**4. Epidemiology and etiology**

are chemotactic to circulating monocytes (c) they enhance adhesion of monocytes (d) they prevent the mobility of macrophages because of this macrophages remain their position and hold on to there (e) they are cytotoxic to endothelium and smooth muscle cells (f) they are

The endothelial damage is like as peeling of the endothelium, because of this damage platelets hold on to the endothelium. Smooth muscle cells derived from media layer migrate to here and starts to duplicate and some of them absorb lipids inside and turns to the foam like cells.

After this stage macrophages take a leading role in atherosclerosis. Macrophages secrete interleukin-1 (IL-1) and tumor necrosis factor (TNF), and they are increasing leukocyte adhesion. Again, monocyte chemoattractant protein-1 (MCP-1) produced by macrophages collects leukocytes in the plaque. They have a role to oxidate the LDL. And finally, they secrete stimu-

Fatty streaks are seen in the childhood phase. This lesion starts as a small 1-mm-diameter intimal color change. With the organization of atherosclerosis, this lesion varies 1–3 mm in

Atheromatous plaque is the definitive lesion, and it is rich in lipids, but more often it is a lipid and fibrotic lesion. Sometimes, this solid and fibrotic characterized plaque can be rich with cells. Plaques' diameter can reach to a few cm. Its color changes according to the amount of

Atheromatous plaques can be seen in the different parts of the body. The prevelence of involvement is in order; Abdominal aorta, coronary arteries, popliteal arteries, descending

Finally, microscopically atherosclerotic plaque has got the main components. These are lipids, vascular smooth cells, monocytes/macrophages, rarely lymphocytes, connective tissue

But more importantly, atherosclerotic plaque changes to four different types. These are com-

**a.** Calcification of the arteries. They can be seen as a consecutive island, and some of them

**c.** Platelet aggregation can occur on the ulcerated plaque. This can lead to total occlusion of the artery. The most devastating effect of atherosclerosis such as heart attack and stroke is

**e.** This ulceration can break endothelial integrity, and this can causes rupture of the plaque

**b.** Ulceration of the surface of the atherosclerotic plaque. This can cause embolization.

diameter and 1–2 cm long. Some of them are raised and some of them not.

the lipid. It is changed to a round shape and has an irregular shape.

thoracic aorta, internal carotid arteries and the circle of Willis.

immunogenic.

And this is shown as fatty streaks.

6 Atherosclerosis - Yesterday, Today and Tomorrow

matrix, and fibrils (**Figure 1**).

can be in the whole artery.

and can cause bleeding.

caused by the superimposed thrombosis.

**d.** Atherosclerotic aneurysm can occur due to atherosclerosis.

plicated plaques:

lators to affecting the smooth muscle cell growth [5].

Due to the asymptomatic phase of atherosclerosis, it is impossible to say the frequency of atherosclerosis, because the process of atherosclerosis starts with fatty streak in the first decade of lifetime. More advanced lesions begin to develop when individuals are in their second and third decade. Complicated coronary atherosclerosis causes coronary artery disease (CAD) after all. CAD remains the most common pathology with which cardiologists and cardiac surgeons are facing. It is the most common cause of death in Turkey in 2013 [6]; 38.8% of the deaths were due to the ischemic cardiovascular disease. Ischemic heart disease is the most common cause of death in the world as reported by the World Health Organization (WHO) in 2012 [7].

Inactivation of genes coding for monocyte chemotactic protein-1 (MCP-1), its receptor on monocyte/macrophages (CCR2), and macrophage colony-stimulating factor has a profound impact on the development of atherosclerosis in otherwise identical mice that have been shown in the experimental studies [8]. The etiology of atherosclerosis is unknown, but in the development process of atherosclerosis, the pathophysiology is important to explain the nature. There are some important risk factors in this process. We have to classify risk factors in two. These are modifiable and non-modifiable risk factors.
