DISCUSSION

representing (31.6% of this class), 9 individuals with stroke (34.6%), 21 individuals with CAD (70%), and 18 individuals with POAD (60%). Thus, Spearman correlations indicated that only individuals with CAD were associated with increased levels of Lp(a).

values of the biochemical parameters belonging to the group with CAD. (ii) if the HDL value found in Table II (between 35.5 and 47.2 mg / dL) are in fact reduced values, implying lower values of the biochemical parameter belonging to the group with PAD, and finally ( iii) point:

the small percentage of individuals with stroke (38.46%) and CAD (33.3%) who, in turn, present indices of Lp(a) < 30 mg / dL is significant.

As opposite, the LDL values are very similar to the LDL values recorded in Table II, which in turn are higher than 100 mg / dL, confirming that there is no significant difference.

The maximum value of 100 mg / dL correlates with diabetic individuals of the PAD group. If these individuals are smokers or hypertensive, the probability of developing PAD is even greater, and consequently, higher values of Lp(a) (> 30 mg / dL) would be noticed, which did not happen because 70% of the individuals presented Lp (a) < 30 mg / dL. However, the individuals belonging to the stroke and POAD groups presented values above 50 mg / dL.

These considerable values of Lp(a) may be related to family history, or even type 2 diabetes mellitus, according to the results recorded in table I.

Recent recommendations state that lipoprotein (a) screening is not warranted for primary prevention and assessment of cardiovascular risk at present but that lipoprotein (a) measurement can be of use in patients with a strong family history of cardiovascular disease or if risk of cardiovascular disease is judged intermediate on the basis of conventional risk factors. In addition to measurement difficulties, a number of factors contribute to lipoprotein (a) levels not being incorporated into routine cardiovascular risk assessment presently, considering that there are no effective drugs that selectively reduce plasmatic levels of lipoprotein (a) (MOHANRAJ; SANDHYA, 2019).

Moreover, values found for the LDL of the four groups (ranging from 111.7 mg / dL for the control group to 124.7 mg / dL for the POAD group) are in fact high values. Levels of Lp(a) were, in turn, higher than normal in the individuals belonging to the CAD and POAD groups (twice the levels in the control group). It should be noted that no association so far has been observed in the stroke group since the values of Lp(a) for this group are within the reference range (<30 mg / dL).

Levels of Lp(a) were, in turn, higher than normal in the individuals belonging to the CAD and POAD groups (twice the levels in the control group). From Table III, however, it was possible to associate only the high values of Lp(a) with CAD and not with POAD, both with relative risk within the confidence range and p ~ 0.003. It is likely that individuals who developed POAD only had high Lp(a) values because they are diabetic, and these diabetic individuals did not develop CAD. It should be noted that no association so far has been

observed in the stroke group since the values of Lp(a) for this group are within the reference range (< 30 mg / dL). Similarly, there is controversy in the literature if Lp(a) determines risk of stroke (GOLDSTEIN, 2001).

According to the results to date, the response obtained for Lp(a) was very varied, as plasma levels were found to be slightly below 30 mg / dL, and high values (above 50 mg / dL) were found. This result shows that Lp(a) is a variable parameter, which depends on the individual response of each patient, and this may have influenced the absence of significant differences between the medians of the studied groups. However, as there was a tendency for a higher Lp(a) elevation, even above the reference levels, in the group with CAD and POAD, this parameter can be considered a marker with potential value to signal a higher risk of atherosclerosis and cardiovascular event in these patients, with reduction of HDL.

The association of Lp (a) with CAD can be doubly explained: by high concentrations of Lp(a) and by the inflammatory process itself of atherosclerosis. Thus, elevated plasmatic levels of Lp(a) may also be part of the consequence and not only the cause of the atherosclerotic process (MILIONIS et al., 2000). It was found a risk of developing CAD 2.3 times higher with Lp (a) > 25 mg / dL, other researchers (RICHES; PORTER, 2012), calculated the risk as being twice as high with Lp(a) above 20 mg / dL. Furthermore, in pro- inflammatory states, Apo-AI becomes a substrate for myeloperoxidase (MPO), a protein released by macrophages, monocytes and neutrophils, which catalyzes the chlorination or nitration of tyrosyl residues of ApoA-I molecules in HDL. MPO promotes oxidative damage of the HDL particle, which leads to a significant reduction of its anti-inflammatory properties, thus rendering HDL dysfunctional (KAMEDA et al., 2015). Oxidized LDL is a powerful inducer of atherogenesis due to its role in endothelial dysfunction and foam cell formation. The mechanism by which oxidized LDL promotes atherogenesis involves the promotion of monocyte adhesion to the endothelium via activation of macrophages and mast cells (CHEN;

KHISMATULLIN, 2015).

The results indicate that the relationship between Lp(a) levels and arterial diseases is not random because r ≠ 0. There was a direct correlation between the high levels of Lp(a) and atherosclerosis and also between the high Lp levels ( a) and CAD, with a moderate Spearman index (r = 0.29). However, there was an inverse relationship between high levels of Lp(a) and stroke (r = -0.09).

In this case, the Spearman index is an alternative that estimates linear correlations in situations where there is a violation of the joint normality assumption between Lp(a) levels