Información del artículo
Resumen
Diversas evidencias procedentes de estudios experimentales y observacionales sugieren que la infección por el virus de la inmunodeficiencia humana (VIH) per se y el estado proinfl amatorio asociado pueden aumentar el riesgo de enfermedad cardiovascular. La infección por VIH puede activar diversas vías infl amatorias de la pared vascular con liberación de citocinas y expresión de moléculas de adhesión endotelial. El tratamiento antirretroviral de gran actividad (TARGA) es capaz de suprimir muchas de estas alteraciones. El papel del VIH en el riesgo cardiovascular se ha puesto de manifiesto en los estudios de interrupción de tratamiento, fundamentalmente en el estudio SMART, en el que se demostró una mayor mortalidad cardiovascular en el grupo que interrumpía el TARGA. El cambio brusco a un estado más proinfl amatorio producido por la reanudación repentina de la replicación viral podría inducir un aumento de la adhesión plaquetaria y la migración de células infl amatorias con inestabilización de la placa. Algunos estudios sugieren que el VIH puede producir también daño endotelial y se ha descrito un descenso de los marcadores de activación endotelial y una mejoría de la función endotelial tras el inicio del TARGA, que se ha correlacionado con el descenso de la carga viral del VIH. Finalmente, el VIH podría inducir enfermedad cardiovascular a través de su efecto sobre el colesterol unido a lipoproteínas de alta densidad que puede descender en pacientes con infección no controlada. Aunque la relación del VHC con el riesgo cardiovascular es controvertida, la coinfección por el VHC se ha asociado con una mayor frecuencia de resistencia insulínica y de infarto agudo de miocardio en algunas cohortes.
Palabras clave:
VIH
Arteriosclerosis
Riesgo cardiovascular
Episodios cardiovasculares
Virus de la hepatitis C
Enfermedad cardiovascular
Abstract
Evidence from experimental and observational studies suggests that HIV infection per se and the associated proinfl ammatory state can increase the risk of cardiovascular disease. HIV infection can activate several infl ammatory pathways in the vascular wall with cytokine release and expression of endothelial adhesion molecules. Many of these alterations can be suppressed by highly-active antiretroviral therapy (HAART). The role of HIV in cardiovascular risk has been demonstrated in studies of treatment interruption, mainly in the SMART trial, in which greater cardiovascular mortality was observed in the group interrupting HAART. The abrupt change to a more proinfl ammatory state produced by sudden resumption of viral replication could induce an increase in platelet adhesion and migration of infl ammatory cells with plaque instability. Some studies suggest that HIV can also produce endothelial damage; a decrease in markers of endothelial activation and improvement of endothelial function after initiation of HAART have been described, and these changes have been correlated with the decrease in HIV viral load. Finally, HIV can induce cardiovascular disease through its effect on high-density lipoprotein cholesterol, which can decrease in patients with uncontrolled infection. Although the association of HIV with cardiovascular risk is controversial, coinfection with hepatitis C infection has been associated with a higher frequency of insulin resistance and acute myocardial infarction in some cohorts.
Keywords:
HIV
Arteriosclerosis
Cardiovascular risk
Cardiovascular events
Hepatitis C virus
Cardiovascular disease
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