Comparison Between Soluble ST2 and High-Sensitivity Troponin I in Predicting Short-Term Mortality for Patients Presenting to the Emergency Department With Chest Pain

BACKGROUND: High-sensitivity cardiac troponin I (hs-cTnI) and the soluble isoform of suppression of tumorigenicity 2 (sST2) are useful prognostic biomarkers in acute coronary syndrome (ACS). The aim of this study was to test the short term prognostic value of sST2 compared with hs-cTnI in patients with chest pain. METHODS: Assays for hs-cTnI and sST2 were performed in 157 patients admitted to the Emergency Department (ED) for chest pain at arrival. In-hospital and 30-day follow-up mortalities were assessed. RESULTS: The incidence of ACS was 37%; 33 patients were diagnosed with ST elevation myocardial infarction (STEMI), and 25 were diagnosed with non-ST elevation myocardial infarction (NSTEMI). Compared with the no acute coronary syndrome (NO ACS) group, the median level of hs-cTnI was higher in ACS patients: 7.22 (5.24-14) pg/mL vs 68 (15.33-163.50) pg/mL (P35 ng/mL at ED arrival died during the 30-day follow-up. CONCLUSIONS: sST2 has a greater prognostic value for 30-day cardiac mortality after discharge in patients presenting to the ED for chest pain compared with hs-cTnI. In STEMI patients, an sST2 value >35 ng/mL at ED arrival showed the highest predictive power for short-term mortality.

Can a Point-of-Care Troponin I Assay be as Good as a Central Laboratory Assay? A MIDAS Investigation

BACKGROUND: We aimed to compare the diagnostic accuracy of the Alere Triage Cardio3 Tropinin I (TnI) assay (Alere, Inc., USA) and the PathFast cTnI-II (Mitsubishi Chemical Medience Corporation, Japan) against the central laboratory assay Singulex Erenna TnI assay (Singulex, USA). METHODS: Using the Markers in the Diagnosis of Acute Coronary Syndromes (MIDAS) study population, we evaluated the ability of three different assays to identify patients with acute myocardial infarction (AMI). The MIDAS dataset, described elsewhere, is a prospective multicenter dataset of emergency department (ED) patients with suspected acute coronary syndrome (ACS) and a planned objective myocardial perfusion evaluation. Myocardial infarction (MI) was diagnosed by central adjudication. RESULTS: The C-statistic with 95% confidence intervals (CI) for diagnosing MI by using a common population (n=241) was 0.95 (0.91-0.99), 0.95 (0.91-0.99), and 0.93 (0.89-0.97) for the Triage, Singulex, and PathFast assays, respectively. Of samples with detectable troponin, the absolute values had high Pearson (R(P)) and Spearman (R(S)) correlations and were R(P)=0.94 and R(S)=0.94 for Triage vs Singulex, R(P)=0.93 and R(S)=0.85 for Triage vs PathFast, and R(P)=0.89 and R(S)=0.73 for PathFast vs Singulex. CONCLUSIONS: In a single comparative population of ED patients with suspected ACS, the Triage Cardio3 TnI, PathFast, and Singulex TnI assays provided similar diagnostic performance for MI.

Avaliação dos valores de troponina I, eletrocardiograma e ecocardiograma em felinos sedados com cetamina e midazolam, suplementados ou não com oxigênio / Troponin I, electrocardiography and echocardiography values in felines sedated with ketamine and midazolam, supplemented or not with oxygen

Lesões no miocárdio, causadas por baixa perfusão e oxigenação cardíaca, podem ser ocasionadas por fármacos anestésicos, como a cetamina. Essas lesões podem ser identificadas por meio de biomarcadores específicos e, dentre estes, destaca-se a troponina I. O objetivo deste estudo foi avaliar as alterações cardiovasculares com base nos valores de troponina I (TnI), eletrocardiograma (ECG) e ecocardiograma em gatos sedados com cetamina e midazolam, suplementados ou não com oxigênio. Utilizaram-se 12 gatos machos, hígidos, nos quais se avaliaram os valores de troponina I, eletro e ecocardiografia, frequência cardíaca (FC) e pressão arterial sistólica (PAS) no momento basal (M0). Na sequência, os animais foram sedados com a associação de 10mg.kg-1 de cetamina e 0,5mg.kg-1 de midazolam pela via intramuscular. Decorridos aproximadamente 10 minutos, os animais foram alocados aleatoriamente em dois grupos: com e sem suplementação de oxigênio via máscara facial (GCO e GSO, respectivamente), sendo submetidos novamente aos exames citados. Foram coletadas amostras sanguíneas, para dosagem de TnI em seis, 12 e 24 horas após a administração dos agentes anestésicos. Não foram observadas alterações significativas na FC, na PAS e no ECG após a administração dos tratamentos em ambos os grupos. Os valores médios de TnI elevaram-se significativamente em T6 quando comparados ao basal em ambos os grupos, com médias de 0,507±0,335ng/mL no GSO e 0,777±0,505ng/mL no GCO. Na ecocardiografia, o débito cardíaco (DC) reduziu em M1 em ambos os grupos, quando comparados aos valores basais, sendo M0 0,472±0,115 e M1 0,234±0,08 no GSO e M0 0,356±0,095 e M1 0,222±0,09 no GCO, expressos em L/min. Conclui-se que a administração de cetamina e midazolam em gatos hígidos não promove alterações eletrocardiográficas, aumenta os valores de troponina I, com pico de seis horas após a administração, reduz o débito cardíaco, e que a suplementação de oxigênio 100% via máscara facial não atenua tais alterações.

Myocardium injuries caused by low myocardial oxygenation and perfusion might be induced by anesthetics agents like ketamine. These injuries can be detected by specific biomarkers and, among them, troponin I. The aim of this study was to evaluate the cardiovascular changes based on troponin I (TnI) values, electrocardiography (ECG) and echocardiography in cats sedated with ketamine and midazolam, supplemented or not with oxygen. Blood samples were collected from 12 intact male healthy cats for troponin I (T0) and they were then submitted to electrocardiographic and echocardiographic evaluation, as well as measurements of heart rate (HR) and systolic blood pressure (SBP) (M0). Subsequently, they were ketamine-midazolam (10mg.kg-1 and 0,5 mg.kg-1 respectively) anesthetized by intramuscular route. After about 10 minutes, the animals were randomly allocated into two groups with or without oxygen supplementation (GCO or GSO, respectively), again being subjected to the tests mentioned. Blood samples for troponin I were collected at 6, 12 and 24 hours after sedation. HR, SBP and ECG did not change among groups. The TnI values rise significantly in T6 comparing to baselines in both groups (0,507±0,335 ng/mL in GSO and 0,777±0,505 ng/mL in GCO). In echocardiography, the cardiac output decreased at M1, in both groups compared to baseline (M0 0,472±0,115 and M1 0,234±0,08 in GSO and M0 0,356±0,095 and 0,222±0,09 in GCO, L/min). We concluded that ketamine and midazolam sedation in healthy cats did not cause changes electrocardiography, increase troponin I values, with an 6 hours peak after administration, reduces cardiac output and oxygen supplementation, via facial mask, did not attenuated these alterations.

Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats

This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.

Association between Angiotensin-Converting Enzyme Inhibitors and Troponin in Acute Coronary Syndrome / Relação entre Inibidores da Enzima de Conversão da Angiotensina e Troponina na Síndrome Coronariana Aguda

Background: Cardiovascular disease is the leading cause of mortality in the western world and its treatment should be optimized to decrease severe adverse events. Objective: To determine the effect of previous use of angiotensin-converting enzyme inhibitors on cardiac troponin I measurement in patients with acute coronary syndrome without ST-segment elevation and evaluate clinical outcomes at 180 days. Methods: Prospective, observational study, carried out in a tertiary center, in patients with acute coronary syndrome without ST-segment elevation. Clinical, electrocardiographic and laboratory variables were analyzed, with emphasis on previous use of angiotensin-converting enzyme inhibitors and cardiac troponin I. The Pearson chi-square tests (Pereira) or Fisher's exact test (Armitage) were used, as well as the non-parametric Mann-Whitney's test. Variables with significance levels of <10% were submitted to multiple logistic regression model. Results: A total of 457 patients with a mean age of 62.1 years, of whom 63.7% were males, were included. Risk factors such as hypertension (85.3%) and dyslipidemia (75.9%) were the most prevalent, with 35% of diabetics. In the evaluation of events at 180 days, there were 28 deaths (6.2%). The statistical analysis showed that the variables that interfered with troponin elevation (> 0.5 ng / mL) were high blood glucose at admission (p = 0.0034) and ST-segment depression ≥ 0.5 mm in one or more leads (p = 0.0016). The use of angiotensin-converting inhibitors prior to hospitalization was associated with troponin ≤ 0.5 ng / mL (p = 0.0482). The C-statistics for this model was 0.77. Conclusion: This study showed a correlation between prior use of angiotensin-converting enzyme inhibitors and reduction in the myocardial necrosis marker troponin I in patients admitted for acute coronary syndrome without ST-segment elevation. However, there are no data available yet to state that this ...

Fundamento: A doença cardiovascular é a maior causa de mortalidade no mundo ocidental, devendo seu tratamento ser otimizado, para a redução de eventos adversos graves. Objetivo: Determinar o efeito do uso prévio de inibidores da enzima de conversão da angiotensina na mensuração da troponina I cardíaca em pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST (SCASST), e avaliar os desfechos clínicos em até 180 dias. Métodos: Estudo prospectivo, observacional, em um centro terciário, em pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST (SCASST). Foram analisadas variáveis clínicas, eletrocardiográficas e laboratoriais, com ênfase no uso prévio de inibidores da enzima de conversão da angiotensina e dosagem de troponina I cardíaca. Foram usados os testes qui quadrado de Pearson ou exato de Fischer , além do teste não paramétrico de Mann-Whitney. Variáveis com níveis de significância < 10% foram submetidas a modelo de regressão logística múltipla. Resultados: Incluídos 457 pacientes, com idade média de 62,1 anos, dos quais 63,7% eram do sexo masculino. Fatores de risco como hipertensão arterial sistêmica (85,3%) e dislipidemia (75,9%) foram os mais prevalentes, com 35% de diabéticos. Na avaliação de eventos em 180 dias, observaram-se 28 óbitos (6,2%). Na análise estatística, as variáveis que interferiram no aumento de troponina (> 0,5 ng/mL) foram a glicemia de admissão elevada (p = 0,0034) e o infradesnivelamento do segmento ST ≥ 0,5 mm, em uma ou mais derivações (p = 0,0016). Relacionada com troponina ≤ 0,5 ng/mL, esteve o uso de inibidores da enzima de conversão da angiotensina prévio à internação (p = 0,0482). ...

Prediction of anthracycline induced cardiotoxicity: study of thirty-one Iraqi adult patients

To look for a nearly ideal tool for prediction of anthracycline-induced cardiotoxicity. Thirty-one patients with various hematological malignancies were included in the study which was conducted from Sept. 2005 to Sept. 2006 in Baghdad Teaching Hospital - Hematology Unit. Initial cardiovascular assessment including cardiac troponin I, electrocardiography and echocardiography were done and repeated one month after the commencement of anthracycline-based regimen. Cardiotoxicity was considered present if the patient has clinical and electrocardiographic evidences, troponin positivity, echocardiographic evidence, or any combination of these. The mean age for the study sample was 34.1 +/- 17.2 years comprising of 17 male and 14 female patients. Increasing age, body surface area, anthracycline dose as well as the concomitant use of cyclophosphomide/ All Trans Retinoic were associated with increased risk of cardiotoxicity. The cut-off point of body surface area above which the risk of anthracycline-induced cardiotoxicity is increased was 1.88 m[2] while the cut-off point for anthracyclines dose was 145.5 mg/m[2]. The constellation of clinical data, ECG, and cTnI was 92% predicitive of early evidence of anthracycline-induced cardiotoxicity. More weight is added when echocardiography is used as a diagnostic tool. The incidence of cardiotoxicity attributed to treatment was 38.7%. The predictive power of cardiac troponin I alone was 58.3%, whereas it increases to 91% when combined with electrocardiography and to 95% when combined with echocardiographic study. The age, anthracyclines dose and the use of other chemotherapeutics increase the risk of anthracylince-induced cardiotoxicity. Cardiac troponin I is a simple non-invasive indicator for the presence of anthracycline- induced cardiotoxicity especially when used in combination with other parameters

Seguimiento alejado de pacientes evaluados en una Unidad de Dolor Torácico / Long term follow up of patients consulting in a Chest Pain Unit

Background: Chest pain (CT) constitutes an important cause of consultation and diagnostic dilemma in the emergency room, especially due to the possible presence of coronary disease. Its presentation, diagnosis and prognosis are different between men and women. Aim: To report a follow-up of patients attended at a Chest Pain Unit (CPU), evaluating gender differences. Material and Methods: Prospective evaluation of patients that consulted for chest pain in a period of 4 years. Baseline characteristics and the final diagnosis from CPU or hospitalization were registered. Telephonic follow-up was performed for at least one year. Mortality was determined using the national mortality registry. Results: A total of 1,168 patients aged 62 ± 23 years, 69 percent men, were followed for a mean of 28 ± 20 months. A definitive diagnosis of coronary disease (CD) was done in 32 percent. Mortality among women and men with CD was 28 and 14 percent respectively (p = 0,02). Predictor variables for mortality were the presence of a complete left branch block in the initial electrocardiogram, with an odds ratio (OR) of 12,5 (95 percent confi dence intervals (CI): 1,98-25,8), the presence of coronary disease with an OR of 3,98 (95 percent CI: 1,45-13,8) and elevated troponin I with an OR 2,12 (95 percent CI: 1,05-7,89). Female gender lost significance in the adjusted model. Conclusions: Complete left branch block, elevated troponin I and coronary etiology of CP are indicators of bad prognosis among patients that consult for CP. Women have twice the mortality of men after 28 months of follow-up.

Níveis cardíacos de troponina I em pacientes com epilepsia do lobo temporal refratária após cortico-amígdalo-hipocampectomia / Cardiac troponin I levels in patients with refractory temporal lobe epilepsy after cortico-amygdalo-hippocampectomy

OBJETIVOS: A morte súbita em epilepsia (SUDEP) é a principal causa de morte entre os pacientes com epilepsia. Alterações morfológicas e funcionais do coração estão relacionadas com a SUDEP. Nesse sentido, o objetivo deste estudo foi avaliar a concentração de troponina I, um importante marcador de lesão do miocárdio, em pacientes com epilepsia do lobo temporal de difícil controle e que foram submetidos à ressecção cirúrgica e que não obtiveram sucesso com esta abordagem terapêutica. METODOLOGIA: Onze pacientes participaram do estudo e todos continuaram a apresentar crises após o tratamento cirúrgico. Os valores de troponina I indicativos de lesão seriam aqueles maiores de 1 ng/ml e o valor mínimo detectável pelo kit utilizado em nosso estudo foi de 0,15 ng/ml. RESULTADOS: Apenas três pacientes apresentaram níveis de troponina I detectáveis. Em relação aos níveis detectáveis de troponina I, não encontramos nenhuma relação com sexo, idade e lateralidade da lesão. CONCLUSÕES: APESAr de não termos encontrado resultados positivos em nosso estudo, o papel do coração na SUDEP não pode ser descartado, já que algumas lesões, embora não sendo capazes de alterar os níveis séricos de troponina I, podem ser suficientes na gênese de focos arritmogênicos.

PURPOSE: Sudden unexpected death in epilepsy (SUDEP) is the main cause of death in patients with epilepsy. Morphologic and functional changes in the heart are related to SUDEP. The aim of our study was to verify the concentration of troponin I, an important marker of myocardium damage, in patients with temporal lobe epilepsy who were submitted to surgical resection and were not seizure-free after the procedure. METHODS: Eleven non-consecutive patients participated in the study and all of them presented poor seizure control after surgical procedure. Troponin I levels higher then 1 ng/ml indicate myocardium damage. The detection level of the kit used in our study was 0,15 ng/ml. RESULTS: Only three patients showed detectable troponin I levels. The troponin I levels found in our study is not related with sex, age or side of the lesion. CONCLUSIONS: In spite of we did not find positive results in our study, an active role of the heart in SUDEP cannot be discarded, since some injuries, even so not being capable to modify troponin I levels, can be enough to generate arrhythmogenic foci.

Cardiac trauma confirmed by cardiac markers in dogs: two case reports

Two clinical cases of cardiac contusion in dogs were studied Radiographic evaluation showed pneumothorax and alveolar pattern on diaphragmatic pulmonary lobe in one dog, and arrhythmias in both dogs. Cardiac troponin I and CK-MB serum analysis associated with clinical history and eletrocardiographic findings indicated accurately the extension of myocardial injury secondary to trauma.

Relatam-se dois casos de miocardite em cães. A avaliação radiográfica mostrou pneumotórax e padrão alveolar no lobo diafragmático pulmonar em um cão e arritmia em ambos os cães. As análises das proteínas cardíacas altamente sensíveis, como a CK-MB e a troponina I cardíaca, associadas ao histórico clínico e aos achados eletrocardiográficos, indicaram, com acurácia, a extensão da injúria miocárdica secundária ao trauma.

Proteção miocárdica com betabloqueador oral em cirurgia de revascularização miocárdica: avaliação pela troponina I / Myocardial protection with oral metoprolol during coronary artery bypass grafting surgery: evaluation by troponin I

Avaliar se metoprolol oral profilático (200mg/d) reduz a troponina I (cTnI) após cirurgia de revascularização miocárdica isolada. Randomizados 33 pacientes para betabloqueador (GB) e 35 para grupo controle (GC). Sem diferença significativa entre o GC e GB quanto às variáveis pré-cirúrgicas e cirúrgicas, incidência de complicações (15 por cento versus 14 per cent; p=0,92) e eventos hospitalares (21 por cento versus 14 per cent; p=0,45). O valor da mediana da cTnI com 12 horas foi de 3,3 ng/ml, sendo menor no GB do que no GC (2,5 ng/ml versus 3,7 ng/ml; p<0,05). O valor de corte para eventos hospitalres foi > 4,4 ng/ml. O metoprolol oral conferiu proteção miocárdica nestes pacientes avaliada pela redução da cTnI./Evaluate if the oral prophylactic administration of metoprolol (200 mg/d) reduces troponin I (cTnI) after isolated coronary artery bypass grafting surgery. 33 patients randomized to betablocker (BC) and 35 to control (CG). CG and BG had no different clinical and surgical characteristics, incidence of complications (15 per cent versus 14 per cent, p=0.92) and hospital events (21 per cent versus 14 per cent; p=0.45). The median value of cTnI with 12 hours was 3.3 ng/ml, and it was lower in the BG than in the CG (2.5 ng/ml versus 3.7 ng/ml; p<0.05). The hospital event cut-off point was > 4.4 ng/ml in this study. The oral administration of metoprolol conferred myocardial protection in these patients by a reduction release of cTnI...

Ausencia de interferencias por anticuerpos heterófilos en la cuantificación de Troponina I Cardíaca, en pacientes con insuficiencia renal crónica terminal en tratamiento de hemodiálisis / Absence of interferences for heterophilic antibodies in the quantification de cardiac

El presente estudio pretende valorar el comportamiento de la adición del reactivo bloqueador de anticuerpos heterófilos (HBR) en la cuantificación de Troponina I cardíaca (TnIc) en pacientes con insuficiencia renal crónica terminal (IRCt) sometidos a tratamiento de hemodiálisis.Acada uno de los70 pacientes con IRCt en tratamiento de hemodiálisis en el Hospital Universitario Clínica San Rafael de Bogotá, se le tomó una muestra de suero y una de plasma heparinizado en la prediálisis, en las cuales se cuantificaron las concentraciones de TnIc con y sin adición de HBR, mediante el enzimoinmunoensayo Axsym. Se utilizó la prueba estadística de Wilcoxon. Los valores de TnIc en plasmas y sueros con y sin la adición de HBR no mostraron diferencias significativas (0.113 y 0.666 respectivamente), tanto en el total de los pacientes como en aquellos con enfermedad cardíaca crónica. El no haber encontrado diferencias en los valores de TnIc con y sin HBR nos lleva a pensar en la ausencia de anticuerpos heterófilos o en que el reactivo bloqueador HBR no tiene acción en esta población de pacientes.

Valor diagnóstico da CK-MB assa, à mioglobina e à troponina I nas síndromes isquêmicas agudas / Diagnostic Value of CK-MB Activity Compared to Mecglobin, CK-MB Mass, Traponin 1 in Acute Coronary Syndrome

A síndrome isquêmica aguda varia de angina instável a infarto agudo do miocárdio, e seu manuseio atual requer rapidez e eficácia. O diagnóstico do infarto agudo do miocárdio foi estabelecido pela Organização Mundial da Saúde, e a CK-MB atividade foi considerada a enzima padrão. O objetivo deste estudo foi comparar o valor diagnóstico e o desempenho da CK-MB atividade à CK-MB massa, à troponina I e à mioglobina em portadores de dor precordial prolongada, atendidos no pronto-socorro. A casuística incluiu 217 pacientes, com dor precordial de duração igual ou superior a 20 minutos, distribuídos em três grupos: grupo I, 29 pacientes com infarto agudo do miocárdio, diagnosticado por supradesnivelamento do segmento ST e dor; grupo II, 24 pacientes com infarto agudo do miocárdio, diagnosticado por elevação da CK-MB atividade e dor, e grupo III, 164 pacientes, com dor, sem alteração da CK-MB atividade e do eletrocardiograma compatível com infarto agudo. As dosagens dos marcadores bioquímicos foram realizadas na ocasião da inclusão do paciente no estudo, duas, quatro, seis, oito, dez, 12 e 24 horas após, e as análises foram realizadas em relação à hora do início da dor. As características demográficas dos grupos foram semelhantes, exceto o tabagismo, que foi menor no grupo III. Quanto às alterações eletrocardiográficas, todos os pacientes com eletrocardiograma normal situaram-se no grupo III, e os níveis dos marcadores bioquímicos foram mais elevados nos pacientes com alterações eletrocardiográficas compatíveis com isquemia aguda. A sensibilidade e a especificidade da CK-MB massa (5,6 ng/ml), da cTnI (1,5 ng/ml), da CK-MB massa (9,4 ng/ml) e da mioglobina (110 ng/ml), em relação à CK-MB atividade, foram 98% e 78,6%, 98% e 74,4%, 98% e 84,5%, 85,7% e 85,1% respectivamente. O valor preditivo positivo variou de 52,7% a 64,8% e o valor preditivo negativo variou de 95,3% a 99,3%. A CK-MB atividade não se elevou em níveis compatíveis com IAM em 13,8% dos pacientes do grupo I, tendo ocorrido um resultado falso positivo no grupo II...