Panoramic Endocardial Optical Mapping Demonstrates Serial Rotors Acceleration and Increasing Complexity of Activity During Onset of Cholinergic Atrial Fibrillation.

BACKGROUND: Activation during onset of atrial fibrillation is poorly understood. We aimed at developing a panoramic optical mapping system for the atria and test the hypothesis that sequential rotors underlie acceleration of atrial fibrillation during onset. METHODS AND RESULTS: Five sheep hearts were Langendorff perfused in the presence of 0.25 μmol/L carbachol. Novel optical system recorded activations simultaneously from the entire left and right atrial endocardial surfaces. Twenty sustained (>40 s) atrial fibrillation episodes were induced by a train and premature stimuli protocol. Movies obtained immediately (Initiation stage) and 30 s (Early Stabilization stage) after premature stimulus were analyzed. Serial rotor formation was observed in all sustained inductions and none in nonsustained inductions. In sustained episodes maximal dominant frequency increased from (mean±SD) 11.5±1.74 Hz during Initiation to 14.79±1.30 Hz at Early Stabilization (P<0.0001) and stabilized thereafter. At rotor sites, mean cycle length (CL) during 10 prerotor activations increased every cycle by 0.53% (P=0.0303) during Initiation and 0.34% (P=0.0003) during Early Stabilization. In contrast, CLs at rotor sites showed abrupt decreases after the rotors appearances by a mean of 9.65% (P<0.0001) during both stages. At Initiation, atria-wide accelerations and decelerations during rotors showed a net acceleration result whereby post-rotors atria-wide minimal CL (CLmin) were 95.5±6.8% of the prerotor CLmin (P=0.0042). In contrast, during Early Stabilization, there was no net acceleration in CLmin during accelerating rotors (prerotor=84.9±11.0% versus postrotor=85.8±10.8% of Initiation, P=0.4029). Levels of rotor drift distance and velocity correlated with atria-wide acceleration. Nonrotor phase singularity points did not accelerate atria-wide activation but multiplied during Initiation until Early Stabilization. Increasing number of singularity points, indicating increased complexity, correlated with atria-wide CLmin reduction (P<0.0001). CONCLUSIONS: Novel panoramic optical mapping of the atria demonstrates shortening CL at rotor sites during cholinergic atrial fibrillation onset. Atrial fibrillation acceleration toward Early Stabilization correlates with the net result of atria-wide accelerations during drifting rotors activity.post-print3906 K

Spectral analysis-based risk score enables early prediction of mortality and cerebral performance in patients undergoing therapeutic hypothermia for ventricular fibrillation and comatose status

Background: Early prognosis in comatose survivors after cardiac arrest due to ventricular fibrillation (VF) is unreliable, especially in patients undergoing mild hypothermia. We aimed at developing a reliable risk-score to enable early prediction of cerebral performance and survival. Methods: Sixty-one out of 239 consecutive patients undergoing mild hypothermia after cardiac arrest, with eventual return of spontaneous circulation (ROSC), and comatose status on admission fulfilled the inclusion criteria. Background clinical variables, VF time and frequency domain fundamental variables were considered. The primary and secondary outcomes were a favorable neurological performance (FNP) during hospitalization and survival to hospital discharge, respectively. The predictive model was developed in a retrospective cohort (n = 32; September 2006 September 2011, 48.5 ± 10.5 months of follow-up) and further validated in a prospective cohort (n = 29; October 2011 July 2013, 5 ± 1.8 months of follow-up). Results: FNP was present in 16 (50.0%) and 21 patients (72.4%) in the retrospective and prospective cohorts, respectively. Seventeen (53.1%) and 21 patients (72.4%), respectively, survived to hospital discharge. Both outcomes were significantly associated (p &lt; 0.001). Retrospective multivariate analysis provided a prediction model (sensitivity = 0.94, specificity = 1) that included spectral dominant frequency, derived power density and peak ratios between high and low frequency bands, and the number of shocks delivered before ROSC. Validation on the prospective cohort showed sensitivity = 0.88 and specificity = 0.91. A model-derived risk-score properly predicted 93% of FNP. Testing the model on follow-up showed a c-statistic &#8805; 0.89. Conclusions: A spectral analysis-based model reliably correlates time-dependent VF spectral changes with acute cerebral injury in comatose survivors undergoing mild hypothermia after cardiac arrest.the CNIC is supported by the Spanish Ministry of Economy and Competitiveness and the Pro-CNIC Foundation.Filgueiras-Rama, D.; Calvo Saiz, CJ.; Salvador-Montañés, Ó.; Cádenas, R.; Ruiz-Cantador, J.; Armada, E.; Rey, JR.... (2015). Spectral analysis-based risk score enables early prediction of mortality and cerebral performance in patients undergoing therapeutic hypothermia for ventricular fibrillation and comatose status. International Journal of Cardiology. 186:250-258. doi:10.1016/j.ijcard.2015.03.074S25025818

Diagnostic protocol for bradyarrhythmias in the emergency department

El enlentecimiento de la conducción del estímulo eléctrico puede producirse a cualquier nivel del sistema específico de conducción. Se denomina bradiarritmia o bradicardia a cualquier ritmo cardíaco con una frecuencia cardíaca (FC) por debajo de 60 lpm. El sustrato anatómico y eléctrico puede localizarse en el nodo sinusal, nodo auriculoventricular y sistema His-Purkinje. El espectro de presentación clínica es muy amplio, desde un hallazgo electrocardiográfico en pacientes asintomáticos, hasta situaciones potencialmente mortales que requieren una actuación rápida y certera. En el abordaje diagnóstico y la estratificación del riesgo de las bradiarritmias en urgencias es imprescindible constatar la situación hemodinámica en la evaluación inicial, ya que la necesidad y la urgencia de la actuación terapéutica vendrán determinadas por la misma. Protocolizar el diagnóstico clínico y establecer un algoritmo electrocardiográfico es clave en pacientes con sospecha de bradiarritmias.The slowing of electrical stimulus conduction can occur in any area of the specific conduction system. Any heart rhythm with a heart rate (HR) below 60 bpm is called bradyarrhythmia or bradycardia. The anatomical and electrical underpinnings can be located in the sinus node, atrioventricular node, or His-Purkinje system. The spectrum of clinical presentation is very broad, ranging from an electrocardiographic finding in asymptomatic patients to potentially fatal situations that require quick, decisive action. In the diagnostic approach and risk stratification for bradyarrhythmias in the emergency department, it is essential to verify the hemodynamic condition in the initial evaluation, given that the necessity and urgency of therapeutic action will be determined based on it. Protocolizing the clinical diagnosis and establishing an electrocardiographic algorithm is key in patients with suspected bradyarrhythmia.Sin financiaciónNo data JCR 20210.107 Q4 SJR 2021No data IDR 2021UE

Mujer de 45 años con episodios sincopalesde repetición

Sin financiaciónNo data JCR 20210.107 Q4 SJR 2021No data IDR 2021UE

P6014 - The variable location of the atrioventricular conduction axis. Implications for permanent and safe His bundle pacing

Background/Introduction The deleterious effects of long-term RV apical pacing have been well recognized. Permament His bundle (HB) pacing has emerged as a promising technique for patients who need ventricular pacing. Purpose To describe the anatomy of the HB region and its variations for successfully approaching HB pacing in a safer and more efficient way and to understand selective vs non-selective HB pacing and to avoid permanent damage to it. Methods In 57 structurally normal human heart specimens (48 males, 77±7 years) we examined by dissection techniques and histological sections the course of the penetrating and non-branching His bundle in relation with the membranous septum and the tricuspid valve (TV) annulus. We correlated these anatomic findings with a series of angiographic studies in 60 patients (47% males, 45±16 years old) by recording the largest His electrogram sites within the limits of the triangle of Koch (TK) and the plane of the TV. Results The membranous septum is divided by the attachment on its right side of the septal leaflet of the tricuspid valve into atrioventricular (AV) and interventricular components. The AV component of the membranous septum forms the anterosuperior apex of the TK and showed in cadaveric hearts variable dimensions in length (4.6±1.5 mm, range 1–9 mm). The AV node becomes the His bundle as the AV conduction axis enters the AV component of the membranous septum and is encircled by the fibrous tissue of the central fibrous body in 100% of hearts with none of them having a “naked” entrance to it. In 30 hearts (53%) the HB penetrates the AV membranous septum at the apex of the TK at the hinge point of the septal leaflet of the TV near its commissure with the anterosuperior leaflet. However in 47% of cases the HB crossed the fibrous tissue of the central fibrous body in a lower position in the medial area of the paraseptal right atrial region of the TK with a mean distance to the AV membranous septum of 4±1.4 mm (range 1.5–8 mm) above and behind the TV annulus. These findings correlate with those obtained in patients in which the site of recording of the largest His bundle deflection does not always coincide with the anterosuperior vertex of the triangle as judged angiographically. In 51% of patients the site of the largest His bundle electrograms was found in the medial area of the triangle above (posterior-inferior) the TV annulus while in 49% of patients the His was recorded at the same level (15%) or below (anterior-inferior) the TV annulus (34% of patients) (figure). Conclusions Knowledge of the marked variability in the location of the AV conduction bundle within the paraseptal right atrial region is crucial for approaching permanent HB pacing. An anterior-inferior and ventricular HB location could yield to restriction of the septal leaflet of the tricuspid valve if a lead is to be deployed in the area.Sin financiación22.673 JCR (2019) Q1, 2/138 Cardiac & Cardiovascular Systems5.883 SJR (2019) Q1, 4/364 Cardiology and Cardiovascular MedicineNo data IDR 2019UE

Treatment protocol for syncope in the emergency department

El síncope puede clasificarse en reflejo (neuromediado), por hipotensión ortostática o secundario a patología cardiovascular. Dado que el síncope reflejo tiene buen pronóstico, el tratamiento va dirigido básicamente a la prevención de recidivas. Se debe explicar a todo paciente el diagnóstico, tranquilizarlo y asesorarle sobre el riesgo de recurrencia y la forma de evitar las situaciones y los factores desencadenantes. Las maniobras isométricas de contrapresión de miembros superiores e inferiores pueden evitar el desarrollo de síncope una vez iniciados los síntomas y evitando caídas. Puede considerarse el entrenamiento con basculación para instruir a los pacientes jóvenes. En pacientes con episodios muy recurrentes de la forma ortostática del síncope vasovagal, puede considerarse la administración de fludrocortisona o midodrina. El síncope por hipotensión ortostática se suele presentar en pacientes de edad y con tratamiento hipotensor. Debemos, en primer lugar, ajustar el tratamiento hipotensor. La ingesta de 400-500 ml de agua entre 3-4 veces al día puede ayudar en ambos síncopes reflejo y por hipotensión ortostática. El síncope cardiogénico se presenta en pacientes con cardiopatía de base o electrocardiograma anormal, suele tener peor pronóstico y debe conocerse su mecanismo final para establecer el tratamiento.Syncope can be classified as reflex (neuromediated) syncope, syncope due to orthostatic hypertension, or syncope secondary to cardiovascular pathology. Given that reflex syncope has a good prognosis, treatment is essentially aimed at preventing recurrence. The diagnosis must be explained to all patients and they must be reassured and advised on the risk of recurrence and how to avoid triggering situations and factors. Isometric counterpressure movements in the upper and lower limbs can avoid onset of syncope once symptoms have begun as well as prevent falls. Tilt training can be considered for instructing young patients. In patients with very recurrent episodes of the orthostatic form of vasovagal syncope, administration of fludrocortisone or midodrine can be considered. Syncope due to orthostatic hypotension tends to occur in elderly patients and those with hypotensive treatment. We must first adjust hypotensive treatment. Intake of 400 - 500 ml of water three to four times per day can help in both reflex and orthostatic hypotension syncope. Cardiogenic syncope occurs in patients with underlying cardiopathy or an abnormal electrocardiogram. It tends to have a poor prognosis and its end mechanism must be understood in order to establish treatment.Sin financiaciónNo data JCR 20210.107 Q4 SJR 2021No data IDR 2021UE

El sistema especializado de conducción eléctrico del corazón. Los nodos del corazón y el sistema His-Purkinje. Sustrato anatómico de las vías accesorias

La arquitectura muscular del miocardio del corazón está constituida fundamentalmente por células musculares de trabajo o cardiomiocitos responsables de la contracción miocárdica, y un espacio intersticial con un componente de células productoras de colágeno o fibroblastos, rodeados de una matriz extracelular de tejido conectivo. Pequeños grupos celulares de localización predominante en las aurículas contienen características neuroendocrinas. Para que se produzca la activación del miocardio de trabajo estriado y el acoplamiento excitación-contracción a través del potencial de acción transmembrana, es necesaria la presencia de las células especializadas del sistema específico de conducción. El proceso y la secuencia de activación de las cámaras cardíacas se realiza a través del sistema específico de conducción, modulado por las fibras simpáticas y parasimpáticas del sistema neurovegetativo, que ejercen un control autónomo del mismo. El sistema de conducción auriculoventricular está compuesto por miocitos especializados y consta de un componente auricular: el nodo sinoauricular y el nodo auriculoventricular, que están en contacto con el miocardio auricular. A continuación, el haz de His atraviesa el cuerpo fibroso central y termina dividiéndose en dos haces o ramas, una izquierda y otra derecha, las cuales se ramifican en los ventrículos formando las denominadas fibras de Purkinje. El haz de His y sus ramas se encuentran rodeados de una capa de tejido conectivo, la cual se pierde en las fibras de Purkinje, lo que permite a estas establecer contacto directo con el miocardio de trabajo ventricular. Es necesario el conocimiento detallado del tejido específico de conducción para entender el ritmo normal del corazón y los sustratos anatómicos y eléctricos que constituyen las arritmias cardíacas.The specialized electrical conduction system of the heart. The heart nodes and the His-Purkinje system. Anatomical underpinnings of the accessory pathways The muscular architecture of the heart myocardium is mainly composed of muscle cells, or cardiomyocytes, that are responsible for myocardial contraction as well as an interstitial space with a component of collagen-producing cells, or fibroblasts, surrounded by an extracellular matrix of connective tissue. Small cell groups predominantly located in the atria have neuroendocrine characteristics. In order to activate of the striated myocardium and excitation-contraction coupling through transmembrane action potential, the presence of specialized cells of the specific conduction system is necessary. The process and sequence of activation of the heart chambers occurs through the specific conduction system and is modulated by sympathetic and parasympathetic fibers of the neurovegetative system, which exercise autonomous control of it. The atrioventricular conduction system is composed of specialized myocytes and has an atrial component: the sinoatrial node and atrioventricular node, which are in contact with the atrial myocardium. Next, the bundle of His crosses the central fibrous body and divides into two bundles or branches—the left and the right—which branch into the ventricles, forming what is known as Purkinje fibers. The bundle of His and its branches are surrounded by a layer of connective tissue that is lost in the Purkinje fibers, allowing them to establish direct contact with the ventricular myocardium. Detailed knowledge of the specific conduction tissue is necessary to understand normal heart rhythm and the anatomical and electrical underpinnings that constitute heart arrhythmias.Sin financiaciónNo data JCR 20200.107 SJR (2021) Q4, 2423/2489 Medicine (miscellaneous)No data IDR 2020UE

Heart arrhythmias

Las alteraciones de la normal función, fisiología y periodicidad de la actividad eléctrica cardíaca se agrupan en el término genérico de arritmias. Los mecanismos más frecuentes causantes de las arritmias cardíacas son las reentradas, así como la actividad automática aumentada, en ocasiones desencadenadas por alteraciones electrolíticas o cuadros intercurrentes, pero en la mayoría de los casos sin causa aparente subyacente. Dividimos los tipos de arritmias en bradiarritmias o taquiarritmias, y según su cámara de origen en supraventriculares y ventriculares. Repasamos de forma genérica los estudios diagnósticos y los criterios de sospecha que pasarán de forma fundamental por conseguir una correlación entre los síntomas y el registro de ECG para el diagnóstico de certeza del tipo de arritmia y para un tratamiento personalizado. Hablaremos también de la importancia de los dispositivos implantables tipo Holter de eventos y de los criterios para la derivación a un especialista en arritmias y electrofisiología cardíaca. Los esfuerzos diagnósticos son de gran importancia, pues muchas de estas arritmias tienen una respuesta muy satisfactoria al tratamiento definitivo, con un procedimiento mínimamente invasivo de ablación con catéter con unos riesgos extremadamente bajos, consiguiendo recuperar la calidad de vida y evitar tratamientos farmacológicos a largo plazo.Sin financiaciónNo data JCR 20200.107 SJR (2021) Q4, 2423/2489 Medicine (miscellaneous)No data IDR 2020UE

Protocol for risk stratification in the initial evaluation of patients with syncope

La historia clínica, los hallazgos de la exploración y los resultados de las pruebas complementarias permiten identificar, en la mayoría de los casos, la etiología del síncope. Durante la evaluación inicial del paciente con síncope, debemos establecer una estratificación del riesgo y definir la estrategia inmediata a seguir, el tipo de exploraciones a realizar, su prioridad y la decisión de ingreso o seguimiento ambulatorio. En el siguiente protocolo, presentamos de forma sintética las recomendaciones de la Sociedad Europea de Cardiología en las recientes guías para la estratificación de riesgo de pacientes con síncope tras una evaluación inicial.The medical history, findings upon examination, and results of additional tests allow for identifying the etiology of the syncope in the majority of cases. During the initial evaluation of a patient with syncope, we must establish a risk stratification and define the immediate strategy to follow, the type of examinations to perform, its priority, and decide on admission or outpatient follow-up. In the following protocol, we will concisely present the recommendations of the European Society of Cardiology in the recent guidelines for risk stratification of patients with syncope following an initial evaluation.Sin financiaciónNo data JCR 20210.107 Q4 SJR 2021No data IDR 2021UE