Creatine kinase-MB Measurements Research Articles

Modeling creatine-kinase MB concentrations following coronary artery bypass grafting

BackgroundAn increase in cardiac biomarkers is a prerequisite for diagnosing periprocedural myocardial infarction (PMI) after coronary artery bypass grafting (CABG). Early-phase risk detection may be aided by modeling time-dependent serum creatine kinase-MB (CK-MB) concentrations. This study aimed to model the kinetics of CK-MB while identifying its influencing factors. MethodsPatients who underwent elective CABG and had CK-MB measurements within 72 hours postoperatively were included. The primary outcome was the modeled post hoc kinetics of CK-MB in patients without potential PMI. These patients were defined as having no potential PMI based on the absence of ischemic electrocardiographic abnormalities, imaging abnormalities, in-hospital cardiac arrest, mortality, or postoperative unplanned catheterization. A web-based application was created using mixed-effect modeling to provide an interactive and individualized result. ResultsA total of 1589 CK-MB measurements from 635 patients who underwent elective isolated CABG were available for analysis. Of these, 609 patients (96%) had no potential PMI and 26 (4%) had potential PMI. Male sex, aortic cross-clamp time, and cardioplegia type significantly impacted CK-MB concentrations. The diagnostic accuracy of the model had an area under the receiver operating characteristic curve of 82.8% (95% confidence interval, 72.6%-90.2%). A threshold of 7 μg/L yielded a sensitivity of 94% and a specificity of 80% (positive predictive value, 17%; negative predictive value, 99%) for excluding potential PMI in our study population. ConclusionsCK-MB release after CABG depends on the timing of measurement, patient sex, aortic cross-clamp time, and cardioplegia type. The model (available at https://www.cardiomarker.com/ckmb) can be validated, reproduced, refined, and applied to other biomarkers.

Importance of evaluation of heart-type fatty acid binding protein (H-FABP) in COVID-19 Patients.

Recent studies have documented the cardiovascular consequences of acute coronavirus disease 2019 (COVID-19), although one of the early cardiac markers that can be used for diagnosis, the heart-type fatty acid-binding protein (H-FABP), has not been covered. Through the evaluation of H-FABP levels, we aim to contribute to the early diagnosis and treatment of cardiac problems in COVID-19 infection patients. Seventy-five patients who were admitted to the emergency department of Mehmet Akif Ersoy Hospital with a complaint of chest pain in the last 6 hours and whose corona PCR tests were positive, were included in our study as the case group and 60 healthy volunteers as the control group. The routine cardiac markers such as creatine kinase MB (CK-MB) cardiac troponin T (cTnT), and H-FABP levels were analyzed by routine laboratory methods. The mean age and gender distributions of the groups did not differ statistically (p > 0.05). CK-MB, cTnT, and H-FABP measurements were statistically different between the groups (p = 0.001; p < 0.01). The relationship between AMI and COVID-19 with routine cardiac markers is already supported by recent studies. We also evaluated H-FABP levels in our study, as it affects the prognosis of the disease independent of the chronic disease history. At the same time, we showed that H-FABP levels increase earlier than routine cardiac markers, so it will be useful for COVID-19 patients with cardiac complaints.

Role of Biomarkers of Myocardial Injury to Predict Adverse Outcomes in Hypertrophic Cardiomyopathy.

Serum troponins and CK-MB (creatine kinase-MB) are readily detectable and reliable cardiac-specific biomarkers of subclinical myocardial injury. This study explores the roles of cTnI (cardiac troponin I) and CK-MB in hypertrophic cardiomyopathy (HCM). This study included 1045 patients with HCM who had baseline cTnI and CK-MB measurements at Fuwai Hospital between 1999 and 2019. Patients were excluded if they had undergone percutaneous coronary intervention or coronary artery bypass grafting, or had renal failure. Five end points were studied: all-cause death, cardiovascular death, noncardiovascular death, sudden cardiac death, and other cardiovascular death. Cox regression was used to assess the associations of cTnI and CK-MB levels with outcomes. Nine hundred seventy patients with available follow-up data were finally analyzed (mean age, 49.3 years; 36.4% female). During the median 4.3-year follow-up period, 87 patients reached the end points. Higher cTnI (per 0.05 ng/mL increase) and CK-MB (per 1 IU/L increase) levels were associated with increased risks of all-cause death (cTnI: adjusted hazard ratio [HR], 1.038, P<0.001; CK-MB: adjusted HR, 1.021, P=0.004), cardiovascular death (cTnI: adjusted HR, 1.040, P<0.001; CK-MB: adjusted HR, 1.025, P=0.006), and sudden cardiac death (cTnI: adjusted HR, 1.045, P<0.001; CK-MB: adjusted HR, 1.032, P=0.001). Patients with elevated levels of both cTnI and CK-MB had worse prognoses than patients with an elevated level of either biomarker alone and patients who did not have an elevated level of either biomarker. Addition of the binary indicator elevation of both cTnI and CK-MB significantly improved the discrimination and reclassification abilities of the standard HCM Risk- sudden cardiac death model (C statistics: P=0.002; net reclassification improvement, 0.652; integrated discrimination improvement, 0.064). Comprehensive evaluations of biomarkers of myocardial injury, cTnI and CK-MB, have considerable value for predicting adverse outcomes among patients with HCM. Routine cTnI and CK-MB assessments may help to guide implantable cardioverter defibrillator implantation for primary prevention in HCM.

Body fat percentage and infarct size in patients with non-ST segment elevation myocardial infarction.

Obesity is a global health problem that increases the risk of coronary artery disease (CAD). However in studies, it has been observed that when the disease develops, obese patients have a more favorable prognosis than leaner patients. This is called the "obesity paradox." This study aims to evaluate the effect of obesity assessed with body fat percentage (BFP) and relative fat mass (RFM) besides body mass index (BMI) on infarct size (IS) estimated from peak creatine kinase-MB (CK-MB) levels in patients with non-ST-segment elevation myocardial infarction (NSTEMI). Patients with a diagnosis of NSTEMI who underwent coronary angiography between January 2017 and January 2022 were retrospectively evaluated. Patients without available anthropometric data to calculate BMI, BFP, and RFM and serial CK-MB measurements were excluded from the study. BMI was calculated using weight(kg)/(height[m])2 formula. Patients were dichotomized as obese (BMI≥30 kg/m2) and non-obese (BMI<30 kg/m2) to compare baseline characteristics. BFP and RFM were calculated from anthropometric data. Linear regression analysis was performed to define predictors of IS. Final study population consisted of 748 NSTEMI patients (mean age was 59.3±11.2 years, 76.3% were men, 36.1% of the patients were obese). Obese patients were more likely to be female, hypertensive, and diabetic. Smoking was less frequently observed in obese patients. Peak CK-MB levels were similar among groups. Obese patients had higher in-hospital left ventricular ejection fraction, and less severe CAD was observed in coronary angiographies of these patients. Multivariable regression analysis identified diabetes mellitus, systolic blood pressure, white blood cell count, hemoglobin, and BFP (β=-4.8, 95% CI=-8.7; -0.3, p=0.03) as independent predictors of IS. Higher BFP is associated with smaller IS in NSTEMI patients. These findings support the obesity paradox in this patient group, but further, randomized controlled studies are required.

Adropin reduces hypoxia/reoxygenation‑induced myocardial injury via the reperfusion injury salvage kinase pathway

Adropin is a secreted polypeptide that has been demonstrated to serve an important role in protecting the vascular endothelium. Pharmacological activation of pro-survival kinases, such as PI3K-Akt and ERK1/2, are involved in the reperfusion injury salvage kinase (RISK) pathway. In the present study, the effects of adropin in cardiomyocyte injury induced by simulated ischemia/reperfusion (SI/R) were assessed. Additionally, the current study also assessed the mechanisms that govern SI/R in a H9c2 cardiomyoblast cell model. Cell viability was measured using an MTT assay. Cell injury was assessed using creatine kinase MB measurements. Apoptosis was assessed using flow cytometry and caspase-3 activity. The inflammatory response was measured using tumor necrosis factor α and interleukin-10 expression. Oxidative stress was assessed using malondialdehyde and superoxide dismutase. The expression levels of Akt, ERK1/2, glycogen synthase kinase 3β (GSK3β), Bcl-2 and Bax were determined using western blot analysis. The results of the current study revealed that moderate-dose adropin increased cell viability, reduced early apoptosis and caspase-3 activity, promoted Bcl-2 expression, inhibited Bax and increased the Bcl-2/Bax ratio. Adropin significantly increased the phosphorylation of Akt, ERK1/2 and GSK3β, whereas inhibitors of PI3K and ERK1/2, respectively, LY294002 and PD98059, abolished the cardioprotective role of adropin. Furthermore, no significant difference was observed in phosphorylated-STAT3/total-STAT3 expression between the adropin and SI/R groups and Janus kinase 2 inhibitor AG490 did not significantly inhibit the protective role of adropin. These results indicate that adropin exerts a protective effect against SI/R injury through the RISK pathway instead of the survivor activating factor enhancement pathway.

An Outbreak of Human Trichinellosis in the Village of Subotinac near the Town of Aleksinac

Abstract An outbreak of trichinellosis affecting 13 individuals, of whom 8 with severe form presented as myocarditis, occurred in the village of Subotinac near the town of Aleksinac in Serbia. The source of this epidemic was smoked pork from a domestic pig that had not undergone meat inspection procedures. The most striking clinical features among all the 13 patients were muscular pain (84.6%), malaise (69.2%), upper eyelid edema (61.5%), and difficulty in chewing (53.9%). These symptoms and signs were associated with significant elevations of creatine phosphokinase and lactate dehydrogenase levels. As high as 61.5% of the patients with trichinellosis were diagnosed with myocarditis (determined by means of electrocardiography, echocardiography, troponin I and creatine kinase-MB measurements). The patients had Trichinella-specific IgG antibodies in an enzyme-linked immunosorbent assay and positive indirect immunofluorescence test results. Patients seemed to respond well to treatment with mebendazole. Corticosteroid therapy was administered to patients with myocarditis. Since high percentage of our patients presented with myocarditis, an infectious diseases specialist should always keep in mind doing cardiac biomarkers analyses, echocardiography and electrocardiography.

Differential Rates and Clinical Significance of Periprocedural Myocardial Infarction After Stenting or Bypass Surgery for Multivessel Coronary Disease According to Various Definitions

ObjectivesThis study sought to estimate the differential incidence and prognostic significance of periprocedural myocardial infarction (MI) according to various definitions. BackgroundIn trials comparing percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), the primary composite endpoint is very sensitive to the definition of MI. Especially, the definition of periprocedural MI has considerably varied, and uniform criteria are still unsettled. MethodsWe evaluated 7,697 patients with multivessel disease who received PCI (n = 4,514) or underwent CABG (n = 3,183) between 2003 and 2013, and for whom serial measurement of creatine kinase-MB was available. According to various MI definitions (second and third universal definitions and the Society for Cardiovascular Angiography and Interventions definition), we assessed the prevalence and prognostic significance of periprocedural MI after both PCI and CABG. Patients were followed for major cardiovascular events (death from cardiovascular causes and spontaneous MI) and death for a median of 4.7 years. ResultsAccording to various definitions of MI, there was a substantial difference in the rates of periprocedural MI after PCI and CABG (18.7% vs. 2.9% by second universal; 3.2% vs. 1.9% by third universal; and 5.5% vs. 18.3% by Society for Cardiovascular Angiography and Interventions definition). The presence of periprocedural MI was associated with increased risks of major cardiovascular events after both PCI and CABG regardless of MI definition. The risk-adjusted 5-year rates of future major cardiovascular events after occurrence of periprocedural MI were similar after PCI and CABG in second and third universal definition. However, using Society for Cardiovascular Angiography and Interventions definition, the rates of major cardiovascular events were significantly higher after PCI than after CABG (24.3% vs. 20.4%; hazard ratio: 1.61; 95% confidence interval: 1.07 to 2.41; p = 0.02). ConclusionsThere were substantial differences in incidence and clinical relevance of periprocedural MI according to various contemporary, widely used definitions of MI.

The Effect of Atenolol on CK-MB Levels in Hypertensive Patients

Atenolol is one of beta-adrenergic receptor blocking agent. It is widely used for the treatment of hypertension as a selective antihypertensive drug. But long term usage of atenolol may cause one of the cardiovascular diseases like myocardial infarction. To prove the relationship between atenolol and cardiovascular disease, measurement of creatinekinase-MB as a diagnostic indicator in early and long term usage of this drug by hypertensive patients is recommended. A comparative study was conducted in Al-Yarmouk Teaching Hospital–Emergency Department- on 30 hypertensive patients using atenolol. They were divided into (2) groups A and B according to the duration of the drug usage. Group A- (15) patients with a mean age (56+6) years. They used atenolol for a period of (1-5) years. Group B- also (15) patients with mean age (60+6) years. They used atenolol for (6-20) years. Both groups were with nearly the same number of males and females. All subjects of the study groups were screened to exclude evidence of hyper or hypothyroidism, diabetes and chronic renal failure. Venous blood samples were taken in first 8 hours after onset symptoms of cardiac attack from each patients and the levels of creatine kinase-MB were estimated and compared between the (2) groups. There is a significant correlation between levels of serum creatine kinase-MB of group A and group B (P&lt;0.05). Atenolol causes increased level of serum CK-MB and this increase was directly proportional to the duration of the drug usage. CK-MB is one of cardiac markers that released from heart muscle when it is damaged as a result of myocardial infraction. So, atenolol has a significant correlation with development of myocardial diseases.&#x0D; Key words: hypertension , Atenolol and side effects , creatine kinase-MB , Atenolol antihypertensive.

Utility of Peak Creatine Kinase-MB Measurements in Predicting Myocardial Infarct Size, Left Ventricular Dysfunction, and Outcome After First Anterior Wall Acute Myocardial Infarction (from the INFUSE-AMI Trial)

Infarct size after ST-segment elevation myocardial infarction (STEMI) is associated with long-term clinical outcomes. However, there is insufficient information correlating creatine kinase-MB (CK-MB) or troponin levels to infarct size and infarct location in first-time occurrence of STEMI. We, therefore, assessed the utility of CK-MB measurements after primary percutaneous coronary intervention of a first anterior STEMI using bivalirudin anticoagulation in patients who were randomized to intralesion abciximab versus no abciximab and to manual thrombus aspiration versus no aspiration. Infarct size (as a percentage of total left ventricular [LV] mass) and LV ejection fraction (LVEF) were evaluated by cardiac magnetic resonance imaging at 30 days and correlated to peak CK-MB. Peak CK-MB (median 240 IU/L; interquartile range 126 to 414) was significantly associated with infarct size and with LVEF (r = 0.67, p <0.001; r = -0.56, p <0.001, respectively). A large infarct size (greater than or equal the median, defined as 17% of total LV mass) and LVEF ≤40% were more common in the highest peak CK-MB tertile group than in the other tertiles (87.6% vs 49.5% vs 9.1%, p <0.001; 43.2% vs 14.0% vs 4.6%, p <0.001, respectively). Peak CK-MB of at least 300 IU/L predicted with moderate accuracy both a large infarct size (area under the curve 0.88) and an LVEF ≤40% (area under the curve 0.78). Furthermore, CK-MB was an independent predictor of 1-year major adverse cardiac events (hazard ratio 1.42 per each additional 100 IU/L [1.20 to 1.67], p <0.001). In conclusion, CK-MB measurement is useful in estimating infarct size and LVEF and in predicting 1-year clinical outcomes after primary percutaneous coronary intervention for first anterior STEMI.

Prognostic implications of creatine kinase–MB measurements in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention

Peak creatine kinase (CK)-MB concentration is related to reperfusion success and clinical outcomes after fibrinolytic therapy for acute myocardial infarction. However, prognostic implications of CK-MB measurements after primary percutaneous coronary intervention (PCI), which provides more predictable and consistent reperfusion, are unknown. We pooled 2,042 primary PCI-treated ST-segment elevation myocardial infarction (STEMI) patients from 3 trials with serial core laboratory-determined CK-MB measurements; 1,799 patients (88.1%) who survived to 36 hours and had ≥4 CK-MB measurements were studied. Cox regression modeling was performed to quantify the association between peak CK-MB concentration (and area under the time-concentration curve [AUC]) and mortality at 6 months, and death or congestive heart failure at 90 days. The median (25th-75th percentiles) peak CK-MB concentration and AUC measurement through 36 hours were 239 (109-429) ng/mL and 4,263 (2,081-7,124) ng/(mL h), respectively. By multivariable analysis, peak CK-MB concentration and AUC measurement were independently associated with 6-month mortality (adjusted hazard ratio [HR] 1.15, 95% CI 1.05-1.25, per 100-ng/mL increase, P = .002; and adjusted HR 1.09, 95% CI 1.03-1.14, per 1,000-ng/[mL h] increase, P < .001, respectively) and 90-day death or congestive heart failure (adjusted HR 1.26, 95% CI 1.18-1.34, P < .001; and adjusted HR 1.15, 95% CI 1.11-1.19, P < .001, respectively). Peak CK-MB concentration and AUC measurement are independent predictors of 3- to 6-month cardiovascular outcomes in primary PCI-treated STEMI patients. Our findings guide application of these measurements as efficacy end points in early-phase studies evaluating new therapies for STEMI.

TCT-239 Clinical Utility of Peak Creatine Kinase-MB Measurements in Predicting Left Ventricular Dysfunction and Clinical Outcomes After First Anterior Myocardial Infarction: An INFUSE-AMI Sub-study

TCT-239 Clinical Utility of Peak Creatine Kinase-MB Measurements in Predicting Left Ventricular Dysfunction and Clinical Outcomes After First Anterior Myocardial Infarction: An INFUSE-AMI Sub-study

Peak Cardiac Troponin-T Level, Scintigraphic Myocardial Infarct Size and One-Year Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for Acute Myocardial Infarction

Current guidelines recommend troponin T (TnT) as the biomarker of choice in the diagnosis of myocardial infarction. In patients with ST-elevation myocardial infarction (STEMI) however, its role in providing a measurement of infarct size and its association with survival is less well established. We sought to assess the correlation of TnT and creatine kinase-MB (CK-MB) with scintigraphically determined infarct size and to assess the predictive value of all 3 parameters on 12-month mortality. Patients presenting with STEMI managed with primary percutaneous intervention underwent serial TnT and CK-MB measurements at admission and for ≥72 hours after presentation. Before hospital discharge patients underwent assessment of infarct size by technetium-99m sestamibi single-photon emission computed tomographic (SPECT) scan. Clinical follow-up was performed up to 1 year. Data were available for 1,237 patients. Mean age was 62.9 ± 12.9 years. Infarct location was anterior in 509 patients (41%); 75 (6.1%) had cardiogenic shock. Median admission and peak TnT were 0.74 μg/L (0.10 to 2.70) and 3.70 μg/L (1.69 to 6.99), respectively. Corresponding values for CK-MB were 44.1 U/L (21.0 to 108.8) and 160.0 U/L (69.0 to 301.0), respectively. Median infarct size on SPECT scan was 12.0% (3.0 to 25.0) of the left ventricle. Peak TnT and CK-MB demonstrated similar moderate correlation with final infarct size (r = 0.45, p <0.001, and r = 0.41, p <0.001 respectively). This correlation was not affected by Thrombolysis In Myocardial Infarction flow grade after intervention. At 1 year, 47 patients (3.8%) had died. Final infarct size at SPECT scanning better predicted mortality than peak TnT or CK-MB. In conclusion, this study is the largest investigation on the value of cardiac troponin for assessment of infarct size in acute STEMI. Compared to peak CK-MB, peak TnT shows similar correlation with scintigraphic infarct size, although scintigraphic infarct size remains a better correlate of 1-year mortality than either biomarker.

Cardiac multi-marker strategy for effective diagnosis of acute myocardial infarction

Background Heart-type fatty acid-binding protein (H-FABP) is a heart-specific and highly sensitive biomarker for early diagnosis of acute myocardial infarction (AMI). We investigated the effectiveness of H-FABP for diagnosis of AMI in patients with different ethnic background and different time from symptom onset. Methods Venous blood was withdrawn from consecutive patients with acute chest pain admitted to the First Affiliated Hospital of Xinjiang Medical University. The blood samples were used for measurement of creatine kinase MB (CK-MB) and cardiac troponin I (cTnI) using Beckman Coulter DC-800 analyzer, and detection of H-FABP using a one-step bedside immunotest. Results Two hundred and eighty-nine patients admitted within 12 h after the onset of symptoms were recruited in the study. The H-FABP immunotest was found to have higher diagnostic accuracy than cTnI and CK-MB in patients admitted within 3 h. The combination of H-FABP and cTnI was found to have the highest diagnostic accuracy (91%) among different cardiac markers and the other combinations. It gave the highest sensitivity [96% (95% CI: 91–98%)] and a comparable specificity [84% (95% CI: 76–89%)] to cTnI alone. Conclusion A cardiac panel consisting of H-FABP and troponin is recommended.

Requiem for a Heavyweight

The development of rapid, automated, and accurate laboratory testing for creatine kinase MB (CK-MB) revolutionized the treatment of patients with acute cardiac events in the 1970s and 1980s.1 To clinicians, CK-MB values augmented a thorough history, physical, and ECG findings, and elevations rapidly became the gold standard for identifying cardiac injury.1 CK-MB allowed earlier diagnosis of acute myocardial infarction (AMI), and detection of reinfarction, and measurements could be used to provide a facile clinical estimate of infarct size. Elevations of CK-MB were never intended to be synonymous with myocardial infarction, only indicative of cardiac injury.1 However, because of the relative insensitivity of measurements, increased concentrations occurred predominantly with larger insults such those associated with acute ischemic heart disease. For that reason, AMI was rarely diagnosed, assuming appropriate timing of the samples, in the absence of a CK-MB elevation.2,3 CK-MB assays initially relied on the measurement of enzyme activity, but over time, improved accuracy and ease of use were established by the use of mass assays. Mass assays allowed earlier detection of abnormal values and improved both clinical sensitivity and specificity. However, mass assays unmasked an increased frequency of CK-MB elevations due primarily to skeletal muscle injury because of their increased sensitivity.4–6 Clinical use of the percent relative index was then initiated. This approach improved the specificity of elevations for cardiac muscle injury but was insensitive when concurrent cardiac injury and skeletal muscle injury were present because elevations from skeletal muscle often are of a large magnitude.7–10 A large number of analytical confounds such as macrokinases and interfering substances also were substantial problems with these assays.10,11 Attempts to standardize assays12 have been partially successful, but differences still exist between manufacturers and even between the same testing antibodies used on different analytical platforms (ie, …

Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome

IntroductionIt is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event.MethodFifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5–10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T3), free T3, thyroxine (T4), free T4, troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group.ResultsThe T3 and free T3 levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T4, free T4 and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T3 and free T3 levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T3, free T3, T4 and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively).ConclusionTFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state.

The effect of blood gas and Apgar score on cord blood cardiac Troponin I

The aims of this study were to (a) establish a reference range for cardiac troponin I (cTnI) in the cord blood of healthy infants, and (b) investigate the effect of Apgar score, cord blood gas, gestational age, and creatine kinase (CK) and creatine kinase MB (CK-MB) fraction levels on cord blood cTnI levels. 112 perinatal hypoxic and 84 control newborns without perinatal hypoxia were enrolled in this study. Cord blood samples were collected from the babies for arterial blood gas analysis, cTnI, CK and CK-MB measurements. Gestational age, birth weight, sex, Apgar score and history of fetal distress were recorded. Hypoxic ischemic encephalopathy (HIE) group, hypoxic but without HIE group and control groups were identified according to clinical observations during the first 72 h in the newborn unit. HIE and perinatal hypoxic without HIE groups had a significantly higher cord blood cTnI level according to the control group (1.8 ng/mL (0-13), 0 ng/ml (0-1.1) and 0 ng/ml (0-0.3) respectively). Cord blood cTnI level did not have a correlation with birth weight and gestational age (r = -0.02, p > 0.05 and r = 0.08, p > 0.05 respectively). Cord blood cTnI level also had a negative correlation with pH, bicarbonate, base deficit, and Apgar score (r = -0.40, p < 0.001; r = -0.39 p < 0.001; r = -0.45 p < 0.001; r = -0.41, p < 0.001) respectively). Cord blood cTnI level showed a positive correlation with CK and CK-MB levels (r = 0.45, p < 0.001 and r = 0.37, p < 0.001 respectively). Receiver operator curve analysis revealed that the most sensitive factor for prediction of perinatal hypoxia is cord cTnI value [area under curve = 0.929]. The optimal cut-off value of cord cTnI was 0.35 ng/ml for hypoxia. cTnI levels in the cord blood are not affected by gestational age and birth weight. cTnI together with CK and CK-MB has been found to be elevated in hypoxic infants compared to normal infants. Therefore cTnI may be an indicator for perinatal hypoxia in neonates.

The effect of blood gas and Apgar score on cord blood cardiac Troponin I

Objectives: The aims of this study were to (a) establish a reference range for cardiac troponin I (cTnI) in the cord blood of healthy infants, and (b) investigate the effect of Apgar score, cord blood gas, gestational age, and creatine kinase (CK) and creatine kinase MB (CK-MB) fraction levels on cord blood cTnI levels. Methods: 112 perinatal hypoxic and 84 control newborns without perinatal hypoxia were enrolled in this study. Cord blood samples were collected from the babies for arterial blood gas analysis, cTnI, CK and CK-MB measurements. Gestational age, birth weight, sex, Apgar score and history of fetal distress were recorded. Hypoxic ischemic encephalopathy (HIE) group, hypoxic but without HIE group and control groups were identified according to clinical observations during the first 72 h in the newborn unit. Results: HIE and perinatal hypoxic without HIE groups had a significantly higher cord blood cTnI level according to the control group (1.8 ng/mL (0-13), 0 ng/ml (0-1.1) and 0 ng/ml (0-0.3) respectively). Cord blood cTnI level did not have a correlation with birth weight and gestational age (r = −0.02, p > 0.05 and r = 0.08, p > 0.05 respectively). Cord blood cTnI level also had a negative correlation with pH, bicarbonate, base deficit, and Apgar score (r = −0.40, p < 0.001; r = −0.39 p < 0.001; r = −0.45 p < 0.001; r = −0.41, p < 0.001) respectively). Cord blood cTnI level showed a positive correlation with CK and CK-MB levels (r = 0.45, p < 0.001 and r = 0.37, p < 0.001 respectively). Receiver operator curve analysis revealed that the most sensitive factor for prediction of perinatal hypoxia is cord cTnI value [area under curve = 0.929]. The optimal cut-off value of cord cTnI was 0.35 ng/ml for hypoxia. Conclusion: cTnI levels in the cord blood are not affected by gestational age and birth weight. cTnI together with CK and CK-MB has been found to be elevated in hypoxic infants compared to normal infants. Therefore cTnI may be an indicator for perinatal hypoxia in neonates.

Cord Blood Cardiac Troponin T and Troponin I Levels in Multiple-Gestation Neonates

The increased mortality and morbidity rates in multiple-gestation neonates are not completely understood. Troponin measurements have a role in situations where the evaluation of the cardiac damage is difficult, such as in cases of unexplained intrauterine fetal growth restriction or death. These conditions, along with perinatal hypoxic risk and in utero ischemic damage, are frequently found in multiple gestations. In this context, a myocardial damage could be expected more frequently in multiple than in singleton births. We hypothesized that cord blood cardiac troponin T and troponin I, markers of myocardial damage, could be different between singleton and multiple pregnancies and, among twins, between the first- and the second-born twin. Troponins T and I and creatine kinase MB concentrations were not increased in twins at birth and were not different between the first- and the second-born twin. These data suggest that myocardial damage, evaluated by cardiac troponin T, troponin I, and creatine kinase MB measurements, does not seem to be a relevant problem in multiple-gestation neonates.

Probability Stratification and Systematic Diagnostic Approach for Chest Pain Patients in the Emergency Department

Management of chest pain patients in the emergency department has been a dilemma because of difficulty in identifying those who can be immediately discharged and those who need to be hospitalized. We assessed the efficacy of a probability stratification model and a systematic diagnostic strategy in 1003 consecutive chest pain patients prospectively evaluated and stratified for acute coronary syndromes according to chest pain characteristics and admission electrocardiogram. Patients with no suspicion of acute coronary syndromes (n = 224) were immediately discharged, whereas those with very-high probability (n =119) were admitted to the coronary care unit. Remaining patients were evaluated in a Chest Pain Unit and investigated during a 9-hour period (intermediate-probability, n = 433) (route 2) and a 6-hour period (low-probability, n = 277) (route 3). Sensitivity and negative predictive value of chest pain type for the diagnosis of acute myocardial infarction (94% and 97%, respectively) was much better than the admission electrocardiogram (49% and 86%, respectively) and admission creatine kinase-MB (46% and 86%, respectively). Serial creatine kinase-MB determinations ruled out acute myocardial infarction by the third-hour postadmission in all route 3 patients but only at the ninth-hour in route 2 patients. For patients with no ST-segment elevation, chest pain type was the strongest independent predictor of acute coronary syndromes. It is concluded that chest pain type is the best single diagnostic tool to rule in/out acute coronary syndromes on admission to the emergency department. Patients with suspicious chest pain must have serum creatine kinase-MB measurements up to 9 hours postadmission to rule out acute myocardial infarction.

The prognostic value of markers of inflammation in patients with troponin T–negative chest pain before discharge from the emergency department

Purpose To assess the prognostic value of markers of inflammation for rule-out purposes in patients admitted to the emergency department with troponin T–negative chest pain. Methods Patients presenting to the emergency department within 6 hours of symptom onset and who had a normal or nondiagnostic electrocardiogram were eligible. The standard rule-out protocol, which included serial creatine kinase and creatine kinase-MB measurements, was applied, and markers of inflammation (C-reactive protein, erythrocyte sedimentation rate, and total white blood cell count and differential count) were measured. The study group comprised patients with negative serial troponin T results (<0.06 μg/L) who were discharged home after unstable coronary artery disease was ruled out. Endpoints during the 6-month follow-up were cardiac death, myocardial infarction, or rehospitalization for unstable angina. Results A total of 382 troponin T–negative patients were discharged, of whom 2 died, 2 had a myocardial infarction, and 7 were rehospitalized for unstable angina. A positive C-reactive protein test result (>0.3 mg/dL) was associated with future clinical events (hazard risk [HR] = 4.5; 95% confidence interval [CI]: 1.2 to 17.0; P = 0.03), as was a positive test (>13 mm/h) for erythrocyte sedimentation rate (HR = 5.6; 95% CI: 1.5 to 22.2; P = 0.01). Patients with positive results for both tests were at highest risk of clinical events (9.3%) compared with patients with other combinations of test results (1.1% to 2.1%; HR = 7.5; 95% CI: 2.2 to 25.5; P = 0.001). Conclusion The combination of C-reactive protein and erythrocyte sedimentation rate had prognostic value in patients with troponin T–negative chest pain and a normal or nondiagnostic electrocardiogram in whom unstable coronary artery disease was ruled out.