English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

It is acknowledged that local and systemic inflammatory processes play an important role in the development and progression of atherosclerotic lesions, and in the pathophysiology of acute coronary syndromes. Established cardiovascular risk factors do not completely explain the epidemiological changes of, and the diverse presentations of, coronary heart disease. This had led to increasing interest in the contribution of certain infectious agents as atherogenic risk factors. The evidence for Chlamydia pneumoniae as a potential causative agent is strong, and is largely based on the findings of (1) seroepidemiological studies, (2) examination of atheromatous plaque specimens, (3) in-vitro experiments and animal models and recently, (4) preliminary antichlamydial antiobiotic intervention studies. This review aims to focus on the scientific evidence of the implication of C. pneumoniae (and other infective agents) as a culprit aetiological agent in atherogenesis and coronary heart disease.

Chlamydia pneumonia (and other infective agents) in atherosclerosis and acute coronary syndromes. How good is the evidence?