**1. Introduction**

Cardiovascular pathologies are still one of the most serious diseases in the world and are also known to be an important reason of mortality and morbidity. Furthermore, they cause a significant burden on the health costs. The understanding of pathophysiology of cardiovascular diseases has an important role for the treatment success. In this chapter, vascular calcification mechanism and its results will be discussed.

There are several reasons leading to vascular calcifications (**Table 1**). Vascular calcifications often occur in the advanced stage of the atherosclerosis [1]. In addition to this, these calcifications may also occur as a complication of metabolic disorders in the end stage of chronic renal failure. Calcium deposits accumulate in vascular tissues as a result of secondary hyperparathyroidism that occurs in chronic renal failure [2, 3]. Another cause of vascular calcifications is familial hypercholesterolemia. Particularly severe aortic calcifications are seen in these patients [4]. Vascular calcifications associated with diabetes mellitus also affect the media and intima layer of vessels [5]. Hypertension is associated with calcifications in the abdominal aorta [6]. The other causes of vascular calcification include smoking [7], male gender [6], and older age [7]. Recently, it has been observed thanks to intravascular invasive images that the use of statins increases vascular calcification. Despite the antilipidemic and anti-inflammatory effects of it, statins cause an


#### **Table 1.**

*The causes of vascular calcification.*

increased calcification in vascular tissue with an unknown mechanism. This effect is defined as the statin paradox [8].

### **2. Pathophysiology**

Vascular smooth muscle cells (VSMCs) play an important role in the pathology of vascular calcifications. Vascular smooth muscle cells are of mesenchymal origin. These cells may turn into osteoblasts and chondrocytes under stress. Osteoblast-like cells that contain hydroxyapatite crystals appear in the extracellular matrix during vascular smooth muscle calcification. Subsequently, the number of osteochondrogenic cells increases, and calcification inhibitors are suppressed; an increased regulation of bone mineralization regulating genes and the release of calcified membrane-dependent carriers from smooth muscle cells in these calcifications are observed. In addition, intracellular phosphate concentration increases in osteoblastlike cells due to developing hyperphosphatemia in chronic renal failure. Apoptosis in smooth muscle cells, oxidative stress, remodeling in extracellular matrix, and high levels of metalloproteinases increase vascular calcification, resulting in endothelial dysfunction [9].

Vascular smooth muscle cells are the predominant cell type in the arterial wall. VSMCs are mainly composed of the medial layer of the blood vessels, which are subjected to mechanical stress and pressure of blood flow, and maintain vascular tone and resistance [10]. Calcium functions as a stimulator, and under physiological conditions, intracellular calcium is present in VSCMs to regulate many biophysical and biochemical processes [11]. Although the agents responsible for production of vasospasm have not yet been clearly identified, recently the molecular mechanisms involved in the development of vasospasm mainly based on experimental data in canine two-hemorrhage model are reviewed. The blood products after subarachnoid hemorrhage most likely stimulate many cell membrane receptors to activate the tyrosine kinase pathway of WSCMs. The activation of the tyrosine kinase pathway is associated with continuous elevation of intracellular Ca++ levels and activation of mu-calpain. The increased intracellular Ca++ concentration stimulates Ca++/calmodulin and depends on myosin light-chain kinase to phosphorylate myosin light-chain continuously during vasospasms [12]. Cerebral vasospasm is the most frequent and troublesome complication after aneurysmal subarachnoid hemorrhage. Cerebral vasospasm is considered a treatable clinicopathological entity; it is still responsible for many deaths and serious disabilities among patients suffering from intracranial aneurysm rupture [13].

**47**

*Vascular Calcifications*

**3. Classification**

ing of the lumen diameter.

**4. Imaging methods**

*The classification of vascular calcification.*

**4.1 Noninvasive methods**

accumulation, fibrotic tissue, and calcifications.

seen in three ways:

**Figure 1.**

resulting in arterial stiffness [9].

*DOI: http://dx.doi.org/10.5772/intechopen.90287*

Vascular calcifications are divided into two subtypes (**Figure 1**). These are called

Medial calcifications are characterized by concentric calcium deposits in the tunica media layer. Here, elastin lamellae occur between the smooth muscle cells and the elastin fibers. Medial calcifications cause loss of elasticity in the arteries,

Various methods are used to visualize calcifications. Macrocalcifications can be

2.Sheetlike fragments: linear or wide single focus of calcium, >2 mm in diameter

Computerized tomography (CT) is the gold standard for imaging calcifications. 400 μm of calcification can be shown as 2D and 3D with the help of CT. However, the calcifications sometimes can be seen as more exaggerated than usual because of the absorption of high X-rays by neighboring tissues in CT imaging. This exaggerated image (artifact) may mask parts of calcification in the proximal region of the lesions. In this case, the artifact can be distinguished from the surrounding soft tissue with the help of magnetic resonance imaging (MRI). MRI is also superior to CT in differentiating multiple components including the coexistence of lipid

Microcalcifications can be detected by the use of positron emission tomography (PET) which is one of the other noninvasive methods. Early microcalcifications are shown using indirect gamma rays with the aid of 18F-sodium fluoride. With the use

Imaging methods can be performed as noninvasive and invasive (**Table 2**).

1.Speckled: spotty calcification flecks, up to 50 μm diameters

3.Diffuse: segments of continuous calcification, ≥5 mm in diameter

intima and media calcifications according to the localization of calcification. Intimal calcifications or the so-called atherosclerotic calcifications begin to occur in the presence of chronic inflammations and/or lipid accumulations. Lipidloaded calcifications in the intima cause intimal thickening and subsequent narrow-
