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Infección por Chlamydia pneumoniae y aterosclerosis carotídea asintomática temprana y temprana

H S Markus¹, M Sitzer, D Carrington

¹Department of Clinical Neuroscience, King's College School of Medicine,Institute of Psychiatry, London, UK. h.markus@iop.kcl.uk

|August 24, 1999

Resumen

Este estudio no encontró ningún vínculo entre la infección por Chlamydia pneumoniae y los marcadores tempranos de aterosclerosis como el grosor de la intima-media. Se necesita más investigación para explorar posibles asociaciones con la enfermedad de la arteria carótida más avanzada.

Área de la Ciencia:

Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
Enfermedades infecciosas Enfermedades infecciosas.
Diagnóstico médico Diagnóstico médico

Sus antecedentes:

La infección crónica por Chlamydia pneumoniae se sospecha en el desarrollo de la aterosclerosis.
El papel de C. pneumoniae en la aterosclerosis temprana sigue sin estar claro.
El espesor íntima-medio de la arteria carótida (IMT) y la evaluación de la placa ofrecen información temprana sobre la aterosclerosis.

Objetivo del estudio:

Para investigar la asociación entre la infección por Chlamydia pneumoniae y la aterosclerosis temprana.
Para determinar si la seropositividad de C. pneumoniae se correlaciona con el IMT de la arteria carótida o la presencia de placa.

Principales métodos:

La imagen por ultrasonidos midió el IMT de la arteria carótida y el grosor de la placa en 983 individuos (30-70 años).
Se midieron los títulos de anticuerpos IgA e IgG de Chlamydia pneumoniae.
Se analizaron las asociaciones entre la seropositividad y las mediciones de la arteria carótida, ajustando los factores de riesgo.

Principales resultados:

No se encontró una asociación significativa entre la seropositividad IgA o IgG de C. pneumoniae y el grosor de la carótida íntima-media o la presencia de placa.
Se observó una asociación potencial entre la seropositividad de IgA y la estenosis carotídea >50%, pero perdió importancia después de ajustar los factores de riesgo cardiovascular.
No se encontró correlación entre la seropositividad de C. pneumoniae y los marcadores inflamatorios (fibrinógeno, proteína C reactiva, recuento de leucocitos).

Conclusiones:

La evidencia serológica de la infección por C. pneumoniae no está asociada con la aterosclerosis temprana.
Un posible vínculo con la aterosclerosis avanzada justifica una mayor investigación en poblaciones relevantes.
La infección por C. pneumoniae no parece inducir un estado inflamatorio sistémico crónico.

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