Zusammenfassung
Objectives: Oxidative modification of low-density-lipoprotein (LDL) increases its atherogenic potential to induce the accumulation of lipids and cells in the vascular wall. Patients have different lipoprotein profiles according to their LDL-subgroup pattern. The subgroup of LDL, which is most susceptible to oxidation, is most likely the dense LDL3 subfraction. In order to study an assumed ...
Zusammenfassung
Objectives: Oxidative modification of low-density-lipoprotein (LDL) increases its atherogenic potential to induce the accumulation of lipids and cells in the vascular wall. Patients have different lipoprotein profiles according to their LDL-subgroup pattern. The subgroup of LDL, which is most susceptible to oxidation, is most likely the dense LDL3 subfraction. In order to study an assumed association between hypertension, LDL subgroup distribution and the susceptibility of LDL to oxidation, 14 normotensive patients without family histories of hypertension (NT), 13 normotensive patients with family histories of hypertension (NT-FH), 10 hypertensive patients without family histories of (HT) and 11 hypertensive patients with family histories of hypertension (HT-FH) were evaluated. Patients and methods: LDL was oxidatively modified by incubation with copper ions (1.6,muM/L). The course of LDL-oxidation was measured in vitro by continuous photometric monitoring and the quantitative distribution of 3 LDL-subgroups by capillary isotachophoresis (ITP). Results: The lag-phases of NT-FH and hypertensive patients were shorter than those of the control group (NT 116 +/- 36 minutes; NT-FH 92 +/- 32 minutes, p < 0.05; HT 95 +/-41 minutes; HT-FH: 76 +/- 33 minutes, p < 0.05). Compared to NT a significant difference in the relative preponderance of LDL3 subgroup was observed for HT-FH(23.5 +/- 4.6% versus NT: 19.3 +/- 66%), additionally, statistical analysis showed a similar trend amongst the other patient groups (NT-FH: 20.4 +/- 7.4%, HT 21.4 +/- 4.6%). Conclusions: The increased occurence of the LDL3 subgroup might contribute to a higher susceptibility to LDL oxidation and therefore create an increased risk of vascular disease in the genotypic and phenotypic hypertensive patient population.
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