Desde el punto de vista molecular, la cardiopatía hipertensiva se caracteriza por un conjunto de cambios en la expresión de genes y proteínas del miocardio que provocan una serie de modificaciones en su composición, dando lugar a su remodelado estructural y geométrico, así como a alteraciones de su función, perfusión y actividad eléctrica. El remodelado es la consecuencia tanto de la sobrecarga mecánica hipertensiva como de la activación local de diversos factores humorales que afectan a los cardiomiocitos (facilitando su muerte por apoptosis) y a la matriz extracelular miocárdica (dando lugar a cambios en la cuantía y el depósito de las fibras de colágeno). La relevancia clínica de estas lesiones radica en que contribuyen a la transición de la hipertrofia ventricular izquierda a la insuficiencia cardiaca en los pacientes con cardiopatía hipertensiva. Hallazgos recientes señalan nuevos mecanismos de apoptosis y fibrosis (p. ej., alteraciones del receptor alfa activado por proliferadores de peroxisomas) en el ventrículo hipertenso que abren vías nuevas para la prevención de la insuficiencia cardiaca en los pacientes con cardiopatía hipertensiva.
Palabras clave
Apoptosis
Fibrosis
Hipertensión arterial sistémica
Hipertrofia
Insuficiencia cardiaca
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