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Fisiopatología de la enfermedad arterial coronaria
1Donald W. Reynolds Cardiovascular Clinical Research Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA. plibby@rics.bwh.harvard.edu
Circulation
|June 29, 2005
Resumen
La enfermedad de las arterias coronarias (CAD) ahora se entiende como una condición inflamatoria, no solo como una acumulación de colesterol. El tratamiento se centra en la estabilización de la placa y la inflamación para prevenir los síndromes coronarios agudos (SAC).
Área de la Ciencia:
- Medicina Cardiovascular La medicina cardiovascular es una especialidad de la salud.
- Fisiopatología Fisiopatología.
- Enfermedades Inflamatorias Las enfermedades inflamatorias.
Sus antecedentes:
- La comprensión de la enfermedad de las arterias coronarias (CAD) ha evolucionado significativamente en la última década.
- La aterosclerosis ahora se ve como un trastorno inflamatorio, yendo más allá del concepto de una enfermedad de almacenamiento de colesterol.
- La remodelación arterial y las placas no estenóticas ahora se reconocen como factores importantes en la CAD.
Objetivo del estudio:
- Revisar los avances en la comprensión de la fisiopatología de la CAD.
- Discutir cómo estos avances impactan los enfoques clínicos para la CAD crónica y aguda.
- Para resaltar el cambio en la perspectiva de la enfermedad localizada a la inflamación generalizada y la inestabilidad de la placa.
Principales métodos:
- Revisión de la literatura científica reciente y los hallazgos clínicos.
- Análisis de los conceptos en evolución en la aterosclerosis y la biología de la placa.
- Síntesis de nuevos conocimientos en recomendaciones de práctica clínica.
Principales resultados:
- Los síndromes coronarios agudos (SCA) a menudo son causados por placas interrumpidas, incluso las no críticas.
- La inflamación juega un papel central en el SCA, que implica tanto la ruptura de la placa como los factores transmitidos por la sangre.
- Los pacientes con SCA presentan inflamación generalizada y múltiples placas de alto riesgo, lo que desafía la visión de la EAC como una enfermedad segmentaria.
Conclusiones:
- La gestión de CAD requiere abordar tanto la lesión culpable inmediata como la estabilización de otras placas para evitar eventos recurrentes.
- Las estrategias de tratamiento para el SCA deben incluir el tratamiento de la "fase líquida" (mediadores protrombóticos / antifibrinolíticos) y los aspectos del "estado sólido" (disrupción de la placa).
- La cardiología intervencionista debe expandirse para incluir estrategias preventivas más allá de la revascularización mecánica para mitigar futuros eventos cardiovasculares.
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