**6. Conclusions**

The presence of *C. pneumoniae* in human atherosclerotic plaques is now a generally accepted fact. Numerous studies in various centers have repeatedly confirmed this with many different diagnostic methods, laboratory tests, and imaging techniques.

The association between *C. pneumoniae* and the atherosclerosis process leads to new questions. Is *Chlamydia* a cause of atherosclerosis, or is it a risk factor that participates in the process and predisposes to its complications?

The active pathogenic mechanism of the bacteria, which involves the ability to live within the cytoplasm, persist long-term and even multiple within vacuoles, cause cell necrosis and lysis, and infect the surrounding cells, and its detection even in the fatty streaking stage, which is the initial stage of atherosclerosis, can be regarded as evidence of its role as a triggering factor. However, its ability to survive in macrophages and lymphocytes, cause cell necrosis and fibrosis, and exist and reproduce in plaque inclusion bodies can be regarded as evidence that it is a co-factor associated with and contributing to the atherosclerotic process.

As a result, the pathophysiological mechanisms of Chlamydial infection shown to play a role in atherosclerosis can be summarized under the main headings as follows:


Considerable research continues on atherosclerosis and related cardiovascular diseases, which are leading causes of mortality and morbidity worldwide. Vascular interventional techniques and bypass surgeries are performed as palliative interventions. However, atherosclerosis is a major disease that has no definitive treatment and is still awaiting a solution.

Studies on the role of *C. pneumoniae* in the pathogenesis of atherosclerosis, vaccine studies, and advances in immune response regulation remain scientists' focus of attention for the treatment of atherosclerosis.
