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.

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.

In spite of the first trials on the effect of cholesterol reduction and its beneficial impact on morbidity and mortality in the elderly many have already proven the antecipated positive results. The high risk attributable to the elderly is a guarantee for an effort in primary prevention, especially when a high level of serum cholesterol is combined with other risk factors linked to coronary artery disease. There are elements of similarity for primary prevention in the elderly over 65 years of age, compared to middle-aged patients. This consideration opened the need for scientific evidence with confirmed levels of evidence. The first studies were WOSCOPS, AFCAPS/TEXCAPS, Heart Protection Study, PROSPER, ALLHAT (Antihipertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial-Lipid Lowering Trial), REVERSAL, Health Study, ASCOT (Anglo Scandinavian Cardiac Outcomes), MIRACL, Post CABG, AVERT, ACCESS, ASSET, ATGOAL, CHALLENGE, CURVES, BELLS, ARBITER, NASDAC, PROVE-IT and DEBATE. Positive evidences were shown from the first to the last trial recalled in this historical beginning.

Mini reviewIn women, 46% of deaths result from cardiovascular disease (CVD) and 50% of them refer to coronary heart disease.Women, more than men, have angina pectomy as the initial manifestation of the disease (65% vs. 35%, respectively). Men, on the other hand, have acute myocardial infarction (AMI) as an initial manifestation in a higher proportion than in women (29% vs. 43%, respectively). The varied initial manifestations of ischemic diseases result in different diagnostic approaches; thus, as women report milder symptoms, despite a more severe disease, they are less submitted to diagnostic procedures, even having a positive stress test and, when they are, they are already in a more advanced state of the disease. [1][2][3][4][5][6][7][8][9][10][11]

The concomitance of diabetes metabolic markers, as Glycated Hemoglobin and blood glucose, together with lipid changes; Cholesterol and fractions and Triglycerides, occurs very frequently but not always in the same pairs of markers, being its peculiarities important factors for the estimation of the cardiovascular risk. Not only has the association of high glucose levels and high triglycerides pointed to an augmented risk. The study of the correlations of the parameter Glycated Hemoglobin with all the values of the lipid profile may help gain a broader insight as to the associated risks. A database of 548 individuals with concomitant results of HbA1C, triglycerides, CT and HDL-c were applied statistical tests of ANOVA and Tukey. Most of the 546 individuals tested for glycated hemoglobin (HbA1C) and lipid profile had HbA1C levels within normal range (49.8%), 15.4% were classified as prediabetic, and 34.8% had HbA1C levels above 6.4% (diabetics). The overall mean HbA1C observed was 6.3%, and triglycerides was 236.8 mg/dL. Data from HbA1C-lipid profile comparations are not superimposed, as expected, to the combinations of fasting glucose and triglycerides. In not accompanying lipids concomitantly with HbA1C, the correct assessment of the overall risk calculation for atherosclerosis can be omitted. In conclusion, HbA1C levels should be added to the lipid profile for a more accurate estimation of the cardiovascular risk.

This work is licensed under Creative Commons Attribution 4.0 License OJCR.MS.ID.000544. IntroductionChronic kidney disease (CKD) is currently considered an important public health issue [1]. It is estimated that its prevalence worldwide is around 8 to 16% and that the numbers tend to increase, as has been happening over the last years [2]. It is responsible for high morbidity and mortality rates due to numerous associated complications -cardiovascular, bone and mineral disorders, anemia, among others -and is a costly disease for the system, mainly due to the fact that several of the risk factors responsible for

This work is licensed under Creative Commons Attribution 4.0 License OJCR.MS.ID.000559.