IJCS | Volume 31, Nº4, July / August 2018

364 Gomes et al. Atherosclerosis and hypertension in pregnancy Int J Cardiovasc Sci. 2018;31(4)359-366 Original Article Table 5 - Logistic regression of variables with p < 0.20 in the univariate analysis with carotid atherosclerosis Variables B p value* LDL 0.002 0.0005 Glycemia 0.001 0.0005 Diastolic blood pressure - 0.006 0.003 Systolic blood pressure 0.005 0.002 LDL: low-density lipoprotein-cholesterol. et al. 22 believe that the effects of pregnancy, mediated by metabolic and immunological responses, could take up to more than one year to return to basal levels. When comparing the CIMT of womenwho developed hypertension during pregnancy and those who had uneventful pregnancies, the literature data show to be similar to those found in our study. Akhter et al. 23 did not detect a statistically significant difference during pregnancy and up to one year postpartum when evaluating 55 women. Blaauw et al. 22 also found no differences 5 years after the pregnancy. Moreover, when women between 40 and 50 years of age were assessed, there was no statistical difference regarding CIMT between those who had hypertension during pregnancy and those with uneventful pregnancies. 24 Nevertheless, several observational studies have shown an association between gestational hypertensive disorder and cardiovascular clinical outcomes. Haukkama et al., 25 when assessing 141 women, identified an almost three- fold higher cardiovascular risk in those with a history of gestational hypertension disorder. In the study byKessous et al., 26 the previous history of gestational hypertensive disorder was associated with a greater number of hospitalizations secondary to atherosclerosis 11 years after the pregnancy complicated by hypertensive disorder, even after statistical adjustment for maternal age, parity, diabetes and obesity. Canoy et al. 27 identified in a large cohort that pregnancy-inducedhypertension increased the risk of CVD in women in the menopausal period. Similarly, studies with longer follow-up periods also showed an increase in severe cardiac complications in womenwith a history of pregnancy-inducedhypertension. AsverifiedbyArnadottiretal.,womenwhohadhypertensive complications during pregnancy had a higher risk of death due to ischemic heart disease and cerebrovascular diseases after 30 years, in addition to a shorter time of survival. 28 One of the explanations for not finding an association between carotid atherosclerosis and a history of pregnancy-induced hypertension would be the method used to measure CIMT. That would be caused by the fact that CIMT measured in the common carotid artery would not be a good parameter for the determination of cardiovascular outcomes, as it estimates the total thickness of the intima and media layers. Some authors have shown that only the increase in the intima layer in association with the reduction in the media layer would be important to increase cardiovascular risk. 21,23,24 In our study, we did not analyze themeasurements of the intima and media layers separately. In agreement with the literature, 19,29 we have identified an association between carotid atherosclerosis and traditional cardiovascular risk factors, such as systemic arterial hypertension and hypercholesterolemia. A possible explanation is that both atherosclerosis and gestational hypertension share several common metabolic abnormalities, such as obesity, insulin resistance, dyslipidemia and hypertension itself, as well as the favoring of endothelial dysfunction. 30 According to Brandão et al., 31 endothelial dysfunction precedes the clinical manifestations of a gestation complicated by hypertension and, therefore, it would accelerate the atherogenic process. 32 According to McDonald et al., 33 the persistence of classic risk factors is the foundation of carotid atherosclerosis development, since even after two decades, women with a history of pregnancy-induced hypertension still had more cardiovascular risk factors than those with uncomplicated pregnancies. In our study, women with a history of pregnancy-induced hypertension had a higher prevalence of obesity and chronic hypertension (data not shown in the tables). Although our population consists of outpatients from the public health care system, the sociodemographic characteristics did not differ from those of the general population. Moreover, it was not possible to evaluate information prior to the pregnancy, due to the proposal of the original study. Conclusion Carotid atherosclerosis was positively associatedwith some classic cardiovascular risk factors, such as increased systolic blood pressure and higher levels of LDL- cholesterol. Ahistory of pregnancy-induced hypertension was not associatedwith carotid atherosclerosis in a group