**3. Pathophysiology**

The predominant type is often seen with intimal fatty plaque formation including central

The second morphologic type of atherosclerosis, Mönckeberg's medial calcific sclerosis, is seen in the muscular arteries with a medial calcification. This form is not prominent as classic atherosclerosis and mostly seen after the age of 50. This can be seen radiologically and can be

The third type is the disorders of the small arteries and arterioles, named arteriosclerosis. This is seen mostly with hypertensive and diabetic patients. This refers to stiffening or hardening

The final result of atherosclerosis is that arteries become narrowed and hardened due to an excessive buildup of plaque around the artery wall. The disease disrupts the flow of blood

Atherosclerosis can be seen in all arteries in the body. But we will instruct about the coronary atherosclerosis. Atherosclerosis is the most common cause of death in the western countries [1].

Arteries contain what is called an endothelium, a thin layer of cells that keeps the artery smooth and allows blood to flow easily. Endothelial damage starts the first step of atherosclerosis. After this LDL cholesterol accumulates in the artery wall. Inflammatory process starts after this accumulation, and macrophages reach the endothelium to clean up cholesterol. But some macrophages stuck in the affected part of the artery wall in this process. Over time this results in plaque being built up, consisting of cholesterol and macrophage

The plaque clogs up the artery, disrupting the flow of blood. This potentially causes blood clots that can result in life-threatening conditions such as *heart attack* and other cardiovascular

Some risk factors are follows: age, sex, familial predisposition, hyperlipidemia, hypertension, diabetes mellitus, smoking, obesity, insufficient physical activity, etc. Whatever the main reason or the risk factor is, once atherosclerosis is formed, several life-threatening cardiovascular

The role of the circulation is to service the needs of the tissues. It includes transporting nutrients to thecells of the body and waste products away from the cells of the body. And finally transporting hormones from one part of the body to another. Naturally, circulation maintains an appropriate environment in all the tissue fluids of the body for optimal survival and func-

Systemic circulation, pulmonary circulation, peripheral circulation, etc. have some details to maintain the blood flow. The arteries are the large conductive vessels that transport blood

lipid-rich core. We want to mention about this type of atherosclerosis.

around the body, posing serious cardiovascular complications.

disorders can be seen. So, it has to be revealed.

felt with palpation.

4 Atherosclerosis - Yesterday, Today and Tomorrow

of the artery walls.

white blood cells.

**2. Background**

tion of the cells.

diseases.

Atherosclerosis is a chronic, inflammatory, fibroproliferative disease of medium- and largesized arteries [3]. There are different stages to form the atherosclerotic plaque. The initiation phase is the beginning and the progression of the plaque and the final complication stage.

Chronic or recurrent endothelial damage is the cornerstone of the "response to damage" hypothesis. Hyperlipidemia, hypertension, smoking, immunoreactions, hemodynamic factors, toxins, and viruses can cause this chronic endothelial damage. Hemodynamic deformities such as endothelial shear stress, turbulent flow, or unfavorable effects of hypercholesterolemia have a role in the initiation phase. Due to endothelial damage and turbulent flow, endothelial permeability, cell regeneration, and receptor-mediated LDL endocytosis and leukocyte adhesion to endothelium increase.

Hyperlipidemia has an important role in the atherogenesis [4]. Chronic hyperlipidemia especially hypercholesterolemia can start the endothelial damage. After all, lipoproteins accumulate in these damaged endothelial sites. The cellular response after endothelial damage continues with increased permeability, leukocyte adhesion, monocyte migration, and increased adhesion. This is no longer the initiation phase after this stage; progression has started.

Some cellular events take an important part in this phase. Smooth muscles migrate from the media layer to intima and macrophages activated. Monocytes turn to macrophages. Activated macrophages, and smooth muscle cells absorb lipids. Modified lipid molecules due to the oxidative mechanisms of modified LDL arise. Oxide LDL makes some additive affects, in order; (a) with the help of altered receptors LDL absorbed easily by macrophages (b) they 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 immunogenic.

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. And this is shown as fatty streaks.

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

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

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

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

Finally, microscopically atherosclerotic plaque has got the main components. These are lipids, vascular smooth cells, monocytes/macrophages, rarely lymphocytes, connective tissue matrix, and fibrils (**Figure 1**).

**4. Epidemiology and etiology**

**Figure 1.** The stages of the progression of atherosclerosis.

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

Focus on Coronary Atherosclerosis

7

http://dx.doi.org/10.5772/intechopen.77301

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

death in the world as reported by the World Health Organization (WHO) in 2012 [7].

in two. These are modifiable and non-modifiable risk factors.

But more importantly, atherosclerotic plaque changes to four different types. These are complicated plaques:



**Figure 1.** The stages of the progression of atherosclerosis.
