Doença arterial coronariano na pós-menopausa: fatores de risco e influência da apolipoproteína E no metabolismo lipídico

Abstract

Coronary artery disease (CAD) affects women, especially after menopause. Risk factors include age, familial history (FH), smoking, diabetes mellitus, systemic arterial hypertension (SAH), hyperlipidemia and obesity, and postprandial triglycerides. Apolipoprotein E (apo E), represented by 2, 3 and 4, influences lipid serous levels.The aim was to evaluate risk factors for CAD, the prevalence of alleles and genotypes of apo E and their influence on the lipid profile, and the triglyceride metabolic kinetics after a lipid-rich diet considering their association with apo E polymorphisms in women with and without CAD. A total of 180 post-menopausal women, divided into CAD and control groups, with mean ages of 60.7±5.8 and 60.7±5.5, respectively were evaluated. The weight, height, body mass index, systemic arterial pressure, FH, smoking and medicines taken of all the participants were evaluated. Venous blood samples were drawn to measure the total cholesterol (TC), low-density (LDLc), high-density (HDLc) and very low-density (VLDLc) lipoprotein cholesterol fractions and triglycerides during fasting at 3 to 6 hours after the ingestion of a single high-lipid meal. Both groups were subdivided according to levels of TC: ≤200 mg/dL; 201-239 mg/dL and ≥ 240 mg/dL. The genomic DNA was extracted from leukocytes and submitted to amplification by polymerase chain reaction, followed by polymorphism analysis using restriction fragment sizes. Comparing the CAD and control groups, there was significant association of the disease with FH (70% and 44.4% respectively; p<0.0001) and with SAH (76% and 44.4% respectively; p<0.0001). The 4 allele presented with a higher frequency in patients (0.15) compared to controls (0.07; p=0282). There were also increases in CT, LDLc and VLDLc serum levels in patients (25965.7; 170.660.1; 38.621.1mg/dL, respectively) in respect to controls 227.542.3; 136.036.9; 30.717.2mg/dL; P<0.0001; P<0.0001; P=0.025 (respectively). The mean concentration of HDLc, on the other hand, was lower in patients (50.212.0 mg/dL) compared to controls (56.516.7 mg/dL; p=0.0091). The mean triglycerides level was higher in patients and controls compared to normal levels (197113.8; 168.093.0, respectively; P=0.056). The lipid profile was not associated to apo E polymorphisms in patients. The control group with -/4 genotypes presented lower triglyceride serous levels in relation to 3/3 (131.249.9; 174.698.6 mg/dL, respectively; P=0.02). There was an increase in the HDLc serous levels of controls compared to patients, when considering the -/4 genotypes. The controls demonstrated significantly lower triglyceride levels (246.0162.8 mg/dL) compared to patients (292.2161.4 mg/dL; P<0.05), 3 to 6 hours after the lipid-rich diet, associated with the -/4 genotypes. In conclusion, FH and SAH are associated with CAD in post-menopausal women. The 4 allele is more prevalent in post-menopausal CAD patients than in control individuals, but it does not influence the lipid profile, however, it exerts a protector effect by its association with high HDLc levels in post-menopausal women without the disease. The triglyceride kinetics, although with similar profiles in both groups, reveal an association between the 4 allele and the accelerated removal of triglycerides only in the control group, suggesting a protector effect in the postprandial stage in post-menopausal women.