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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 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 COVID-19 (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 la cardiovascular fueron significativamente mayores en los pacientes con COVID-19: el 25 frente al 3,8% (p 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 COVID-19 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 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.

Resumen Introduccion y objetivos La ivabradina es un inhibidor de la corriente If, principal determinante de la funcion marcapasos del nodulo sinusal, aprobado como antianginoso y para tratar la insuficiencia cardiaca. Existen indicios sobre su capacidad para inhibir la conduccion a traves del nodulo auriculoventricular (NAV). Sobre esta base, el proyecto BRAKE-AF plantea el uso de ivabradina como agente cronotropico negativo en fibrilacion auricular (FA). Metodos Se realizara un ensayo clinico multicentrico de fase III, aleatorizado, abierto, en paralelo, con diseno 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 reduccion de la frecuencia cardiaca media diurna en un Holter de 24 h a los 3 meses. El ensayo se apoyara en un estudio electrofisiologico que analizara el efecto de la ivabradina en el potencial de accion del NAV humano, utilizando un modelo experimental en celulas de ovario de hamster chino transfectadas con el ADN que codifica la expresion de los distintos canales que componen dicho potencial de accion, registrando las corrientes ionicas mediante la tecnica del parche de membrana. Resultados Se obtendra informacion tanto del efecto de la ivabradina en las corrientes ionicas y el potencial de accion del NAV como de su eficacia y su seguridad en pacientes con FA permanente. Conclusiones Los resultados del proyecto BRAKE-AF podrian permitir que la ivabradina se incluyera en el limitado arsenal de farmacos disponibles actualmente para el control de frecuencia en la FA. Ensayo registrado en ClinicalTrials.gov (Identificador: NCT03718273).

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 .

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.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.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.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.

El uso de los stents recubiertos, mas alla de las recomendaciones de las guias de practica clinica, ha originado nuevas cuestiones que inicialmente no se habian tenido en cuenta. El principal problema que ha surgido es el de la trombosis del stent, la terapia necesaria para prevenirlo y la duracion de esta. Este fenomeno se ha clasificado temporalmente en trombosis precoz (cuando sucede dentro del primer mes), trombosis tardia (entre los 30 dias y un ano) y trombosis muy tardia (despues de un ano). 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 este despues de los 12 meses de su implantacion; ademas, antes de este periodo la trombosis del stent se ha relacionado especialmente con el abandono prematuro de la doble antiagregacion. Actualmente ha crecido el sentir de que despues de la implantacion de un stent recubierto es necesario mantener la doble antiagregacion durante un tiempo prolongado. La necesidad de tratamiento antiagregante durante periodos muy prolongados ha generado un especial interes, por el posible incremento del riesgo hemorragico y por el fenomeno de la resistencia a los antiagregantes. La causa fundamental de resistencia es una mala adhesion terapeutica, pero tambien, posiblemente, una variabilidad genetica a la respuesta de los antiagregantes; asimismo, un factor no menos importante seria el posible tratamiento concomitante con farmacos con un potencial efecto protrombotico. 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 investigacion clinica nuevos farmacos, que es posible que puedan paliar alguno de los problemas actuales de la doble antiagregacion mantenida a largo plazo.

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.

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.

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).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.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.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.

Varon de 71 anos, hipertenso y ex fumador con comorbilidad respiratoria y renal, presentaba estenosis aortica grave y sintomatica. Debido al alto riesgo quirurgico (EuroSCORE del 20,5%), se implanto una protesis aortica percutanea LOTUS Boston Scientific, via transfemoral, de manera eficaz y con profundidad adecuada. Se preciso el implante de un marcapasos definitivo por bloqueo auriculoventricular completo. Dos meses despues, ingreso en situacion de edema agudo de pulmon, y se ausculto un soplo sistolico V/VI en foco mitral de nueva aparicion. El ecocardiograma transtoracico mostro un velo mitral anterior engrosado y perforado que condicionaba una insuficiencia mitral grave (figuras 1A y B). En el ecocardiograma transesofagico se observaba un velo mitral anterior con ecogenicidad heterogenea y bordes irregulares, hallazgos compatibles con un absceso (video 1 del material suplementario). El anillo protesico aortico y sus velos se observaban engrosados con una estructura movil y filiforme compatible con vegetacion (figura 2A y video 2 del material suplementario). Ademas, se observaba una imagen vegetante en el cable de marcapasos (figura 2B y video 3 del material suplementario). En los hemocultivos seriados, se aislo Streptococus gallolyticus. Ante el diagnostico de endocarditis infecciosa protesica aortica precoz complicada con insuficiencia mitral grave por rotura valvular y endocarditis del cable de marcapasos, se presento el caso a cirugia cardiaca, que rechazo la opcion quirurgica debido al alto riesgo. El paciente fallecio a las 48 h en situacion de sepsis grave e insuficiencia cardiaca. La necropsia clinica corroboro el diagnostico (figura 3). Este es el primer caso conocido de endocarditis infecciosa en paciente portador de protesis aortica percutanea LOTUS.