Factores de riesgo de muerte hospitalaria en pacientes con infarto agudo de miocardio durante la pandemia de la COVID-19 / Risk factors for in-hospital mortality in patients with acute myocardial infarction during the COVID-19 outbreak

INTRODUCCIÓN Y OBJETIVOS: A pesar de los avances en el tratamiento del infarto agudo de miocardio (IAM), este sigue presentando un pronóstico desfavorable. Hay poca evidencia acerca de la evolución de los pacientes con IAM y la enfermedad coronavírica de 2019 (COVID-19). El objetivo del estudio es describir la presentación clínica, las complicaciones y los factores predictores de mortalidad hospitalaria en pacientes con IAM durante el brote de COVID-19 en España. MÉTODOS: Se realizó un estudio de cohortes, prospectivo y multicéntrico de todos los pacientes consecutivos con IAM en tratamiento invasivo durante el brote de COVID19 (15 de marzo a 15 de abril de 2020). Se compararon las características clínicas de los pacientes positivos para COVID-19 con las de los negativos, y se evaluó el efecto de la COVID-19 en la mortalidad mediante emparejamiento por puntuación de propensión y regresión logística. RESULTADOS: Se incluyó a 187 pacientes con IAM: 111 con elevación del segmento ST y 76 sin elevación. De ellos, 32 (17%) resultaron positivos para COVID-19. Las puntuaciones GRACE y Killip-Kimball y varios marcadores inflamatorios resultaron significativamente mayores en los pacientes con COVID-19. La mortalidad total y cardiovascular fueron significativamente mayores en los pacientes con COVID-19 (el 25 frente al 3,8%; p < 0,001; y el 15,2 frente al 1,8%; p = 0,001). La puntuación GRACE > 140 (OR = 23,45; IC95%, 2,52-62,51; p = 0,005) y la COVID-19 (OR = 6,61; IC95%, 1,82-24,43; p = 0,02) resultaron factores independientes de mortalidad hospitalaria. CONCLUSIONES: Durante el brote epidémico, la puntuación GRACE elevada y la COVID19 fueron los factores independientes de mortalidad hospitalaria en los pacientes con IAM

INTRODUCTION AND OBJECTIVES: Despite advances in treatment, patients with acute myocardial infarction (AMI) still exhibit unfavorable short- and long-term prognoses. In addition, there is scant evidence about the clinical outcomes of patients with AMI and coronavirus disease 2019 (COVID-19). The objective of this study was to describe the clinical presentation, complications, and risk factors for mortality in patients admitted for AMI during the COVID-19 pandemic. METHODS: This prospective, multicenter, cohort study included all consecutive patients with AMI who underwent coronary angiography in a 30-day period corresponding chronologically with the COVID-19 outbreak (March 15 to April 15, 2020). Clinical presentations and outcomes were compared between COVID-19 and non-COVID-19 patients. The effect of COVID-19 on mortality was assessed by propensity score matching and with a multivariate logistic regression model. RESULTS: In total, 187 patients were admitted for AMI, 111 with ST-segment elevation AMI and 76 with non-ST-segment elevation AMI. Of these, 32 (17%) were diagnosed with COVID-19. GRACE score, Killip-Kimball classification, and several inflammatory markers were significantly higher in COVID-19-positive patients. Total and cardiovascular mortality were also significantly higher in COVID-19-positive patients (25% vs 3.8% [P < .001] and 15.2% vs 1.8% [P = .001], respectively). GRACE score > 140 (OR, 23.45; 95%CI, 2.52-62.51; P = .005) and COVID-19 (OR, 6.61; 95%CI, 1.82-24.43; P = .02) were independent predictors of in-hospital death. CONCLUSIONS: During this pandemic, a high GRACE score and COVID-19 were independent risk factors associated with higher in-hospital mortality

[Risk factors for in-hospital mortality in patients with acute myocardial infarction during the COVID-19 outbreak]. / Factores de riesgo de muerte hospitalaria en pacientes con infarto agudo de miocardio durante la pandemia de la COVID-19.

INTRODUCTION AND OBJECTIVES: Despite advances in treatment, patients with acute myocardial infarction (AMI) still exhibit unfavorable short- and long-term prognoses. In addition, there is scant evidence about the clinical outcomes of patients with AMI and coronavirus disease 2019 (COVID-19). The objective of this study was to describe the clinical presentation, complications, and risk factors for mortality in patients admitted for AMI during the COVID-19 pandemic. METHODS: This prospective, multicenter, cohort study included all consecutive patients with AMI who underwent coronary angiography in a 30-day period corresponding chronologically with the COVID-19 outbreak (March 15 to April 15, 2020). Clinical presentations and outcomes were compared between COVID-19 and non-COVID-19 patients. The effect of COVID-19 on mortality was assessed by propensity score matching and with a multivariate logistic regression model. RESULTS: In total, 187 patients were admitted for AMI, 111 with ST-segment elevation AMI and 76 with non-ST-segment elevation AMI. Of these, 32 (17%) were diagnosed with COVID-19. GRACE score, Killip-Kimball classification, and several inflammatory markers were significantly higher in COVID-19-positive patients. Total and cardiovascular mortality were also significantly higher in COVID-19-positive patients (25% vs 3.8% [P < .001] and 15.2% vs 1.8% [P = .001], respectively). GRACE score > 140 (OR, 23.45; 95%CI, 2.52-62.51; P = .005) and COVID-19 (OR, 6.61; 95%CI, 1.82-24.43; P = .02) were independent predictors of in-hospital death. CONCLUSIONS: During this pandemic, a high GRACE score and COVID-19 were independent risk factors associated with higher in-hospital mortality.Full English text available from:www.revespcardiol.org/en.

Risk factors for in-hospital mortality in patients with acute myocardial infarction during the COVID-19 outbreak.

INTRODUCTION AND OBJECTIVES: Despite advances in treatment, patients with acute myocardial infarction (AMI) still exhibit unfavorable short- and long-term prognoses. In addition, there is scant evidence about the clinical outcomes of patients with AMI and coronavirus disease 2019 (COVID-19). The objective of this study was to describe the clinical presentation, complications, and risk factors for mortality in patients admitted for AMI during the COVID-19 pandemic. METHODS: This prospective, multicenter, cohort study included all consecutive patients with AMI who underwent coronary angiography in a 30-day period corresponding chronologically with the COVID-19 outbreak (March 15 to April 15, 2020). Clinical presentations and outcomes were compared between COVID-19 and non-COVID-19 patients. The effect of COVID-19 on mortality was assessed by propensity score matching and with a multivariate logistic regression model. RESULTS: In total, 187 patients were admitted for AMI, 111 with ST-segment elevation AMI and 76 with non-ST-segment elevation AMI. Of these, 32 (17%) were diagnosed with COVID-19. GRACE score, Killip-Kimball classification, and several inflammatory markers were significantly higher in COVID-19-positive patients. Total and cardiovascular mortality were also significantly higher in COVID-19-positive patients (25% vs 3.8% [P <.001] and 15.2% vs 1.8% [P=.001], respectively). GRACE score> 140 (OR, 23.45; 95%CI, 2.52-62.51; P=.005) and COVID-19 (OR, 6.61; 95%CI, 1.82-24.43; P=.02) were independent predictors of in-hospital death. CONCLUSIONS: During this pandemic, a high GRACE score and COVID-19 were independent risk factors associated with higher in-hospital mortality.

Ivabradina para el control crónico de la frecuencia cardiaca en fibrilación auricular permanente. Diseño del proyecto BRAKE-AF / Ivabradine for chronic heart rate control in persistent atrial fibrillation. Design of the BRAKE-AF project

INTRODUCCIÓN Y OBJETIVOS: La ivabradina es un inhibidor de la corriente If, principal determinante de la función marcapasos del nódulo sinusal, aprobado como antianginoso y para tratar la insuficiencia cardiaca. Existen indicios sobre su capacidad para inhibir la conducción a través del nódulo auriculoventricular (NAV). Sobre esta base, el proyecto BRAKE-AF plantea el uso de ivabradina como agente cronotrópico negativo en fibrilación auricular (FA). MÉTODOS: Se realizará un ensayo clínico multicéntrico de fase III, aleatorizado, abierto, en paralelo, con diseño de no inferioridad, para comparar la ivabradina frente a la digoxina en 232 pacientes con FA permanente no controlada con bloqueadores beta o antagonistas del calcio; el objetivo primario es la reducción de la frecuencia cardiaca media diurna en un Holter de 24 h a los 3 meses. El ensayo se apoyará en un estudio electrofisiológico que analizará el efecto de la ivabradina en el potencial de acción del NAV humano, utilizando un modelo experimental en células de ovario de hámster chino transfectadas con el ADN que codifica la expresión de los distintos canales que componen dicho potencial de acción, registrando las corrientes iónicas mediante la técnica del parche de membrana. RESULTADOS: Se obtendrá información tanto del efecto de la ivabradina en las corrientes iónicas y el potencial de acción del NAV como de su eficacia y su seguridad en pacientes con FA permanente. CONCLUSIONES: Los resultados del proyecto BRAKE-AF podrían permitir que la ivabradina se incluyera en el limitado arsenal de fármacos disponibles actualmente para el control de frecuencia en la FA

INTRODUCTION AND OBJECTIVES: Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). METHODS: A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. RESULTS: New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. CONCLUSIONS: The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF

Infarto agudo de miocardio secundario a infección por Plasmodium ovale / Acute myocardial infarction secondary to infection by Plasmodium ovale

No disponible

Ivabradine for chronic heart rate control in persistent atrial fibrillation. Design of the BRAKE-AF project.

INTRODUCTION AND OBJECTIVES: Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). METHODS: A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. RESULTS: New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. CONCLUSIONS: The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.gov. Identifier: NCT03718273.

Endocarditis infecciosa en paciente con prótesis aórtica percutánea LOTUS / Infective endocarditis in a patient with a transcatheter LOTUS valve

No disponible

Electrocardiographic changes during induced therapeutic hypothermia in comatose survivors after cardiac arrest.

AIM: To assess the safety of therapeutic hypothermia (TH) concerning arrhythmias we analyzed serial electrocardiograms (ECG) during TH. METHODS: All patients recovered from a cardiac arrest with Glasgow < 9 at admission were treated with induced mild TH to 32-34 °C. TH was obtained with cool fluid infusion or a specific intravascular device. Twelve-lead ECG before, during, and after TH, as well as ECG telemetry data was recorded in all patients. From a total of 54 patients admitted with cardiac arrest during the study period, 47 patients had the 3 ECG and telemetry data available. ECG analysis was blinded and performed with manual caliper by two independent cardiologists from blinded copies of original ECG, recorded at 25 mm/s and 10 mm/mV. Coronary care unit staff analyzed ECG telemetry for rhythm disturbances. Variables measured in ECG were rhythm, RR, PR, QT and corrected QT (QTc by Bazett formula, measured in lead v2) intervals, QRS duration, presence of Osborn's J wave and U wave, as well as ST segment displacement and T wave amplitude in leads II, v2 and v5. RESULTS: Heart rate went down an average of 19 bpm during hypothermia and increased again 16 bpm with rewarming (P < 0.0005, both). There was a non-significant prolongation of the PR interval during TH and a significant decrease with rewarming (P = 0.041). QRS duration significantly prolonged (P = 0.041) with TH and shortened back (P < 0.005) with rewarming. QTc interval presented a mean prolongation of 58 ms (P < 0.005) during TH and a significant shortening with rewarming of 22.2 ms (P = 0.017). Osborn or J wave was found in 21.3% of the patients. New arrhythmias occurred in 38.3% of the patients. Most frequent arrhythmia was non-sustained ventricular tachycardia (19.1%), followed by severe bradycardia or paced rhythm (10.6%), accelerated nodal rhythm (8.5%) and atrial fibrillation (6.4%). No life threatening arrhythmias (sustained ventricular tachycardia, polymorphic ventricular tachycardia or ventricular fibrillation) occurred during TH. CONCLUSION: A 38.3% of patients had cardiac arrhythmias during TH but without life-threatening arrhythmias. A concern may rise when inducing TH to patients with long QT syndrome.

Computerized physician order entry in the cardiac intensive care unit: effects on prescription errors and workflow conditions.

PURPOSES: To evaluate the effects of a computerized physician order entry (CPOE) system in the cardiac intensive care unit by detecting prescription errors (PEs) and also to assess the impact on working conditions. METHODS: A longitudinal, prospective, before-after study was conducted during the periods before and after the implementation of the CPOE system. Clinical pharmacists were responsible for the registration, description and classification of PEs, and their causes and severity, according to an international taxonomy. Professionals were also surveyed for their opinion, concerns, and level of satisfaction. RESULTS: A total of 470 treatment orders containing 5729 prescriptions were evaluated. The CPOE resulted in a marked reduction in the number of PEs: error rate was 44.8% (819 errors among 1829 prescriptions) with handwritten orders and 0.8% (16 among 2094 prescriptions) at the final electronic phase (P < .001). Lapses were the main cause of error in both prescription methods. Most errors did not reach the patients. Errors related with the computerized system were scarce. Most users were satisfied with many aspects of this technology, although a higher workload was reported. CONCLUSIONS: Computerized physician order entry in the cardiac intensive care unit proved to be a safe and effective strategy in reducing PEs and was globally well received by professionals.

Obstructive sleep apnea and coronary artery disease: from pathophysiology to clinical implications.

Coronary artery disease (CAD) and obstructive sleep apnea (OSA) are both complex and significant clinical problems. The pathophysiological mechanisms that link OSA with CAD are complex and can influence the broad spectrum of conditions caused by CAD, from subclinical atherosclerosis to myocardial infarction. OSA remains a significant clinical problem among patients with CAD, and evidence suggesting its role as a risk factor for CAD is growing. Furthermore, increasing data support that CAD prognosis may be influenced by OSA and its treatment by continuous positive airway pressure (CPAP) therapy. However, stronger evidence is needed to definitely answer these questions. This paper focuses on the relationship between OSA and CAD from the pathophysiological effects of OSA in CAD, to the clinical implications of OSA and its treatment in CAD patients.

Do patients with ST segment elevation myocardial infarction in Killip class I need intensive cardiac care after a successful primary percutaneous intervention?

BACKGROUND AND OBJECTIVE: There are limited data regarding the need for intensive care or the appropriate length of hospital stay for patients with ST elevation acute myocardial infarction (STEMI). In order to optimize resources, we tried to determine the need of coronary care unit (CCU) admission for patients with STEMI who remained in Killip class I after a successful primary percutaneous coronary intervention (PPCI). METHODS: From August of 2006 till June of 2008, we analyzed data from all patients admitted in our CCU who met these criteria, a total of 278. We prospectively recorded all in-hospital adverse events and event-free survival at 30 and 90 days (all cause death, stroke, new acute coronary syndrome or re-hospitalization due to heart failure). Medical treatment was optimized according to the current guidelines. RESULTS: A coronary stent was implanted in 96% of the patients. None of the patients had any adverse event that could not be resolved in a step-down unit. Survival at 30 and at 90 days was 99.6% and 98.3% respectively. Event-free survival was 97.3% at 30 days and 94.3% at 90 days. The median length of stay was three days in the CCU and five days in the hospital. CONCLUSION: Patients with STEMI treated with PPCI who remained in Killip class I after the procedure and receive optimal pharmacological treatment have an excellent prognosis. All of them can probably be admitted safely to a step-down unit. Wide application of this management strategy may result in substantial cost savings.

Cuestiones planteadas con el tratamiento antiplaquetario en los pacientes portadores de stents recubiertos / Problems associated with antiplatelet treatment in patients with drug-eluting stents

El uso de los stents recubiertos, más allá de las recomendaciones de las guías de práctica clínica, ha originado nuevas cuestiones que inicialmente no se habían tenido en cuenta. El principal problema que ha surgido es el de la trombosis del stent, la terapia necesaria para prevenirlo y la duración de ésta. Este fenómeno se ha clasificado temporalmente en trombosis precoz (cuando sucede dentro del primer mes), trombosis tardía (entre los 30 días y un año) y trombosis muy tardía (después de un año). Actualmente, se ha puesto de manifiesto que es posible que los pacientes a los que se ha implantado un stent recubierto puedan tener trombosis de éste después de los 12 meses de su implantación; además, antes de este período la trombosis del stent se ha relacionado especialmente con el abandono prematuro de la doble antiagregación. Actualmente ha crecido el sentir de que después de la implantación de un stent recubierto es necesario mantener la doble antiagregación durante un tiempo prolongado. La necesidad de tratamiento antiagregante durante períodos muy prolongados ha generado un especial interés, por el posible incremento del riesgo hemorrágico y por el fenómeno de la resistencia a los antiagregantes. La causa fundamental de resistencia es una mala adhesión terapéutica, pero también, posiblemente, una variabilidad genética a la respuesta de los antiagregantes; asimismo, un factor no menos importante sería el posible tratamiento concomitante con fármacos con un potencial efecto protrombótico. Posiblemente, la resistencia a los antiagregantes puede tratarse mediante un incremento de las dosis de antiagregantes, aunque no hay muchos datos sobre su seguridad a largo plazo. Por otra parte, se encuentran en fase de investigación clínica nuevos fármacos, que es posible que puedan paliar alguno de los problemas actuales de la doble antiagregación mantenida a largo plazo (AU)

The use of drug-eluting stents outside of clinical practice guideline recommendations has given rise to novel concerns that were not initially taken into account. The main problem that has arisen is stent thrombosis, and the type and duration of therapy necessary to prevent it. This phenomenon is classified as either early (i.e., occurring in the first month), late (i.e., occurring between the 30th day and one year), or very late thrombosis (i.e., occurring after one year). In fact, it has become clear that stent thrombosis can occur more than 12 months after implantation of a drug-eluting stent. However, stent thrombosis occurring before this time has been associated, in particular, with the premature discontinuation of dual antiplatelet therapy. In fact, it is increasingly felt that dual antiplatelet therapy must be maintained for a prolonged period after implantation of a drug-eluting stent. This need to continue antiplatelet therapy for a prolonged period of time has led to specific concerns about the risk of hemorrhage and the development of antiplatelet resistance. The main cause of antiplatelet resistance is poor compliance with therapy, though it may also be associated with genetic variability in antiplatelet responses and, of no less importance, concomitant treatment with drugs that have a potential prothrombotic effect. Probably, antiplatelet resistance can be managed by increasing the antiplatelet dosage, though few data exist on the long-term safety of this approach. On the other hand, clinical research is taking place into new drugs that could ameliorate some of current problems associated with long-term dual antiplatelet therapy (AU)

[Risk stratification using combined ECG, clinical, and biochemical assessment in patients with chest pain without ST-segment elevation. How long should we wait? ]. / Estratificación de riesgo en pacientes con dolor torácico sin ascenso persistente del segmento ST basado en variables clínicas, ECG y bioquímicas. ¿Cuánto tiempo debemos esperar?

INTRODUCTION: We use clinical, ECG, and biochemical data to stratify risk in patients with chest pain without ST segment elevation. However, the prognostic performance of these studies in relation to time from onset of symptoms is unknown. PATIENTS AND METHOD: In a single-center, prospective study, 321 consecutive patients who had been admitted in the emergency room with a suspected acute coronary syndrome without ST segment elevation were included in the study. Blood samples were collected for CK, CK-MB mass, myoglobin, and cardiac troponin T analysis 6, 12 and 18 hours after the onset of pain and other clinical and ECG data were recorded. Univariate and multivariate analysis was used to identify independent prognostic predictors 6 and 12 hours after the onset of chest pain. RESULTS: Five variables were independent predictors of the recurrence of ischemia. The model correctly classified 82% of the patients. Age, history of coronary artery disease, prolonged chest pain at rest in the preceding 15 days, pain, ST-segment changes with pain, and cardiac troponin T in excess of 0.1 ng/m 12 hours after the onset of chest pain were identified by logistic regression. A similar model was analyzed at 6 hours, after changing the cutoff point for cardiac troponin T. Cardiac troponin T was considered positive with values of 0.04 ng/ml 6 hours after the onset of chest pain. CONCLUSIONS: More than 80% of the patients admitted to the emergency room with chest pain without ST segment elevation can be correctly classified for new ischemic recurrences using clinical, ECG, and biochemical parameters 6 hours after the onset of pain.

Estratificación de riesgo en pacientes con dolor torácico sin ascenso persistente del segmento ST basado en variables clínicas, ECG y bioquímicas. ¿Cuánto tiempo debemos esperar? / Risk stratification using combined ECG, clinical, and biochemical assessment in patients with chest pain without ST-Segment elevation. How long should we wait?

Introducción. Utilizamos datos clínicos, ECG y bioquímicos en la estratificación pronóstica inicial de los pacientes con dolor torácico sin ascenso persistente del segmento ST. Su rendimiento pronóstico global, basado en el tiempo desde el inicio de los síntomas, no ha sido estudiado .Pacientes y método. Estudio unicéntrico y prospectivo de 321 pacientes consecutivos que acudieron a urgencias con sospecha de síndrome coronario agudo sin ascenso persistente del segmento ST y menos de 12 h de evolución. Se determinaron la creatincinasa (CK), la CKMB masa, la mioglobina y la troponina T cardíaca a las 6, 12 y 18 h desde el inicio del cuadro. Analizamos de manera uni y multivariada las variables clínicas, ECG y bioquímicas para identificar predictores pronósticos independientes a las 6 y 12 h, valorando el rendimiento pronóstico global. Resultados. En el análisis de regresión logística, 5 variables obtenidas resultaron predictoras independientes para nuevos acontecimientos cardiovasculares y permitieron clasificar correctamente al 82 por ciento de los pacientes: edad, cardiopatía isquémica previa, dolor prolongado en los 15 días previos, dolor y cambios del segmento ST con dolor y troponina T superior a 0,1 ng/ml a las 12 h del inicio del dolor. La troponina T, considerada positiva con valores superiores a 0,04 ng/ml a las 6 h, permite un modelo a las 6 h similar al de las 12 h. Conclusiones. Es posible identificar correctamente la evolución clínica de más del 80 por ciento de los pacientes que ingresan con dolor torácico sin ascenso del segmento ST con variables clínicas, ECG y bioquímicas en el plazo de 6 h desde el inicio del cuadro (AU)

[Utility of the serum biochemical markers CPK, CPK MB mass, myoglobin, and cardiac troponin T in a chest pain unit. Which marker determinations should be requested and when?]. / Utilidad clínica de los distintos marcadores biológicos CPK, CPK MB masa, mioglobina y troponina T en una unidad de dolor torácico. Cuándo, cuáles y cómo pedirlos?

BACKGROUND: The prognostic value of biochemical markers in relation to time since onset of chest pain was evaluated in an emergency room with a chest pain unit. METHODS: In a single-center, prospective study we included 321 consecutive patients admitted to the emergency room with suspected unstable angina IIIB and an evolution of less than 12 hours. Blood samples were collected for CPK, CPK MB mass, myoglobin, and cardiac troponin T assays 6, 12, and 18 h after the onset of pain. ROC curve analysis was carried out to compare biochemical markers in terms of cutoff values and time since onset of pain. We determined the relation between prognosis and biochemical markers before and after adjustment for baseline characteristics. RESULTS: CPK mass and myoglobin showed the maximum sensitivity and specificity for new ischemic recurrences 6 hours after the onset of chest pain with laboratory cutoff values. We had to wait 12 h after the onset of pain for troponin T to be useful using the laboratory cutoff value (0.1 ng/ml). A single determination 6 hours after onset of chest pain of cardiac troponin T above 0.04 ng/ml was the most sensitive and specific marker for new ischemic recurrences. CONCLUSIONS: A single blood determination of cardiac troponin T 6 hours after the onset of chest pain complete the prognostic stratification in combination with clinical and ECG variables. The best cutoff point of cardiac troponin T, based on univariate and multivariate analysis, was 0.04 ng/ml 6 h after the onset of chest pain.

Utilidad clínica de los distintos marcadores biológicos CPK, CPK MB masa, mioglobina y troponina T en una unidad de dolor torácico. ¿Cuándo, cuáles y cómo pedirlos? / Utility of the serum biochemical markers CPK, CPK MB mass, myoglobin, and cardiac troponin T in a chest pain unit. Which marker determinations should be requested and when?

Objetivos. Se pretende evaluar el rendimiento pronóstico de los marcadores bioquímicos en pacientes que consultan en un servicio de urgencias con una unidad de dolor torácico. Métodos. Estudio monocéntrico y prospectivo de 321 pacientes consecutivos con sospecha de angina inestable IIIB y menos de 12 h de evolución. Se analizó CPK, CPK MB masa, mioglobina y troponina cardíaca T a las 6, 12 y 18 h del inicio del cuadro. Se comparó la utilidad pronostica según el punto de corte y tiempo de evolución de los síntomas, analizando la concordancia entre las determinaciones y comprobando su valor independiente mediante análisis multivariado de regresión logística. Resultados. La CPK masa y la mioglobina alcanzaron las máximas sensibilidad y especificidad para nuevos episodios isquémicos en los límites del laboratorio a las 6 h, no así en la troponina T, en la que hay que esperar a las 12 h con los límites prefijados por el laboratorio. Un punto de corte de troponina cardíaca T superior a 0,04 ng/ml a las 6 h del dolor torácico se convierte en la variable aislada con una mayor relación sensibilidad-especificidad para nuevos episodios isquémicos y aporta, además, una excelente concordancia con la determinación a las 12 h. Conclusiones. Una única determinación bioquímica de troponina T a las 6 h del inicio del dolor torácico parece suficiente para completar la estratificación pronostica añadiéndola a variables clínicas y de electrocardiograma. El mejor punto de corte pronóstico de troponina T se sitúa en 0,04 ng/ml a las 6 h del inicio del dolor torácico (AU)