Información del artículo
La fibrilación ventricular, la isquemia miocárdica y la muerte súbita son fisiopatologías cardiacas inseparables. La influencia de la distribución de células del medio miocardio en la formación de arritmias en la pared heterogénea cardiaca en presencia de isquemia sub-epicárdica, no está del todo dilucidada. En este estudio se modela una porción plana de la pared transmural con diferentes configuraciones de células del medio miocardio que se adjuntan a las heterogeneidades bioquímicas presentes en isquemia sub-epicárdica para cuantificar su influencia en la formación de arritmias.
Se obtuvieron reentradas lobulares no sostenidas en torno de la lesión isquémica que interfieren con las células M, alterando la repolarización del tejido. La función de vulnerabilidad que cuantifica la prospección a reentradas es aproximada por una función logística, y su mayor expresión ocurre en el minuto 8,75 de isquemia modelada.
La heterogeneidad bioquímica y morfológica en el tejido virtual estudiado dan como resultado una arritmia por reentrada; su secuela en la vulnerabilidad del tejido aumenta a medida que crece la severidad de la hiperkalemia. Los electrogramas obtenidos muestran depresión TQ y elevación ST con una morfología de taquicardia ventricular polimórfica.
Palabras clave:
células M
electrogramas
función de vulnerabilidad
isquemia sub-epicárdica
modelo de Luo-Rudy
reentrada transmural
taquicardia polimórfica
Ventricular fibrillation, myocardial ischemia and sudden cardiac death are inseparable cardiac pathophysiologies. The influence of the distribution of myocardial cells in the formation of arrhythmias in the heterogeneous cardiac wall in the presence of sub-epicardial ischemia is not entirely elucidated. This study models a flat portion of the transmural wall under different myocardial cell configurations attached to the biochemical heterogeneity present in sub-epicardial ischemia to quantify their influence on the development of arrhythmias.
Lobular non-sustained reentries were obtained around the ischemic lesion that interfere with M cells, altering the tissue repolarization. Vulnerability function that quantifies prospection to reentries is approximated by a logistic function, and its main expression occurs in 8.75 minutes of modeled ischemia.
The biochemical and morphological heterogeneity in the virtual tissue studied results in a reentrant arrhythmia; its sequel to the tissue vulnerability increases as the severity of hyperkalemia grows. Electrograms obtained show TQ depression and ST elevation with a morphology of polymorphic ventricular tachycardia.
Key words:
M cells
electrograms
vulnerability function
sub-epicardial ischemia
Luo-Rudy model
transmural reentry
polymorphic tachycardia
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