**4. Endotelial disfunction**

#### **4.1 Atherosclerosis in obesity**

The process to atherosclerosis begins with fatty streaks resulting in thickening of the intima arterial layer. Obesity is considered a storm, which accelerates this process by several mechanisms such as insulin resistance through adipocytokines, endothelial dysfunction, hypercoagulability, and inflammation. The VAT makes systemic and vascular inflammation that promotes atherogenesis. Further, insulin resistance has been associated to metabolic syndrome, proinflammatory, and prothrombotic states.

Endothelial dysfunction in obesity has two principal causes: diminished bioavailability of nitric oxide and increased oxidative stress. A good marker of early atherosclerosis is carotid intima media thickness [18].

Several prospective epidemiological studies demonstrate that obesity and higher risk of incident coronary artery disease (CAD) are strongly linked. Excess visceral fat rather than body weight has been linked to increased risk of cardiovascular events. BMI, higher measures of central adiposity, including WC and waist-to-hip ratio (WHR), were aligned with a higher risk of CAD and cardiovascular mortality independently of BMI [19, 20].

Another important concept is the duration of obesity and abdominal adiposity, expressed as excess BMI-years and WC-years, which are stronger predictors of CAD, highlighting these measurements must be evaluated together [21].

#### **4.2 Microvascular disease and obesity**

The chronic inflammatory conditions developed from the obesity are linked to abnormalities in the coronary microvasculature. Coronary microvascular disease is pathophysiologically associated with endothelial dysfunction and possibly to small vessel remodeling and also disturbing coronary blood flow; this microvascular disease is independently associated with higher BMI [22].

Obesity has implications in macrophages and adipocytes that generate a proinflammatory state that increases the cytokines and reduces the nitric oxide. All this cascade promotes endothelial dysfunction (**Figure 1**).

**Proinflamatory state:** IL1β, IL 6, Leptin, TNFα, PCR, NO.

**Endothelial Dysfunction:** ROS, angiotensinogen, calprotectin NO, Ghrelin. **Metabolic disorders:** Changes in glucose and lipid metabolism, insulin resistance, hypertension, atherosclerosis.

*IL1* β*: Interleukin 1* β*, IL6: Interleukin 6, TNF Tumor Necrosis Factor, Nitric Oxide, ROS: Reactive Oxygen Species*.

Normally the endothelium regulates vascular homeostasis; it is the natural inner lining of the vessels. Its layers are: tunica intima, tunica media, and the vascular smooth muscle cell (VSMC). But there is a combination-coordination of multiple factors such as blood flow, distribution of nutrients, hormones, and other macronutrients, and migration and proliferation of VSMC. The VSMC is an important

*Obesity and Cardiovascular Risk DOI: http://dx.doi.org/10.5772/intechopen.106877*
