**5. Treatment strategies**

#### **5.1 Antibiotic studies**

The multitude of studies indicating that *C. pneumoniae* plays a role in the pathogenesis of atherosclerosis led to the investigation of whether this pathogenesis can be treated with antibiotic therapy. Some experimental studies showed that antichlamydial antibiotherapy slowed atherosclerosis to some extent [116].

The ACADEMIC study included 302 coronary artery patients with positive *Chlamydia* IgG tests. Of these, 152 patients received a placebo and 150 patients

#### *A Hidden Organism, Chlamydia in the Age of Atherosclerosis DOI: http://dx.doi.org/10.5772/intechopen.109745*

received azithromycin for 6 months. At the end of the study, there were significant decreases in CRP, IL-1, IL-6, and TNF levels in the azithromycin group, but the expected significant change in serological tests was not observed. In addition, there was no difference in terms of rates of clinical events related to coronary artery disease [117]. This supports the theory that inflammation can be reduced with antichlamydial antibiotherapy.

However, in a multi-center antichlamydial antibiotic study including more than 15,000 people in total, although there were significant changes in laboratory parameters, it unfortunately did not yield the expected results in terms of reducing rates of clinical symptoms and events [118–120].

The failure of antibiotic therapy to provide secondary protection against atherosclerosis complications in individuals infected with *C. pneumoniae* has been attributed to the treatment being too late. It is believed that the atherosclerosis process is already triggered in people infected with *C. pneumoniae* and that antichlamydial treatment does not protect against infection. Experimental studies have indicated that antibiotic treatment initiated immediately after chlamydial infection may protect against atherosclerosis [121, 122]. Research on this subject is ongoing.
