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BACKGROUND: Left atrial peak systolic strain (LA-PSS) imaging is an emerging index of left atrial function, and it was shown to be decreased in heart failure with preserved ejection fraction (EF). We aimed to determine whether LA-PSS could be used as an additional diagnostic parameter to current existing guidelines for the presence of left ventricle diastolic dysfunction (LVDD). MATERIALS AND METHODS: A total of 190 consecutive adult patients with cardiovascular risk factors and normal left ventricle EF with no prior history of heart failure were included in the study. Speckle tracking software was used to study ventricular parietal deformity, left ventricle global longitudinal systolic strain, and LA-PSS. RESULTS: The median left ventricle global longitudinal systolic strain was -19%, with a significant difference ( P < 0.001) between patients with normal diastolic function versus those with LVDD. The median LA-PSS was 33% (30% to 38%) ( P < 0.001). Most patients (61%) had grade 1 atrial dysfunction based on PSS (range 24%-35%). The analysis of the area under the receiver operating characteristic curve of the LA-PSS as a potential indicator pathway of LVDD was 67% [95% confidence interval (CI), 62-72], and 75% (95% CI, 70-80), when the indeterminate pattern was included. The decreased LA-PSS made it possible to reclassify patients with an indeterminate pattern of diastolic function in 96% of cases. CONCLUSIONS: These results support the potential role of LA-PSS as an additional parameter for the diagnosis of LVDD in patients with normal EF, and may be integrated into the guidelines for routine evaluation of patients.

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BACKGROUND: There is a global tendency to emphasize the prevention and early diagnosis of diseases that have a great impact on public health. Atrial fibrillation (AF) has a prevalence affecting 1.5-2% of the general population. Certain variables of the P wave allow us to identify and stratify patients at risk of developing AF. MATERIALS AND METHODS: This is an observational, descriptive, and longitudinal study to determine the applicability of the electrocardiographic (ECG) morphology, voltage, and P wave duration (MVP) risk score to predict the development of AF in consecutive patients with systemic hypertension (SH) in an initial follow-up of 12 months. RESULTS: Initially, 104 patients were included, of whom 12 died during follow-up and 17 did not attend subsequent checkups during the COVID-19 pandemic; therefore, they were excluded. The study patients were 75, of whom AF was detected in 25 patients (33%). The average duration of the P wave was 120 ± 26 ms, the average voltage was 0.1 ± 0.5 Mv. The high-risk MVP ECG score had an [area under the curve, 0.69; 95% confidence intervals (CI), 0.59-0.79] and demonstrated a specificity and a positive predictive value of 100%, a negative predictive value of 76%, and a sensitivity of 40% for predicting the development of AF. CONCLUSIONS: The present study establishes for the first time that SH patients who possess a high-risk MVP ECG score have a significantly higher incidence of developing AF. The high-risk MVP Score has a specificity and a positive predictive value of 100% and a high negative predictive value with a moderate sensitivity for the prediction of the development of AF in SH patients.

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El Bloqueo Interauricular (BIA) puede servir como un valioso marcador electrocardiográfico para evaluar el riesgo del desarrollo de arritmias auriculares, y nueva aparición de fibrilación auricular (FA). El BIA se produce por un deterioro en la conducción auricular que implica un retraso en la conducción del estímulo eléctrico desde la aurícula derecha a la aurícula izquierda. Las causas probables de interrupción del haz de Bachmann incluyen isquemia, enfermedad degenerativa del envejecimiento, enfermedades infiltrativas, enfermedad coronaria difusa y afecciones inflamatorias. Los factores de riesgo para el BIA avanzado, la fibrilación auricular (FA) y el accidente cerebrovascular (ACV) parecen ser muy similares, y la patogénesis subyacente probablemente se deba a fibrosis miocárdica y remodelación auricular. El bloqueo interauricular se relaciona clínicamente a la aparición de taquiarritmias supraventriculares y está relacionado al remodelamiento auricular. Aunque el agrandamiento auricular y el BIA comparten un patrón electrocardiográfico similar, son dos entidades separadas. Sin embargo, muchos autores aún asocian una duración de la onda P mayor a 120 ms con agrandamiento de la aurícula izquierda. El remodelamiento auricular modifica la velocidad de conducción, la arquitectura cardiaca, los canales iónicos dependientes de voltaje, y los componentes de resistencia y capacitancia, como son el espacio extracelular y las uniones celulares. La alteración de estas propiedades afecta las propiedades electrofisiológicas de la conducción auricular y favorece el BIA, los trastornos auriculares y la génesis de FA.

Interatrial block (IAB) can serve as a valuable electrocardiographic marker to assess the risk of developing atrial arrhythmias, and new onset of atrial fibrillation (AF). The IAB is produced by a deterioration in atrial conduction that implies a delay in the conduction of the electrical stimulus from the right atrium to the left atrium. Probable causes of Bachmann bundle interruption include ischemia, degenerative disease of aging, infiltrative diseases, diffuse coronary disease, and inflammatory conditions. The risk factors for advanced IAB, atrial fibrillation (AF), and cerebrovascular accident (CVA) appear to be very similar, and the underlying pathogenesis is probably due to myocardial fibrosis, and atrial remodeling. The interatrial block is clinically related to the appearance of supraventricular tachyarrhythmias and is related to atrial remodeling. Although atrial enlargement and IAB share a similar electrocardiographic pattern, they are separate entities. However, many authors still associate P wave duration greater than 120 ms with left atrial enlargement. Atrial remodeling modifies conduction velocity, cardiac architecture, voltage-gated ion channels, and resistance and capacitance components, such as the extracellular space and cell junctions. The alteration of these properties affects the electrophysiological properties of atrial conduction and favors IAB, atrial disorders, and the genesis of AF.

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RESUMEN El bloqueo interauricular (BIA) es un marcador significativo en la predicción del desarrollo de Fibrilación Auricular (FA). El sustrato histopatológico que se observa en el proceso de remodelación auricular es la fibrosis del miocardio auricular induciendo disincronía interauricular. La disfunción electromecánica de la aurícula izquierda (AI) produce una activación anormal de sus paredes, el aumento de la presión, la dilatación, la disfunción endotelial, y la fibrosis de la AI. Estas alteraciones favorecen la conducción lenta, el bloqueo unidireccional y el desarrollo de mecanismos de reentrada con la aparición de la FA con sus nefastas complicaciones, entre ellas el accidente cerebrovascular (ACV). El BIA está presente hasta en un 59% de los pacientes mayores de la población general y se asoció con un aumento del riesgo de unas 3 veces más de FA de nueva aparición y ACV isquémico. Es evidente el interés académico, clínico, y terapéutico en el diagnóstico electrocardiográfico certero del BIA avanzado, ya que el mismo se asocia con arritmias supraventriculares, fibrilación auricular, ACV embólicos y mortalidad. La detección de BIA avanzado en pacientes con ACV isquémico previo permite identificar a pacientes de alto riesgo de recurrencia en los que algunas terapias farmacológicas podrían ser beneficiosas. Los pacientes con BIA avanzado sin episodios previos de FA documentada también presentan un riesgo aumentado de ACV embólico. Por lo tanto, es necesario realizar ensayos clínicos randomizados cuyos resultados podrían avalar el uso de anticoagulantes en ausencia de FA documentada en pacientes con BIA avanzado.

ABSTRACT Interatrial block (IAB) is a significant marker in the prediction of the development of Atrial Fibrillation (AF). The histopathological substrate observed in the atrial remodeling process is fibrosis of the atrial myocardium, inducing interatrial desynchrony. Electromechanical dysfunction of the left atrium (LA) produces abnormal activation of its walls, increased pressure, dilation, endothelial dysfunction, and fibrosis of the LA. These alterations favor slow conduction, unidirectional block and the development of reentry mechanisms with the appearance of AF with its disastrous complications, including cerebrovascular accident (CVA). IAB is present in up to 59% of older patients in the general population and was associated with a 3-fold increased risk of new-onset AF and ischemic stroke. The academic, clinical, and therapeutic interest in the accurate electrocardiographic diagnosis of advanced IAB is evident, since it is associated with supraventricular arrhythmias, atrial fibrillation, embolic stroke and mortality. The detection of advanced IAB in patients with previous ischemic stroke allows the identification of patients at high risk of recurrence in which some pharmacological therapies could be beneficial. Patients with advanced IAB with no prior documented AF episodes are also at increased risk of embolic stroke. Therefore, it is necessary to conduct randomized clinical trials whose results might be available in the use of anticoagulants in the absence of documented AF in patients with advanced IAB.