Conceptos epidemiológicos y mecanismos arritmogénicos en pacientes con fibrilación auricular
DOI:
https://doi.org/10.52379/mcs.v9.529Palabras clave:
fibrilación auricular, Electrogramas auriculares anormales, rotoresResumen
Muchos aspectos fundamentales de la fibrilación auricular (FA) han sido poco conocidos hasta hace unos pocos años atrás, y hay varias características en los mecanismos de FA que dificultan su evaluación adecuada. Diversos factores externos inducen un proceso lento pero progresivo de remodelado estructural en las aurículas. La activación de fibroblastos, el aumento de depósitos de tejido conectivo y la fibrosis son los elementos más importantes de este proceso. El remodelado estructural produce una disociación eléctrica entre los haces musculares y heterogeneidad de la conducción local que favorece el fenómeno de reentrada y la perpetuación de la arritmia. Los focos ectópicos, rotores y otros circuitos estables de reentrada, causan una conducción no homogénea y anisotrópica lejos de la fuente. Esta conducción es difícil de diferenciar de la propagación de múltiples ondas que mantiene la FA, y cualquiera de estos fenómenos puede generar rotores detectados en registros intracardiacos. El mecanismo de la actividad focal por una fuente en las venas pulmonares puede desencadenar episodios de FA debido tanto a la actividad desencadenada como al mecanismo de reentrada localizada. Los pacientes con FA que en ritmo sinusal presentan una alteración de la morfología de la onda P y dispersión de la onda P, tienen una gran susceptibilidad a desarrollar FA y generalmente poseen electrogramas auriculares anormalmente prolongados y fraccionados. Además, poseen una duración de la onda P más larga, un tiempo de conducción intraauricular e interauricular más largo de los impulsos sinusales; y una mayor incidencia de inducción de FA sostenida.
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Derechos de autor 2025 Orlando Robert Sequeira, Laura Beatriz García, Christian Osmar Chávez, Rocío del Pilar Falcón, Alfredo Javier Meza, Osmar Centurión

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