Blood lipids variations of persons with family history of severe arterial hypertension

Abstract

Background: Despite large research on impact of lipoprotein (a) and apolipoprotein B100 on the development of atherosclerosis and its effect on the human body, the problem of the onset of their variations in blood serum has not yet been clarified. Aim: To compare the variations of parameters of lipid metabolism in hypertension-diseased patients and in persons with family history of severe arterial hypertension. Patients and methods: Ninety subjects were examined. Group 1 comprised 41 patients with arterial hypertension disease, grade 2, 22 men and 19 women aged from 35 to 70 (the average age 52.4 ± 0.6 years). The comparison Group 2 comprised 23 practically healthy persons, but with family history of severe arterial hypertension. The control Group 3 consisted of 26 practically healthy subjects of comparable age and gender. Apart from full clinical examination, all the 90 persons under research were tested for overall cholesterol level, high density lipoproteins cholesterol, triglycerides, lipoprotein (a), apolipoprotein B100, apolipoprotein A-1. The statistical calculations were carried out applying the set of programs Microsoft Excel, Statistics for Windows 6.0. Results: The patients in Group 1 affected by hypertension disease, grade 2 have shown lipid metabolic disorder manifested by the increase of overall cholesterol levels, proatherogenic lipoprotein classes low density lipoproteins and very low density lipoproteins, lipoprotein(a), apolipoprotein B100, and decrease of high density lipoproteins cholesterol and apolipoprotein A-1 which significantly differ from the related levels in the control Group 3. Persons in Group 2 with family history of severe arterial hypertension have shown similar proatherogenic changes in lipid fractions of blood serum as the patients with arterial hypertension i. e., remarkable (p < 0.001) rise of overall cholesterol levels, low density lipoproteins cholesterol and lipoprotein (a), as compared to the control Group 3, which can testify a genetic cause of the detected lipid metabolic disorder. The lipoprotein (a) level by 67.0 % exceeded the values in the control Group 3 (p = 0.0005), but was reliably lower (p < 0.05) than in hypertension disease-affected patients (Group 1). Conclusions: The detected changes in lipid metabolism in persons with family history of arterial hypertension testify the possible relation of these disorders to a genetic susceptibility. The increased lipoprotein (a) level can be regarded as an additional high risk marker of onset of both ischemic heart disease and arterial hypertension in this population, as well as their unfavorable outcome.