Background: Several novel criteria can improve detection of subclinical atherosclerosis. In particular, the clinical interest has focused on lipoprotein(a), a modified LDL particle which presents a structurally homologue protein to plasminogen.
Aim: The aim of our work was to evaluate the levels of lipoprotein(a), in hypertensive patients with or without atherogenic dyslipidemia comparative with a control group and to estimate the relationship of Lp(a) with other biological and functional parameters.
Methods: The study included 40 hypertensive patients with atherogenic dyslipidemia (HTN+DYS), 43 hypertensive patients without atherogenic dyslipidemia (HTN-DYS) and 35 control subjects, aged and sex matched. The hypertensive patients were not receiving pharmacological therapy and had no clinical signs of associated pathologies or organ damage. We determined in all groups the levels of Lp(a), apolipoprotein A-I and apolipoproteinB and fibrinogen. Lipoprotein(a) was measured by enzyme immuno assay (ELISA) test. Using B-mode ultrasonography we determined carotid intima-media thickness (IMT) and flow mediated vasodilatation (FMD) in all patients.
Results: Lp(a) was significantly higher in HTN+DYS group than in HTN-DYS group and than in control group (77.18 ± 48.51 mg/dL versus 58.14 ± 47.31 mg/dL versus 22.64 ± 11.86 mg/dL versus , p<0.001). A significant correlation was found between Lp(a) and IMT (r = 0.64, p < 0.001), between Lp(a) and fibrinogen (r = 0.78, p < 0.001), and between Lp(a) and brachial FMD (r = -0.29, p < 0.001). Lp(a) levels were not correlated with total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoproteins A-I or B or apoA-I/apoB.
Study Limitations: Potential limitations of our study are the relative small number of patients and controls and missing apo(a) phenotype.
Conclusion: Lp(a) levels are related to early structural changes of the carotid arteries as shown by ultrasound measurements of IMT and to early functional changes evaluated by brachial FMD and can be considered an emerging risk factor for premature atherosclerosis.
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