Oxidized Low-Density Lipoprotein Autoantibodies, Chronic Infections, and Carotid Atherosclerosis in a Population-Based Study

Objective Physical activity is associated with improved carotid atherosclerosis in spinal cord injury (SCI) subjects independent of variation in hemodynamic, metabolic and inflammatory variables. The present study investigated the role of oxidized low-density lipoprotein (Ox-LDL), matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) in this regard. Design and Methods We studied 40 men with chronic (>1 year of injury) SCI and no voluntary motor activity [17 sedentary (47% tetraplegic) and 23 athletes (52% tetraplegic)] by clinical, anthropometric, laboratory (glucose, lipid profile and C-reactive protein), hemodynamic (blood pressure and cardiac output) and carotid ultrasound analysis. All enrolled subjects were normotensive, non-diabetics, non-smokers and normolipemic. Plasmatic Ox-LDL, MMP2, MMP8, MMP9, TIMP1 and TIMP2 were determined by ELISA. Data are presented as mean±SEM. A p-value <0.05 was considered significant. Results Sedentary SCI subjects and SCI athletes presented similar clinical, anthropometric, laboratory and hemodynamic features. Carotid intima-media thickness (IMT) of SCI athletes was lower than that of SCI sedentary individuals (0.54±0.01 vs 0.69±0.02 mm; p<0.001). SCI athletes presented lower Ox-LDL (38.4±2.1 vs 54.1±4.1 U/L; p<0.001) levels in comparison with SCI sedentary individuals. Conversely, MMPs and TIMPs levels as were as MMP8/TIMP1, MMP9/TIMP1 and MMP2/TIMP2 ratios were similar between the SCI groups. Bivariate correlation analysis including all SCI subjects showed that carotid IMT correlated with Ox-LDL (r=0.54; p<0.001), but not with any MMPs or MMP/TIMP ratios. Further linear regression analysis adjusted for the presence or not of physical activity showed that Ox-LDL was still associated with carotid IMT (beta=0.293±0.141; p=0.044) in the whole sample. Conclusions Plasmatic Ox-LDL levels are associated with increased carotid IMT in SCI subjects and are lower in physically active SCI individuals than in sedentary SCI ones. These findings may provide a potential mechanism by which physical activity attenuates SCI-induced atherosclerosis.

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Circulating oxidized low-density lipoprotein is increased in hypertension

Clinical Science ◽

10.1042/cs20030152 ◽

2003 ◽

Vol 105 (5) ◽

pp. 615-620 ◽

Cited By ~ 41

Author(s):

Johan FROSTEGÅRD ◽

Ruihua WU ◽

Carola LEMNE ◽

Thomas THULIN ◽

Joseph L. WITZTUM ◽

...

Keyword(s):

Carotid Atherosclerosis ◽

Screening Programme ◽

Diastolic Pressure ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Disease Stage ◽

Low Density ◽

Oxidized Low Density Lipoprotein ◽

Swedish Population

Oxidized low-density lipoprotein (OxLDL) and autoantibodies to OxLDL (aOxLDL) are implicated in the development of atherosclerosis. The objective of this study was to determine the importance of these factors in hypertension, a major risk factor for atherosclerosis. Samples were obtained from 111 men with established hypertension (diastolic pressure >95 mmHg) from the Swedish component of an ongoing hypertension study (European Lacidipine study on Atherosclerosis, ELSA) and from 75 normotensive control men, who were from a Swedish population-screening programme (diastolic pressure <80 mmHg). The presence of carotid atherosclerosis and the intima-media thicknesses were determined by ultrasonography. A monoclonal antibody to OxLDL, EO6, was used to determine oxidation epitopes in LDL. aOxLDL of IgG and IgM subclass were tested by ELISA against OxLDL. Hypertensive men had increased OxLDL levels compared with normotensives (P=0.002), whereas autoantibodies tested were largely similar between groups. There was no association between the antibodies tested, or OxLDL and carotid atherosclerosis. Age was not associated with OxLDL or aOxLDL measurements. Taken together, our findings indicate that OxLDL is elevated in hypertensive men, which may predispose to atherosclerosis in hypertension. In contrast, aOxLDL levels were unchanged and the role of aOxLDL may depend on disease stage and/or type.

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