The Atrioventricular Conduction Axis and its Implications for Permanent Pacing

Extensive knowledge of the anatomy of the atrioventricular conduction axis, and its branches, is key to the success of permanent physiological pacing, either by capturing the His bundle, the left bundle branch or the adjacent septal regions. The inter-individual variability of the axis plays an important role in underscoring the technical difficulties known to exist in achieving a stable position of the stimulating leads. In this review, the key anatomical features of the location of the axis relative to the triangle of Koch, the aortic root, the inferior pyramidal space and the inferoseptal recess are summarised. In keeping with the increasing number of implants aimed at targeting the environs of the left bundle branch, an extensive review of the known variability in the pattern of ramification of the left bundle branch from the axis is included. This permits the authors to summarise in a pragmatic fashion the most relevant aspects to be taken into account when seeking to successfully deploy a permanent pacing lead.Sin financiaciónNo data JCR 20211.035 Q1 SJR 2021No data IDR 2021UE

Optimization of decrementing evoked potential mapping for functional substrate identification in ischaemic ventricular tachycardia ablation

Ventricular tachycardia (VT) ablation approaches based on high-density mapping, which enable the rapid acquisition of thousands of mapping points in order to delineate slow conduction zones, have been widely adopted.1 The identification of functionally relevant substrates has been advanced by the identification of potentials participating in the initiation and/or maintenance of scar-dependent VT. During right ventricular apical (RVA) pacing with an extra-stimulus (S2), these potentials display delayed conduction (decremental) behaviour (DeEP).2 This methodology has been shown to be more specific in identifying the critical isthmus of re-entrant VT.3 An important factor accounting for decrement is conduction velocity (CV) restitution.2 With a short-coupled S2, CV will decrease, and further delay occurs in the near-field signal with respect to the far-field signal, creating DeEPs. Conventionally, the S2 has been delivered at ventricular effective refractory period (VERP) + 20 ms to elicit decrement.3–5 However data are lacking on justifying the delivery of the S2 at VERP + 20 ms, which may result in areas defined as DeEP due to intrinsic CV restitution properties, thus creating larger-than-required ablation target areas. We hypothesized that DeEPs are better identified with longer S2 coupling intervals. The second hypothesis was to consider the definition of a DeEP as the range of decrement beyond 10 ms has not been previously explored and to identify the best combination of these parameters

Incidence, clinical characteristics, risk factors and outcomes of meningoencephalitis in patients with COVID-19

We investigated the incidence, clinical characteristics, risk factors, and outcome of meningoencephalitis (ME) in patients with COVID-19 attending emergency departments (ED), before hospitalization. We retrospectively reviewed all COVID patients diagnosed with ME in 61 Spanish EDs (20% of Spanish EDs, COVID-ME) during the COVID pandemic. We formed two control groups: non-COVID patients with ME (non-COVID-ME) and COVID patients without ME (COVID-non-ME). Unadjusted comparisons between cases and controls were performed regarding 57 baseline and clinical characteristics and 4 outcomes. Cerebrospinal fluid (CSF) biochemical and serologic findings of COVID-ME and non-COVID-ME were also investigated. We identified 29 ME in 71,904 patients with COVID-19 attending EDs (0.40‰, 95%CI=0.27-0.58). This incidence was higher than that observed in non-COVID patients (150/1,358,134, 0.11‰, 95%CI=0.09-0.13; OR=3.65, 95%CI=2.45-5.44). With respect to non-COVID-ME, COVID-ME more frequently had dyspnea and chest X-ray abnormalities, and neck stiffness was less frequent (OR=0.3, 95%CI=0.1-0.9). In 69.0% of COVID-ME, CSF cells were predominantly lymphocytes, and SARS-CoV-2 antigen was detected by RT-PCR in 1 patient. The clinical characteristics associated with a higher risk of presenting ME in COVID patients were vomiting (OR=3.7, 95%CI=1.4-10.2), headache (OR=24.7, 95%CI=10.2-60.1), and altered mental status (OR=12.9, 95%CI=6.6-25.0). COVID-ME patients had a higher in-hospital mortality than non-COVID-ME patients (OR=2.26; 95%CI=1.04-4.48), and a higher need for hospitalization (OR=8.02; 95%CI=1.19-66.7) and intensive care admission (OR=5.89; 95%CI=3.12-11.14) than COVID-non-ME patients. ME is an unusual form of COVID presentation (<0.5‰ cases), but is more than 4-fold more frequent than in non-COVID patients attending the ED. As the majority of these MEs had lymphocytic predominance and in one patient SARS-CoV-2 antigen was detected in CSF, SARS-CoV-2 could be the cause of most of the cases observed. COVID-ME patients had a higher unadjusted in-hospital mortality than non-COVID-ME patients

Ventricular Tachycardia Ablation Guided by Functional Substrate Mapping: Practices and Outcomes

Catheter ablation of ventricular tachycardia has demonstrated its important role in the treatment of ventricular tachycardia in patients with structural cardiomyopathy. Conventional mapping techniques used to define the critical isthmus, such as activation mapping and entrainment, are limited by the non-inducibility of the clinical tachycardia or its poor hemodynamic tolerance. To overcome these limitations, a voltage mapping strategy based on bipolar electrograms peak to peak analysis was developed, but a low specificity (30%) for VT isthmus has been described with this approach. Functional mapping strategy relies on the analysis of the characteristics of the electrograms but also their propagation patterns and their response to extra-stimulus or alternative pacing wavefronts to define the targets for ablation. With this review, we aim to summarize the different functional mapping strategies described to date to identify ventricular arrhythmic substrate in patients with structural heart disease

A 34-year-old female patient who consulted for palpitations of years of evolution

Sin financiaciónNo data SJR 20210.107 SJR (2021) Q4, 2382/2489 Medicine (Miscellaneous)No data IDR 2021UE

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

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