Many research groups on atherosclerosis have sought through prospective large-scale epidemiological studies to better understand which residual factors would be associated with cardiovascular risk. Thus, atherogenic dyslipidemia was defined, such as the presence in an individual of decreased HDL-C levels, increased triglyceride levels, and a relatively high proportion of small and dense LDL-C particles. On the other hand, it was found that atherogenic dyslipidemia is present in cases of insulin resistance and metabolic syndrome (low HDL-C and elevated triglycerides are part of the definition of this syndrome) and consequently in patients with type 2 diabetes mellitus. Regarding treatment, there are studies in diabetic patients with risk reduction with fenofibrate, and the guidelines recommend the association of fenofibrate with statins. Diabetes mellitus is also an important cause of hospitalizations and proportional mortality, also assuming that most deaths register only the immediate cause of this death, which is often the result of diabetes complications. Most of these complications are cardiovascular diseases, which may manifest as coronary heart disease, cerebrovascular disease or peripheral arteriopathies. These are the so-called macrovascular complications of type 2 diabetes and are present even before the onset of hyperglycemia, due to the presence of insulin resistance and associated metabolic syndrome. Metabolic syndrome is characterized by the presence in the patient of at least 3 out of 5 parameters (increased abdominal waist, high glycemia, hypertriglyceridemia, low HDL-C and arterial hypertension) and is one of the factors responsible for the macrovascular changes.

The involvement of inflammation is described in all stages of atherosclerosis as well as in dyslipidemias, particularly in lipoproteins (especially oxidized LDL), coronary syndromes, hypertension, diabetes, infections, obesity, and also in the use of sexual replacement hormones. From the first steps of leukocyte recruitment in the nascent atheromatic lesion to the development of atheroma plaque, culminating in its rupture and thrombosis in the acute coronary event, we found a constant release of inflammatory mediators, soluble in plasma, from macrophages, T lymphocytes, endothelial cells and smooth muscle vessels of the vessels, hepatocytes, and adipocytes. The greatest evidence relating inflammation to the future development of cardiovascular events has been verified in large-scale population studies. High concentrations of inflammatory markers such as TNF-α, IL-6, ICAM-1, P-selectin, E-selectin, C Reactive Protein, fibrinogen, and amyloid serum A, in apparently healthy individuals, have shown predictive value for future vascular events. Considering the multifactorial etiology of coronary artery disease and its inflammatory nature, it was possible to find an association between the presence of risk factors and the increase in the concentration of biomarkers of inflammation. TNF-α is a multifunctional cytokine derived from smooth endothelial and muscle cells, as well as macrophages present in the coronary atheroma. It is involved in a number of cardiovascular processes, being increased in congestive heart failure.

In view of the controversy between hormonal replacement in postmenopausal women and decreased cardiovascular morbidity and mortality, and the effects of estrogens associated with progesterones, or progesterone alone, we developed a protocol to evaluate the repercussions of hormone therapy with progesterone in oophorectomized rabbits submitted to atherogenic diet, on the development of atherosclerotic lesions induced in animals. Forty New Zealand rabbits were oophorectomized and divided into three groups. After 90 days, when the animals were sacrificed and the lesions that developed in the aorta and coronary arteries were evaluated. The results showed an increase in serum cholesterol in the four groups of animals. In groups II, III and IV, there was an increase of approximately fifteen times the baseline values, with no significant differences between these groups observed in 5 time courses. Regarding triglyceride levels, we found that group III showed a significant increase in values in Time 4, but this difference was not verified in Time 5. When quantitatively analyzing the area occupied by the lesion, we found that there were no statistically significant differences between the groups submitted to the atherogenic diet, observing that the coronary arteries presented a lower number of compromised arteries

Definition and functionLipids: are biomolecules, chemically heterogeneous, which are characterized by being insoluble in water. 1 The main lipids for humans are: fatty acids (FA), triglycerides (TG), phospholipids (PL) and cholesterol. 2,3 Fatty acids: the most important for man's nutrition are long-chain (C 12 -C 20 ), containing evenly numbered carbon atoms. They were defined as: saturated (not present double bond inside the molecule, e.g. steariaric C 18:0 ), monounsaturated (have a double bond, e.g. oleic C 18:1 ) and polyunsaturated (have more than a double bond, e.g. linoleic C 18:3 ). In general, saturated FA of animal origin and unsaturated ones of plant origin predominate in the diet. Longchain FA is oxidized for energy production by the process known as β oxidation, which results in sequential reduction of the chain every two carbon atoms, and the production of Acetyl-Coenzyme-A (Acetyl-Co-A) that enters the tricarboxylic acid cycle (Krebs cycle) to generate energy. The FA has an energetic function, participate in the synthesis of prostaglandins and provide Acetyl-Co-A for the synthesis of other lipids.Triglycerides: are obtained by diet or produced by the body, from the esterification of glycerol with three molecules of FA, in liver or adipose tissue. It has an essentially energetic role, for immediate or subsequent storage use. Phospholipids: have a glycerol molecule as the backbone, in which two FA are esterified. The third hydroxyl group is attached to alcohol through phosphodiester binding. Therefore, PL have both domains: one hydrophilic (phosphate group) and another hydrophobic (FA), which give it structural function in the double layer that make up cell membranes and on the surface of lipoprotein particles.Cholesterol: Is the main steroid of man, unsaturated monohydric alcohol, derived from the pentanoperhydrophenantrene cycle and is present in all cells of the body and in most fluids. It may be in free form (structural component of cell membranes and on the surface of lipoprotein), or esterified (stored inside cells or inside lipoproteins). Cholesterol esterification occurs in the blood plasma by the action of the enzyme LCAT (lecithin cholesterol acyl transferase), activated by apo A-I, which transfers an FA of lecithin to the 3-beta-hydroxide cholesterol position. Intracellular esterification occurs by the action of ACAT (acyl-CoA-cholesterol acyl transferase). Cholesterol is present in foods, with the exception of vegetables, but most of it found in the body comes from the synthesis of new from acetate (Acetyl-Co-A). The step that regulates the speed in the synthesis pathway is the conversion of 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, catalyzed by the enzyme hydroxy-methyl-glutariICoA reductase (HMGCoA reductase). The liver is the organ responsible for most of the synthesis of new cholesterol. Cholesterol also serves as a precursor for synthesis of steroid hormones, vitamin D and bile acids.