The Cardiac Troponin T and I are highly cardiac specific biochemical markers of myocardial injury. They are very sensitive markers to detect all kinds of myocardial injury, and are able to distinguish myocardial injury and skeletal injury. Furthermore, They are independent predictor of future cardiac events. Such markers are now widely used in the clinic practice. It is prospective to use them in Forensic Medical Science.
Biomarkers ; Forensic Medicine ; Humans ; Myocardial Infarction/blood* ; Myocardium/metabolism* ; Troponin I/blood* ; Troponin T/blood*

The diagnosis and management of patients with acute coronary syndrome (ACS) have evolved dramatically over the past decade. Biomarkers play an important role in the diagnosis of ACS, especially in unstable angina and non-ST-segment elevation myocardial infarction. Among these, cardiac troponin and creatine kinase appear to be the most sensitive and specific markers of myocardial injury. Recent studies have revealed several novel biomarkers. Elevated levels of C-reactive protein and interleukin-6 are strong independent markers of increased mortality among patients with ACS. However, the ideal biomarkers that offer early detection, risk stratification, selection of therapy, monitoring disease progression, and treatment efficacy remain to be elucidated. This review assesses limitations and contemporary needs for biomarkers in the context of diagnosis of ACS. It also discusses the newly developing technologies for novel biomarkers or novel biomarker protein signatures discovery, and importance of point-of-care testing for future management.
Acute Coronary Syndrome ; blood ; pathology ; Biomarkers ; blood ; Creatine Kinase ; blood ; Electrocardiography ; Humans ; Myoglobin ; blood ; Necrosis ; blood ; Oxidative Stress ; Platelet Activation ; Troponin I ; blood ; Troponin T ; blood

Hyperadrenocorticism (HAC) is a common endocrinopathy among dogs that causes multisystemic signs. This study was conducted to evaluate cardiocirculatory, biochemical, and hemostatic parameters in dogs with HAC at diagnosis, in addition to verifying whether abnormal parameters could be controlled by initial treatment with trilostane. Fifteen dogs with HAC were assessed by systolic blood pressure measurement, electrocardiography, Doppler echocardiography, serum concentration of troponin I, and biochemical and hemostatic profile at diagnosis and after trilostane therapy. Unlike biochemical parameters, hemostatic and cardiocirculatory parameters were not significantly influenced by the onset of treatment. The authors believe that clinical treatment with trilostane for 3 to 4 months might not be sufficient for the stabilization of cardiocirculatory abnormalities such as hypertension. Therefore, dogs with HAC must receive cardiocirculatory monitoring at diagnosis and during drug treatment.
Adrenocortical Hyperfunction* ; Animals ; Blood Pressure ; Cardiology ; Diagnosis* ; Dogs* ; Echocardiography, Doppler ; Electrocardiography ; Endocrinology ; Hypertension ; Troponin I

The objective of this study is to combine troponin and indicators of cardiac acoustics for synthetically evaluating cardiac fatigue of rabbits, analyzing exercise-induced cardiac fatigue (EICF) and exercise-induced cardiac damage (EICD). New Zealand white rabbits were used to conduct a multi-step swimming experiments with load, reaching an exhaustive state for evaluating if the amplitude ratio of the first to second heart sound (S1/S2) and heart rate (HR) during the exhaustive exercise would decrease or not and if they would be recovered 24-48 h after exhaustive exercise. The experimental end point was to complete 3 times of exhaustions or death from exhaustion. Circulating troponin I (cTnI) were detected from all of the experimental rabbits at rest [(0. 02±0. 01) ng/mL], which, in general, indicated that there existed a physiological release of troponin. After the first exhaustive swim, cTnI of the rabbits increased. However, with 24-hour rest, S1/S2, HR, and cTnI of the tested rabbits all returned toward baseline levels, which meant that the experimental rabbits experienced a cardiac fatigue process. After repeated exhaustion, overloading phenomena were observed, which led to death in 3 out of 11 rabbits, indicating their cardiac damage; the troponin elevation under this condition could be interpreted by pathological release. Evaluation of myocardial damage can not be based on the troponin levels alone, but can only be based on a comprehensive analysis.
Animals ; Fatigue ; Heart ; physiopathology ; Heart Rate ; Myocardium ; pathology ; Rabbits ; Swimming ; Troponin I ; blood

p-Nitrophenylphosphate (PNPP) is usually employed as the substrate for enzyme-linked immunosorbent assays. p-Nitrophenol (PNP), the product of PNPP, with the catalyst alkaline phosphatase (ALP), will passivate an electrode, which limits applications in electrochemical analysis. A novel anti-passivation ink used in the preparation of a graphene/ionic liquid/chitosan composited (rGO/IL/Chi) electrode is proposed to solve the problem. The anti-passivation electrode was fabricated by directly writing the graphene-ionic liquid-chitosan composite on a single-side conductive gold strip. A glassy carbon electrode, a screen-printed electrode, and a graphene-chitosan composite-modified screen-printed electrode were investigated for comparison. Scanning electron microscopy was used to characterize the surface structure of the four different electrodes and cyclic voltammetry was carried out to compare their performance. The results showed that the rGO/IL/Chi electrode had the best performance according to its low peak potential and large peak current. Amperometric responses of the different electrodes to PNP proved that only the rGO/IL/Chi electrode was capable of anti-passivation. The detection of cardiac troponin I was used as a test example for electrochemical immunoassay. Differential pulse voltammetry was performed to detect cardiac troponin I and obtain a calibration curve. The limit of detection was 0.05 ng/ml.
Electrochemical Techniques/methods* ; Electrodes ; Graphite ; Immunoassay/methods* ; Ink ; Microscopy, Electron, Scanning ; Troponin I/blood*

OBJECTIVETo study the changes and significance of plasma cardiotrophin-1 (CT-1) in neonates with hypoxic-ischemic encephalopathy (HIE) complicated by myocardial ischemic injury.

METHODSForty-five neonates with HIE (15 mild cases, 24 moderate cases and 6 severe cases) were enrolled and divided into two subgroups based on the presence of myocardial injury (n=19) and not (n=26). Twenty healthy neonates were used as the control group. Plasma CT-1 levels were measured using double-antibody sandwich enzyme immunoassay method. Serum creatinine kinase MB (CK-MB) and cardiac troponin I (CTnI ) levels were also measured.

RESULTSPlasma CT-1 levels in the mild HIE (169±20 pg/mL) and moderate/severe HIE subgroups (287±44 pg/mL) were significantly higher than those in the control group (30±8 pg/mL), and plasma CT-1 levels were associated with the severity of HIE (P<0.01). Plasma CT-1 levels were positively correlated with serum CK-MB and CTnI levels in neonates with HIE in the acute phase (r=0.565 and 0.621 respectively; P<0.01). Plasma CT-1 levels in neonates with myocardial injury were significantly higher than those without myocardial injury (249 ±35 pg/mL vs 177±26 pg/mL; P<0.01). Plasma CT-1 levels were significantly reduced in neonates with myocardial injury in the convalescent phase (157±19 pg/mL) compared with those in the acute phase (249±35 pg/mL; P<0.01).

CONCLUSIONSDetection of plasma CT-1 levels may be useful in the diagnosis of myocardial ischemic injury and the severity evaluation of HIE.

Creatine Kinase, MB Form ; blood ; Cytokines ; blood ; Female ; Humans ; Infant, Newborn ; Male ; Myocardial Ischemia ; blood ; Troponin I ; blood

OBJECTIVETo investigate the association between serum cardiac troponin I (cTnI) and cardiac function/structure in patients with chronic heart failure.

METHODSOne hundred and twenty patients with decompensated chronic heart failure were included. The patients were divided into cTnI normal group (cTnIn; n = 80) and cTnI elevated group (cTnIe; n = 40). Systolic dimension of the left atrium (LAd), the maximal width of the left ventricle (LVd), the thickness of the interventricular septum (IVS) and posterior wall (LVPW) during diastole, left ventricle ejection fraction (LVEF), E and A wave velocities ratio (E/A) were determined. Bivariate correlation analysis was applied to show the correlation of serum cTnI level with above indices. Partial correlation analysis was performed followed by multivariate logistic regression.

RESULTSLAd and LVd dimensions were significantly higher (P < 0.05), IVS, LVPW, LVEF and E/A ratio were significantly lower (P < 0.05) in cTnIe group than in cTnIn group. Moreover, serum cTnI was positively correlated with LAd, LVd, and inversely correlated with IVS, LVPW, LVEF and E/A ratio (P < 0.05). The correlation persistent after adjusting with sex, history of heart failure, NYHA functional class and treatment. In multivariate modeling, cTnI was positively associated with LAd, LVd and the history of heart failure, and negatively related with the treatment with angiotensin-converting enzyme inhibitor.

CONCLUSIONSerum cTnI correlated with cardiac structure and function. Intensively serum cTnI monitoring and suitable therapy strategy may be helpful to attenuate the cardiac remodeling in patients with chronic heart failure.

Adult ; Chronic Disease ; Female ; Heart Failure ; blood ; physiopathology ; Humans ; Male ; Middle Aged ; Myocardium ; chemistry ; Troponin I ; blood ; Ventricular Remodeling

Acetamides ; pharmacology ; Animals ; Bridged-Ring Compounds ; poisoning ; Disease Models, Animal ; Female ; Male ; Rats ; Rats, Sprague-Dawley ; Troponin I ; blood

OBJECTIVE: To observe the changes of electrocardiogram and serum cardiac troponin I at the early stage of severe crush injury in rats. METHODS: Crush injury was produced in Sprague-Dawley rats. The changes of electrocardiogram were recorded with the standard II, the serum levels of cardiac troponin I were studied by automated chemiluminescence assay. RESULTS: The ST segment elevated considerably after crush injury and lasted 24 h, the levels of serum cTnI were much higher than those of the control groupes after 6 h of injury. CONCLUSION Cardiomyocyte injury was induced in the early phase of crush injury.
Animals ; Crush Syndrome/physiopathology* ; Electrocardiography ; Extremities/injuries* ; Female ; Heart Injuries/physiopathology* ; Male ; Rats ; Rats, Sprague-Dawley ; Troponin I/blood*

BACKGROUND AND OBJECTIVES: The purpose of the study was to evaluate the clinical effect of Nicorandil during percutaneous coronary intervention (PCI) in patients with unstable angina (UA). SUBJECTS AND METHODS: Two hundred patients (61+/-10 years, male 143) with UA were randomly assigned to two groups: intravenous Isosorbide dinitrate (Group I, n=100) and intravenous Nicorandil (Group II, n=100). PCI was performed 12-48 hours after infusion of the agents. The post-procedural cardiac enzymes, 6-month MACE (major adverse cardiac event) and left ventricular ejection fraction (LVEF) were compared between the two groups. RESULTS: Successful PCI was performed in 96 patients (Group I=54, Group II=42). Patients requiring either emergent coronary angiography, temporary pacemaker or platelet glycoprotein IIb/IIIa receptor blocker were excluded. No significant differences were observed between the two groups in terms of the clinical and coronary angiographic characteristics. The level of creatine kinase-MB was elevated in 9 (17%) and 6 patients (14%), troponin T in 16 (30%) and 6 (14%) and troponin I in 25 (46%) and 9 (21%) patients of Groups I and II, respectively, after the PCI. The elevation of all troponins was lower in Group II (28 vs. 10 patients, p=0.01). MACE developed in 9 (17%) and 5 (12%) patients of Groups I and II (p=NS), respectively, during the 6-month clinical follow-up. The LVEF was higher in Group II than in Group I on follow-up echocardiography (65.4+/-7.2% vs. 71.0+/-6.7%, p=0.003). CONCLUSION: Nicorandil may have a myocardial protective effect during PCI in patients with UA.
Angina, Unstable* ; Angioplasty ; Blood Platelets ; Coronary Angiography ; Creatine ; Echocardiography ; Follow-Up Studies ; Glycoproteins ; Humans ; Isosorbide Dinitrate ; Male ; Nicorandil* ; Nitroglycerin ; Percutaneous Coronary Intervention* ; Stroke Volume ; Troponin ; Troponin I ; Troponin T