**2.2. Vascular changes**

The spectrum of clinical and morphological changes that can be displayed has changed over time. One of the classifications we find is that proposed by author Gibbons [12]. These changes are shown predominantly in the relationship of light/medium vessel by changing the ratio of wall thickness by an increase in muscle mass or reorganization of the cellular and noncellular components. These changes increase vascular reactivity, which promotes increased peripheral resistance in diseases such as hypertension. Another form of vascular remodeling involves primarily changes in the dimensions of the light. In this example, the restructuring of the active components of cellular and noncellular vascular wall results in significant changes in the dimensions of the vascular lumen, with relatively small changes in wall thickness. The clinical examples of this type include remodeling associated with vascular dilation of blood flow which is consistently high, for example, an arteriovenous fistula or loss in cellularity and proteolysis of extracellular matrix, resulting in the formation of an aneurysm. By contrast, a mass reduction vascular caliber results from a long-term reduction in blood flow. In fact, rarefaction of the microcirculation is another form of vascular remodeling. The architecture of the vascular wall is also markedly changed in response to vascular injury. Neointima is formed as part of a repair response to injury involving thrombosis, migration, and proliferation of vascular cells, production of the matrix, and infiltration of inflammatory cells.

The term "remodeling" is limited to situations in which there is a change in the lumen of a vessel relaxed, measured under a standard intravascular pressure, and where changes in the characteristics of the wall material (i.e., the wall stiffness) do not consider the change in the vascular lumen [13].

Chronic changes in hemodynamic forces produce structural alterations in the vascular wall, as stated above. Furthermore, hemodynamic changes are not the only production mechanisms of vascular remodeling [14], and the role of the inflammatory response and changes in matrix components have been suggested as mediators in this process of vascular adaptation [15].

To complete the above concept, the vascular wall remodeling is the result of changes in cellular and noncellular components, depending on the disease process causing the changes. Changes in growth and migration of VSMC, endothelial dysfunction, the inflammatory process, synthesis, or degradation of extracellular matrix components may be present in this process.

#### **2.3. Vascular remodeling and inflammation**

The traditional view of atherosclerosis as a lipid storage disease crumbles in front of the large and growing evidence that inflammation contributes to the center at all stages of the disease, from initial injury until the final stage of thrombotic complications that compromise the bloodstream. Researchers now appreciate that the mere narrowing of the arterial lumen does not necessarily presage myocardial infarction and that simply treating narrowed blood vessels does not prolong life. Although invasive procedures such as angioplasty and coronary bypass will remain necessary in some cases, we now understand that medical treatment and lifestyle modification (diet and physical activity) produce benefits that may result from reductions in the processes inflammatory [16].
