**1. Introduction**

Cardiovascular diseases are the leading cause of morbidity and mortality in developed societies. The World Health Organization ranked coronary heart disease first and stroke fourth on its list of major life-threatening diseases. More than 40% of deaths from noncommunicable diseases in the community are due to cardiovascular causes.

Cardiovascular disease can manifest in myriad ways, including heart attack, stroke, peripheral artery disease, organ ischemia and necrosis, and aortic and peripheral arterial aneurysms. The main pathogenetic mechanism underlying cardiovascular diseases is atherosclerosis. When evaluated in terms of cost and loss of labor, atherosclerosis is a malignant condition that requires enormous resource allocation and affects all aspects of humanity. Atherosclerosis is progressive and affects all arteries in the body to a varying extent. It is extremely common, occurring in almost all individuals in the population. The main factors associated with a higher rate of atherosclerosis are chronic inflammation, genetic predisposition, advanced age, male sex, hyperlipidemia, hypertension, smoking, diabetes, sedentary lifestyle, and obesity.

Studies conducted in different parts of the world have shown that atherosclerosis begins in childhood. Autopsy studies conducted in Japan demonstrated early atherosclerosis and fatty streaks in the aortas of 29% of infants younger than 12 months and in the coronary arteries of 3.1% of children aged 1–9 years [1]. Similarly, autopsy studies in the USA have shown that the prevalence of fatty streaks in the coronary arteries is 50% between the ages of 2 and 15 years and increases to 85% between the ages of 21 and 39 years. Atherosclerotic plaque formation, a more advanced form of fatty streaking, was observed in 8% of children aged 2–15 years and 69% of adults aged 26–39 years [2].

Atherosclerosis starts with endothelial dysfunction and progresses with subintimal thickening and smooth muscle cell proliferation. The process is characterized with medial thickening due to macrophage infiltration, scavenger cell accumulation, and plaque formation. Lipid deposition is a common vascular condition in which inflammatory and infective processes trigger each other.

Studies on atherosclerosis risk factors have shown that organic pathogenic microorganisms contribute to the inflammatory process. These include *Chlamydia pneumoniae, Helicobacter pylori*, influenza A virus, hepatitis C virus, cytomegalovirus, and HIV. Chronic inflammation induced by microorganisms can cause many chronic diseases, malignancies, autoimmune diseases, and inflammatory atherosclerosis [3, 4]. Some microorganisms have been directly linked to atherosclerotic disease because they can be isolated and cultured from plaques, whereas the presence of other organisms has been demonstrated by biochemical tests [5, 6]. Microorganisms influence the atherosclerosis process by triggering inflammation; inducing endothelial cell damage, macrophage-derived foam cell formation, and vascular smooth muscle cell proliferation; and stimulating the immune system at all of these stages.

Electron microscope images obtained from atheromatous plaques showed that their central nucleus consists of a lipid-rich structure containing lipid clusters, vesicles, and microorganisms mimicking the appearance of a lipid cluster [3]. In analyses of these microorganisms, *C. pneumoniae* is the causative bacteria most frequently associated with atherosclerosis.

This chapter examines the relationship between the atherosclerotic process and *C. pneumoniae* through a review of the relevant literature.
