Evaluation of the vasoactive-inotropic score, mid-regional pro-adrenomedullin and cardiac troponin I as predictors of low cardiac output syndrome in children after congenital heart disease surgery / Evaluación de la escala vasoactiva-inotrópica, pro-adrenomedulina y troponina cardiaca-I como factores predictivos del síndrome de bajo gasto cardiaco en niños tras corrección quirúrgica de cardiopatías congénitas

Objective: To determine the predictive value of the inotropic score (IS) and vasoactive-inotropic score (VIS) in low cardiac output syndrome (LCOS) in children after congenital heart disease surgery involving cardiopulmonary bypass (CPB), and to establish whether mid-regional pro-adrenomedullin (MR-proADM) and cardiac troponin I (cTn-I), associated to the IS and VIS scores, increases the predictive capacity in LCOS. Design: A prospective observational study was carried out. Setting: A Paediatric Intensive Care Unit. Patients: A total of 117children with congenital heart disease underwent CPB. Patients were divided into two groups: LCOS and non-LCOS. Interventions: The clinical and analytical data were recorded at 2, 12, 24 and 48h post-CPB. Logistic regression was used to develop a risk prediction model using LCOS as dependent variable. Main outcome measures: LCOS, IS, VIS, MR-proADM, cTn-I, age, sex, CPB time, PIM-2, Aristotle score. Results: While statistical significance was not recorded for IS in the multivariate analysis, VIS was seen to be independently associated to LCOS. On the other hand, VIS>15.5 at 2h post-CPB, adjusted for age and CPB timepoints, showed high specificity (92.87%; 95%CI: 86.75-98.96) and increased negative predictive value (75.59%, 95%CI: 71.1-88.08) for the diagnosis of LCOS at 48h post-CPB. The predictive power for LCOS did not increase when VIS was combined with cTn-I >14ng/ml at 2h and MR-proADM >1.5nmol/l at 24h post-CPB. Conclusions: The VIS score at 2h post-CPB was identified as an independent early predictor of LCOS. This predictive value was not increased when associated with LCOS cardiac biomarkers. The VIS score was more useful than IS post-CPB in making early therapeutic decisions in clinical practice post-CPB

Objetivo: Estudiar el valor predictivo de la escala inotrópica (IS) y la escala vasoactiva-inotrópica (VIS) en el síndrome de bajo gasto cardiaco (SBGC) en niños poscirugía de cardiopatías congénitas mediante bypass cardiopulmonar (BCP). Determinar si adrenomedulina (MR-proADM) y troponina cardiaca-I (cTn-I) asociadas con IS y VIS incrementan su capacidad predictora de SBGC. Diseño: Estudio prospectivo y observacional. Ámbito: Cuidados intensivos pediátricos. Pacientes: Ciento diecisiete pacientes pediátricos con cardiopatías congénitas corregidos mediante BCP, clasificados en función de la presencia o no de SBGC. Intervenciones: Los datos analíticos y clínicos se midieron a las 2, 12, 24 y 48h post-BCP. Las principales variables se analizaron mediante regresión logística multivariante, considerando SBGC como variable dependiente. Variables de interés principales: SBGC, IS, VIS, MR-proADM, cTn-I, edad, sexo, BCP, PIM-2 y escala Aristóteles. Resultados: El IS no alcanzó significación estadística en el estudio multivariante; sin embargo, el VIS se asoció independientemente a SBGC. El VIS>15,5 a las 2h del ingreso en CIP, ajustado por edad y tiempo de CEC, muestra alta especificidad (92,87%; IC 95%: 86,75-98,96%) y alto valor predictivo negativo (75,59%; IC 95%: 71,10-88,08) para predecir SBGC a las 48h post-BCP. La capacidad predictora no se incrementa al incorporar cTn-I>14ng/ml a las 2h y ADM>1,5nmol/l a las 24h del postoperatorio. Conclusiones: El VIS a las 2h post-BCP es un predictor independiente precoz de SBGC. Este valor no se incrementa al asociarse biomarcadores cardiacos de LCOS. La escala de VIS fue más útil que la escala de IS en la toma de decisiones terapéuticas tras la cirugía cardiaca

Are high-sensitivity troponins always reliable? Donor-recipient troponin transfusion in liver transplantation.

Blood troponins are used to diagnose perioperative myocardial injury and infarction. During liver transplantation, a passive donor-recipient troponin transfer with the graft may result in an increase of troponins in the transplant recipient questioning the diagnosis of myocardial injury. We present a case of liver transplantation with sudden elevation of recipient's serum troponin levels immediately after graft reperfusion and its subsequent normalization in which myocardial damage and other non-ischaemic potential causes were ruled out. Patient consent for publication was obtained prior to submission of the manuscript.

Understanding cardiac troponin part 2: early rule out of acute coronary syndrome.

Chest pain of suspected cardiac origin is a very common emergency department presentation. Over the past decade, there has been an exponential growth in strategies that promote blood sampling at earlier and earlier time points after presentation to facilitate the rule out of acute coronary syndrome.In part 2 of this series, we examine key concepts from the recent literature with the aim of improving clinicians' understanding of the rule-out strategies available to them and provide a structured overview of strategies that facilitate discharge with blood testing over <3 hours.

Troponinas de alta sensibilidad y pronóstico de la insuficiencia cardíaca / High-sensitivity troponins and prognosis of heart failure

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Troponina i en preeclampsia y eclampsia / Troponin i in preeclampsia and eclampsia

Objetivo. Comparar las concentraciones séricas de troponina i en eclámpticas, preeclámpticas y embarazadas normotensas sanas. Materiales y método. Se incluyeron 30 pacientes con preeclampsia leve (grupo A), 30 pacientes con preeclampsia grave (grupo B) y 30 pacientes con eclampsia (grupo C). El grupo control fue seleccionado por tener edad e índice de masa corporal similar con los grupos en estudio y consistió en 30 embarazadas normotensas sanas (grupo D). Solo se incluyeron pacientes nulíparas. Las muestras de suero se recolectaron antes del parto y en los grupos en estudio inmediatamente después del diagnóstico para la determinación de las concentraciones de troponina i. Resultados. Los valores más altos de troponina i fueron más elevados en el grupo de pacientes eclámpticas (0,171 ± 0,025 ng/ml) junto con las preeclámpticas graves (0,168 ± 0,024 ng/ml). Se encontraron valores más bajos en las preeclámpticas leves (0,123 ± 0,015 ng/ml). Los grupos en estudio presentaron valores de troponina i significativamente superiores que los controles (0,049 ± 0,034 ng/ml; p < 0,0001). El análisis de regresión lineal mostró que los factores que se relacionaban significativamente con las concentraciones séricas de troponina i fueron la proteinuria en 24 h y la creatinina (p < 0,05). Conclusión. Las pacientes eclámpticas y preeclámpticas presentan concentraciones séricas de troponina i más altas que las embarazadas normotensas sanas (AU)

Objective. To compare serum troponin i concentrations in eclamptic patients, preeclamptic patients, and normotensive pregnant women. Materials and method. We included 30 patients with mild preeclampsia (group A), 30 patients with severe preeclampsia (group B), and 30 patients with eclampsia (group C). A control group was selected with a similar age and body mass index to the study groups and consisted of 30 healthy normotensive pregnant women (group D). Only nulliparous women were included. Serum samples were collected from all patients before delivery and in the study groups immediately after diagnosis for troponin i determination. Results. Serum troponin i values were higher in eclamptic patients (0.171 ± 0.025 ng/mL) and in severe preeclamptic patients (0.168 ± 0.024 ng/mL) and were lower in mild preeclamptic patients (0.123 ± 0.015 ng/mL). Serum troponin i values were significantly higher in the study groups than in the control group (0.049 ± 0.034 ng/mL; P < .0001). Linear regression analysis revealed that the factors significantly related to serum troponin i concentrations were 24-hour proteinuria and creatinine (P < .05). Conclusion. Tropinin i concentrations were higher in eclamptic and preeclamptic patients than in healthy normotensive pregnant women without these complications (AU)

Determinación de troponina más allá del síndrome coronario agudo / Cardiac troponin beyond acute coronary syndrome

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Respuesta de los autores: Determinación de troponina más allá del síndrome coronario agudo / Author's reply: Cardiac troponin beyond acute coronary syndrome

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Correlação entre marcadores de injúria miocárdica, disfunção ventricular e mortalidade na sepsis / The correlation between markers for myocardial injury, ventricular dysfunction and mortality in sepsis

Introdução: O choque séptico é a principal causa de morte nas unidades de terapia intensiva, sendo a depressão miocárdica um importante fator causal nesse desfecho. Objetivo: Avaliar a função ventricular e o tipo de alteração contrátil (regional ou difusa) presentes em pacientes na fase aguda da sepsis e sua correlação com marcadores de injúrias miocárdica e mortalidade. Método: Foram estudados prospectiva e, consecutivamente, 45 pacientes sépticos, admitidos na unidade de terapia intensiva no período de 24 meses. Foi realizado um ecocardiograma transtorácico (ETT) na fase aguda da sepsis, junto com ecocardiograma (ECG) e dosagem sérica troponina I (TNI). Em um segundo momento, foram analisadas a frequência e a correlação das alterações funcionais ao ecocardiograma, da elevação da TNI e a taxa de mortalidade dos pacientes. O ETT foi repetido nos pacientes que sobreviveram após a resolução do quadro séptico. Resultados: Dos 45 pacientes estudados, o ECG mostrou alterações isquêmicas em 40% e o ecocardiograma apresentou alteração regional ou difusa em 44% dos pacientes estudados. A TNI esteve elevada em 53% dos pacientes, dos quais 77% apresentavam disfunção ventricular esquerda (DVE) na fase aguda da sepsis. O ETT evolutivo foi realizado em 24 pacientes (53%%), mostrando melhora parcial...

Nasal vaccination with troponin reduces troponin specific T-cell responses and improves heart function in myocardial ischemia-reperfusion injury.

Myocardial ischemia with subsequent reperfusion (MI/R) can lead to significant myocardial damage. Ischemia initiates inflammation at the blood-microvascular endothelial cell interface and contributes significantly to both acute injury and repair of the damaged tissue. We have found that MI/R injury in mice is associated with a cellular immune response to troponin. Myocardial cells exclusively synthesize troponin and release the troponin into the bloodstream following injury. Mucosally administered proteins induce T cells that secrete anti-inflammatory cytokines such as IL-10 and transforming growth factor beta at the anatomical site where the protein localizes. We found that nasal administration of the three subunits of troponin (C, I and T isoforms), given prior to or 1 h following MI/R, decreased infarct size by 40% measured 24 h later. At 1.5 months following MI/R, there was a 50% reduction in infarct size and improvement in cardiac function as measured by echocardiography. Protection was associated with a reduction of cellular immunity to troponin. Immunohistochemistry demonstrated increased IL-10 and reduced IFN-gamma in the area surrounding the ischemic infarct following nasal troponin. Adoptive transfer of CD4+ T cells to mice from nasally troponin-treated mice 1 h after the MI/R decreased infarct size by 72%, whereas CD4+ T cells from IL-10-/- mice or nasally BSA-treated mice had no effect. Our results demonstrate that IL-10-secreting CD4+ T cells induced by nasal troponin reduce injury following MI/R. Modulation of cardiac inflammation by nasal troponin provides a novel treatment to decrease myocardial damage and enhance recovery after myocardial ischemia.

Impacto dos níveis séricos da troponina I cardíaca na evolução tardia de pacientes submetidos a ressincronização com estimulação biventricular / Impact of serum levels of cardiac troponin I in later evolution of patients submited to resynchronization with biventricular simulation

Objetivo: Analisar evolução e a influência dos níveis séricos da troponina I cardíaca no prognóstico de pacientes com insuficiência cardíaca congestiva (ICC) submetidos a ressincronização biventricular. Método: 33 pacientes com miocardiopatia dilatada idiopática , classe funcional III/IV da NYHA, submetdios a ressincronização com estímulo biventricular, foram acompanhados por até 59 meses. A qualidade de vida (QV) foi avaliada no pré e pós-operatórios, utilizando-se o Minnesota Code, e a função ventricular foi analisada por meio de ecocardigrafia. Em 23 pacientes, os níveis séricos de troponina I foram dosados para verificar sua relação com o óbito (teste exato de Fisher) e analisar a taxa de sobrevivência (curva de Kaplan-Meier). Resultados: A QV mostrou-se significativamente melhor após a RV, com mediana de 73 pontos no pré e 36 pontos no pós-operatório (p menor que 0,0001). O diâmetro diastólico do VE(DDVE) reduziu-se de 65 mm para 60 mm após o implante (p igual a 0,0014) e a fração de ejeção (FEVE) aumentou de 37 por cento para 47 por cento (p igual a 0,0004). Não ocorreram óbitos entre os 15 pacientes com valores normais de troponina. Já entre os oito com valores elevados, seis vieram a falecer (p igual a 0,0003). A curva mostrou uma taxa de sobrevivência de 47,1 maior ou menor que 13,3 por cento ao final de 59 meses. Conclusões: Em pacientes com ICC, a ressincronização biventricular melhora os parâmetro ecocardiográficos (FEVE e DEVE) e a QV. Constitui uma boa alternativa para pacientes em classe funcional III/IV NYHA. Os níveis séricos elevados da troponina I cardíaca são preditores de risco para óbito.

El papel de las troponinas en el diagnóstico y el pronóstico de los síndromes coronarios agudos / The role of troponins in the diagnostic and prognostic evaluation of acute coronary syndromes

El diagnóstico de infarto de miocardio se ha facilitado con el uso de nuevos marcadores cardíacos. Entre los pacientes con un síndrome coronario agudo, pequeñas elevaciones de troponina T o I se correlacionan con un riesgo aumentado de muerte o recurrencia de eventos isquémicos en comparación con el de los pacientes con valores de troponina por debajo del límite de decisión. Sin embargo, este refinamiento en la capacidad de diagnóstico ocasiona nuevas cuestiones e incertidumbres debido a que las troponinas pueden elevarse en numerosas situaciones clínicas diferentes de las del infarto agudo de miocardio de origen trombótico. De cualquier forma, el aumento de las troponinas fuera del contexto de un infarto de miocardio también conlleva un peor pronóstico, de forma independiente del mecanismo por el que las troponinas son liberadas desde los miocitos a la circulación (AU)

The use of new cardiac markers has improved the diagnosis of acute myocardial infarction. Among patients presenting with an acute coronary syndrome, even a minor elevation in cardiac troponin-T or -I level correlates with an increased risk of death or recurrent ischemic event compared with that in patients with levels below the diagnostic cut-off limits. However, this refinement in diagnostic capability has generated new questions and uncertainties because elevated serum troponin levels have been observed in a number of clinical conditions other than acute myocardial infarction of thrombotic origin. As with acute myocardial infarction, an increase in serum cardiac troponin level in other settings also portends a poor prognosis, irrespective of the precise mechanism by which cardiac troponins are released from cardiac myocytes into the circulation (AU)

O papel das troponinas no infarto agudo do miocárdio / The role of troponin in the early diagnosis of acute myocardial infarction

Nos Estados Unidos, em 1997, dentre 550 mil pacientes com suspeita de infarto agudo do miocárdio, aproximadamente metade apresentou eletrocardiograma inalterado. Pesquisas realizadas demonstraram que isso aumenta o risco de morbidade e mortalidade após a alta hospitalar em pacientes com infarto agudo do miocárdio não-diagnosticado. Esse fato estimulou a pesquisa de novos marcadores sorológicos que fossem capazes de fornecer resultados cada vez mais precoces das agressões sofridas pelo organismo decorrentes de necroses das células miocárdicas ocorridas diante do infarto agudo do miocárdio. Uma das descobertas da atualidade foi a troponina, pela sua sensibilidade e especificidade...

Calcium-calmodulin-stimulated phosphorylation of rat parotid secretion granule proteins.

In studies designed to determine the mechanism by which Ca++ and calmodulin stimulate the fusion of parotid secretion granules with plasma membrane vesicles, the hypothesis tested was that Ca++ and calmodulin act by stimulating protein phosphorylation. It was earlier found that Ca++ and calmodulin, but neither alone, stimulated the phosphorylation of four secretion granule proteins with molecular masses of 64, 58, 55 and 31 kDa, and decreased the degree of phosphorylation of a 36-kDa protein. Further studies have shown that in the presence of an optimal concentration of calmodulin (2.4 microM), half-maximal activation of phosphorylation of the four proteins occurred at approx. 8 microM Ca++, and at a maximally effective Ca++ concentration (10(-4) M), half-maximal stimulation occurred at calmodulin concentrations between 0.13 and 1.1 microM for the different proteins. The studies now described also demonstrate that the need for calmodulin for stimulating the phosphorylation, but not the dephosphorylation, is specific; two other Ca(++)-binding proteins, parvalbumin and troponin, could not replace calmodulin in stimulating phosphorylation of the four secretion granule proteins, but either one could substitute for calmodulin in stimulating dephosphorylation of the 36-kDa protein. Additionally, the phosphorylated proteins appear to be located on the granule surface. When secretion granules were subjected to mild treatment with a concentration of trypsin that did not lyse the granules, the 31-, 36-, 55-, 58- and 64-kDa proteins were no longer observed. In the presence of optimal concentrations of Ca++ and calmodulin, a dose-dependent inhibition of the phosphorylation of the various proteins by two calmodulin antagonists, trifluoperazine and calmidazolium, was observed; 50% inhibition of phosphorylation of the different proteins was obtained at approx. 20-40 microM trifluoperazine and at about 2.5-3.0 microM calmidazolium. Inhibition of the dephosphorylation of the 36-kDa protein required greater concentrations of trifluoperazine and calmidazolium; 128 microM and 50 microM, respectively. These results are consistent with the hypothesis that the phosphorylation of one or more of the 31-, 55-, 58- and 64-kDa proteins, but not the dephosphorylation of the 36-kDa protein, may be involved in the action of Ca++ and calmodulin in secretion granule-plasma membrane fusion.

Molecular basis of depression of Ca2+ sensitivity of tension by acid pH in cardiac muscles of the mouse and the rat.

BACKGROUND: Acid pH decreases the Ca2+ sensitivity of myocardial tension generation, and recent studies have suggested that regulatory proteins are involved. The current study defines the molecular basis of this effect on troponin C (TnC) and troponin I (TnI) and also addresses previous differences between the rat and mouse. METHODS AND RESULTS: Endogenous cardiac TnC and cardiac TnI in isolated trabeculae from mice and rats were exchanged with their fast-twitch skeletal muscle counterparts. A cardiac-skeletal TnC chimera was used to define the target region for proton action on cardiac TnC. Finally, cardiac TnC and skeletal TnC were genetically modified by insertion of a tryptophan for phenylalanine-26 to probe the pH effects with fluorescence spectroscopy. The pH 6.2 effects on Ca2+ sensitivity of force development in mouse and rat cardiotrabeculae are largely accounted for by the proton influences on TnC (23%) and TnI (53%). In cardiac TnC, residues 1 to 41 provide the target region. Comparison of the Ca(2+)-induced fluorescence in isolated cardiac TnC and skeletal TnC also indicated a greater pH effect in the cardiac isoform. CONCLUSIONS: The studies provide firm evidence that both TnC and TnI moieties are involved in the mechanism of acidosis causing reduction in the Ca sensitivity of force development in the myocardium. The findings rule out the possibility of interspecies variations in the underlying mechanisms. The genetically designed TnCs and a chimera demonstrate that the observed TnC-mediated difference in the pH effects on Ca2+ sensitivity of tension between cardiac and skeletal muscles is preserved in these isolated proteins. The N-terminal amino acid residues 1 to 41 in cardiac TnC are established as the pH sensor of this protein in the mouse as in the rat.