed that the intake of meat during the previous week was positively associated with post-race CK (Standardized Coefficients (β) = 0.643; p < 0.01) and myoglobin (β = 0.698; p < 0.001). Vegetables were negatively associated the concentration of post-race CK (β = −0.482; p = 0.002). Butter and fatty meat were positively associated with NT-proBNP (β = 0.796; p < 0.001) and TNI (β = 0.396; p < 0.001) post-marathon values. However, fish intake was negatively associated with CK (β = −0.272; p = 0.042), TNI (β = −0.593; p < 0.001) and TNT (β = −0.640; p = 0.002) post-marathon concentration. Olive oil was negatively associated with TNI (β = −0.536; p < 0.001) and TNT (β = −0.415; p = 0.021) values. In conclusion, the consumption of meat, butter, and fatty meat might be associated with higher levels of EIMD and EICS. On the other hand, fish, vegetables, and olive oil might have a protective role against EIMD and EICS. The selection of an adequate diet before a marathon might help to reduce some of the acute burdens associated with marathon races.

Troponin I as an early biomarker of cardiopulmonary parameters during the first 24 h of intensive care unit treatment in isolated traumatic brain injury patients

ObjectiveCardiopulmonary (CP) complications are well-known phenomena after an isolated traumatic brain injury (iTBI) and they may be associated with an elevated serum troponin I (TnI) value. However, the influence of an elevated TnI level on CP parameters within the first 24 h after an iTBI is still unknown. The current study was conducted to assess the associations between the initial TnI value on admission and CP parameters during the first 24 h of intensive care unit (ICU) treatment in iTBI patients. Patients and MethodsA total of 288 patients with iTBIs, who were admitted to our emergency department between January 2010 and November 2016 were retrospectively analyzed. Blood samples were taken on admission to determine TnI value. Each patient's demographic data, treatment regime, computed tomography results, and intra-hospital outcomes were evaluated, as well as several CP parameters, within the first 24 h of ICU treatment. The entire study population was stratified into patients with an initial TnI elevation (TnI positive) and without an initial TnI elevation (TnI negative). ResultsIncreased TnI values on admission were found in 59 (20.5%) patients. There were significant correlations between an initially elevated TnI value and a lower Glasgow Coma Scale score (p = 0.003), higher head Abbreviated Injury Scale score (p<0.0001), and higher Acute Physiology and Chronic Health Evaluation II score (p = 0.005) on admission, as well as a lower Glasgow Outcome Scale score (p = 0.0002) and higher modified Rankin Scale score (p = 0.0001) at discharge. In addition, a significantly higher norepinephrine application rate (NAR) (p<0.0001) and inspiratory oxygen fraction (FiO2) (p = 0.028) were needed in the TnI positive group. ConclusionPatients with elevated TnI values on admission require more circulation support (NAR and FiO2) within the first 24 h of ICU treatment after an iTBI. Therefore, the TnI may be a useful biomarker to improve ICU treatment of these patients.

Serum Cortisol as an Early Biomarker of Cardiopulmonary Parameters Within the First 24 Hours After Aneurysmal Subarachnoid Hemorrhage in Intensive Care Unit Patients.

Cardiopulmonary complications/stress are well-known phenomena in patients after aneurysmal subarachnoid hemorrhage (aSAH) and might be associated with an elevated serum troponin I (TNI) level. Since the glucocorticoid hormone cortisol is released during stress situations, the present study was conducted to investigate the influence of serum cortisol (SC) on cardiac and pulmonary parameters in patients after aSAH within the first 24 hours of intensive care unit (ICU) treatment. We retrospectively analyzed a cohort of 104 patients with aSAH admitted to our emergency department between January 2008 and April 2017. Blood samples were taken to determine SC and TNI. Demographics, initial Glasgow Coma Scale (GCS) score, World Federation of Neurosurgical Societies (WFNS) score, and Fisher grade were evaluated retrospectively. Mean norepinephrine application rate (NAR) in µg/kg/min and mean inspiratory oxygen fraction (OF) within the first 24 hours were defined as cardiopulmonary parameters. An elevated SC value was found in 44 (42%) patients, and 27 (26%) patients showed an increased TNI value. In patients with initially increased SC value, a significant higher NAR (P = .04) was needed. Furthermore, patients with initially elevated TNI value had a lower GCS score (P = .0013) and a higher WFNS score (P = .003) on admission and required a higher NAR (P = .02) as well as OF (P = .0008) within the first 24 hours of ICU treatment. In the current study, initially elevated SC values were associated with a higher need of NAR within the first 24 hours of ICU treatment after aSAH. Moreover, patients with initially elevated TNI values required an increased NAR and a higher OF so that these biomarkers could be useful to improve ICU treatment.

Serum apelin predicts spontaneous reperfusion of infarct-related artery in patients with ST-segment elevation myocardial infarction.

Spontaneous reperfusion (SR) was associated with significant myocardial salvage, decreased mortality rates, better clinical outcomes, and lower incidences of major adverse cardiovascular events. It was found that apelin inhibited thrombin-induced and collagen-induced platelet activation and aggregation. This study was carried out to assess whether serum apelin correlates with SR of the infarct-related coronary artery in ST-elevation myocardial infarction (STEMI) patients. Blood samples were obtained on admission in 280 consecutive patients with STEMI before primary percutaneous coronary intervention. Blood chemistry and apelin levels were tested. Coronary arteriography and echocardiography were performed after admission. Frequencies of the patients with preinfarct angina, history of smoking, and pathoglycemia were higher in the non-SR group than in the SR group (P=0.03, 0.001, and 0.002, respectively). Peak values of plasma troponin-I and frequencies of the patients with Killip 2-3 were significantly higher in the non-SR group (P<0.05, respectively) compared with the SR group. Left ventricular systolic and diastolic functions improved markedly in the SR group compared with the non-SR group. Gensini scores were lower in the SR group than the non-SR group (P=0.02). Serum apelin was significantly higher in patients with SR compared with patients with non-SR (0.82±0.34 vs. 0.35±0.22 ng/ml, P=0.04). A cut-off value of 0.75 ng/ml had a predictive value of 77% to identify patients with SR. In the non-SR group, patients who died in the hospital had much lower apelin levels compared with those who survived (P<0.001). Apelin level in the high thrombus load group was much lower compared with the other group (P<0.001). Apelin level in the group undergoing successful reperfusion was much higher than that in the group without successful reperfusion (P<0.001). Patients with SR have better cardiac systolic function and improved diastolic function. An increased serum apelin level is an independent and novel predictor of SR for STEMI patients.

Urine catecholamines in children with severe Enterovirus A71 infection: comparison with paediatric septic shock

Purpose: Hypercatecholaminemia-related heart failure has been proposed as the main cause of enterovirus A71-related (EV-A71) early mortality. The purpose of this study was to measure urine catecholamine concentrations in severe EV-A71-infected children. Methods: A total of 35 children, aged 2.5 ± 2.1 years, were divided into three groups. Group I: 15 septic shock patients, group II: 17 EV-A71-stage-2 patients, and group III: 3 EV-A71-stage-4 patients. The laboratory results, cardiac biomarkers and urine catecholamine concentrations were statistically analysed. Results: Group I had the highest C-reactive protein (CRP) levels and group II had the lowest B-type natriuretic peptide (BNP) and its N-terminal prohormone among the groups (p = 0.039, <0.01 and <0.01, respectively). Group III patients had significantly higher urine catecholamine and troponin-I values among the groups. If urine epinephrine (Epi) >134 ug/gCr, norepinephrine (NE) >176 ug/gCr and vanillylmandelic acid (VMA) >11.7 mg/gCr were used as the cutoff points to differentiate groups II and III, the sensitivities and specificity were all 100%. Conclusions: The significantly elevated urine catecholamine concentrations in EV-A71-stage-4 patients support the hypothesis that hypercatecholaminemia-related heart failure is involved in severe EV-A71 infection. Urine catecholamines could be used as reliable biomarkers for differentiation of severe EV-A71 infection with or without heart failure and septic shock.

Troponin I as an Early Biomarker of Cardiopulmonary Parameters Within the First 24 Hours After Nontraumatic Subarachnoid Hemorrhage in Intensive Care Unit Patients.

The elevation of serum cardiac troponin I (TNI) in patients with nontraumatic subarachnoid hemorrhage (ntSAH) is a well-known phenomenon. However, the relation between elevated TNI and different cardiopulmonary parameters (CPs) within the first 24 hours after ntSAH is unknown. The present study was conducted to investigate the association between TNI and different CP in patients with ntSAH within the first 24 hours of intensive care unit (ICU) treatment. We retrospectively analyzed a consecutive group of 117 patients with ntSAH admitted to our emergency department between January 2008 and February 2017. Blood samples were taken to determine TNI values on admission. Demographic data, baseline Glasgow Coma Scale (GCS) score, World Federation of Neurosurgical Societies (WFNS) score, baseline Fisher grade (FG), norepinephrine application rate (NAR) in µg/kg/min, and inspiratory oxygen fraction (OF) were recorded within the first 24 hours. An increased TNI value was found in 32 (27.4%) of 117 patients. There was a significant correlation between initial elevated TNI and a low WFNS score (P = .007), a low GCS score (P = .003) as well as a high OF (P = <.001). The FG (P = .27) and NAR (P = .08) within the first 24 hours of ICU treatment did not show any significant correlation. In the present study, an increased TNI value was significantly associated with a low WFNS score and GCS score on admission. The TNI was a predictor of the need for a higher OF within the first 24 hours after ntSAH so that TNI could be an informative biomarker to improve ICU therapy.

Harmonization of Cardiac Troponin I: Significance of Sample Types.

Cardiac troponin I (TnI) is one of the most crucial biomarkers for the management of acute coronary syndrome. However, the TnI values can vary when using commercial TnI assays from different vendors. We assessed the feasibility of TnI harmonization using plasma and serum samples. Leftover plasma and serum samples were collected from patients and stored for further analysis (n = 200). TnI measurements were performed using 3 different analyzers. The TnI values for plasma and serum were compared, and the mathematical recalibration was performed using the mean of 3 values from each analyzer as a reference value. The number of biased cases was counted before and after recalibration. The final analysis was performed in a total of 140 plasma and serum samples, and constant and/or proportional differences for each analyzer were observed. Mathematical recalibration of the TnI values resulted in improved correlation to the reference values. The number of TnI values that were remote from the reference values decreased after recalibration. The effects were more evident for serum samples. In this study, we reassured the possibility of TnI harmonization among 3 different immunoassays using plasma and serum samples. It is important to note the differences between sample types during TnI harmonization.

Relationship between neutrophil-to-lymphocyte ratio, d-dimer and troponin-I values and pulmonary embolism severity index

Aim: We aimed to determine whether Neutrophil-to-Lymphocyte Ratio (NLR), Monocyte-to-Lymphocyte Ratio (MLR), Platelet-to-Lymphocyte Ratio (PLR), D-dimer, and troponin values were correlated with the simplified Pulmonary Embolism Severity Index (sPESI) in patients diagnosed as having Pulmonary Embolism (PE) in the emergency room. Material and Methods: Forty-three patients diagnosed as having PE in the emergency departmentwere divided into low and high-risk groups according to the sPESI. We investigated whether NLR, MLR, and PLR, d-dimer, troponin-I, and Pulmonary Artery Pressure (PAP) had any effect in determining the severity of PE. Also, patients were divided into groups as those with PAP ≤20 or >20 mm Hg, Systolic Blood Pressure (SBP) ≤100 or >100 mm Hg, and those receiving or not receiving thrombolytic treatment, and compared. Results: There was a statistically significant difference between patients with low sPESI (n=10) and those with high sPESI (n=33) in terms of age (p=0.001), pulse (p=0.016), oxygen saturation (p=0.039), troponin-I (p=0.029) and PAP (p=0.032), but there was no difference between the groups in terms of NLR (p=0.796), MLR (p=0.656), PLR (p=0.863), and d-dimer (p=0.343). There was a statistically significant difference between patients who did (n=6) and did not (n=37) receive thrombolytic treatment in terms of troponin-I (p=0.012), but there was no difference between the groups in terms of NLR (p=0.861), MLR (p=0.335), and PLR (p=0.277). Conclusion: NLR, MLR, PLR and d-dimer levels were found not to be effective in determining the severity of PE. Troponin-I was associated with sPESI and was considered as an effective marker in determining the thrombolytic treatment.