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We compared several "new" risk factors (autoantibodies to oxidatively modified low density lipoprotein (LDL), sialic acid content of LDL, bilirubin and C-reactive protein) with "conventional" risk factors (apolipoprotein (apo) AI, AII and B, lipoprotein(a), triglycerides, and total, LDL and high density lipoprotein (HDL) cholesterol) for the presence and the extent of coronary or carotid atherosclerosis. Forty male patients with angiographically proven coronary atherosclerosis and 31 male patients with ultrasound-proven extracranial carotid atherosclerosis were compared to 40 age matched (53+/-5 years) healthy males as control subjects, with negative parental history of atherosclerosis, no clinical signs of systemic or organ-related ischemic disease and normal extracranial carotid arteries. The apo B/apo All ratio most powerfully indicated the presence and the extent of coronary or carotid atherosclerosis. Elevated lipoprotein(a) contributed significant additional information in the assessment of the atherosclerotic risk. Increase in C-reactive protein indicated the presence (but not the extent) of coronary or carotid atherosclerosis with a similar power as lipoprotein(a). Decreased values of total bilirubin indicated the presence of atherosclerosis only in smokers. Autoantibodies to oxidatively modified LDL additionally described the atherosclerotic process, but were less important than apolipoproteins, lipoprotein(a), C-reactive protein or bilirubin. Sialic acid content of LDL added no information to the parameters discussed above. We demonstrated that in male patients apolipoproteins, especially the apo B/apo All ratio, were better indicators of the presence and the extent of coronary or carotid atherosclerosis than C-reactive protein, bilirubin, autoantibodies to oxidatively modified LDL or sialic acid content of LDL.

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Some cardiovascular complications in patients with chronic kidney disease and end-stage renal disease may be caused by structurally and functionally modified lipoproteins. Redox status (advanced oxidation protein products [AOPPs]), prooxidant-antioxidant balance, total protein sulfhydryl (SH-groups), and paraoxonase 1 (PON1) activity were assessed in 77 renal patients and 20 controls. Lipoproteins were isolated using ultracentrifugation. PON1, PON3, and pentraxin-3 concentration were determined by enzyme-linked immunosorbent assay (ELISA). Dyslipidemia-Oxy-Inflammation (DOI) score was calculated as a sum of dyslipidemia, oxidative stress, and inflammation scores. The dyslipidemia score ( P < .001), oxy score ( P < .01), inflammation score (P < .001), and the DOI score ( P < .001) were higher in patient groups compared with controls. The very-low-density lipoprotein (VLDL) fraction contained the highest amount of AOPP ( P < .001) compared with other lipoprotein fractions in all groups. The low-density lipoprotein (LDL) fraction contained elevated AOPP in all groups compared with the high-density lipoprotein (HDL) fraction ( P < .001). Significant positive correlation was observed between AOPP in LDL fraction and DOI score (ρ = 0.510, P < .01). Dyslipidemia, oxidative stress, and inflammation play an interactive role in renal disease and are mutually associated with redox status in VLDL, LDL, and HDL lipoproteins in plasma of renal patients.

In a randomized study, sequential anticoagulation for hemodialysis (citrate for the first 3.5 h, switching to 30-min anticoagulation-free hemodialysis) was compared to standard citrate anticoagulation. Fifty-two hemodialysis procedures were randomized either to sequential (n = 27) or standard citrate group (n = 25). The antithrombotic effect in the circuit was visually assessed after hemodialysis using a score from 1 (total clotting) to 5 (no clotting). The antithrombotic score for sequential versus standard group was as follows: dialyzer, 4.0 +/- 1.1 versus 4.8 +/- 0.4 (P < 0.01); arterial bubble trap, 4.0 +/- 1.2 versus 4.7 +/- 0.6 (P = 0.013); venous bubble trap, 4.0 +/- 1.3 versus 4.8 +/- 0.6 (P < 0.01). Serum citrate levels during sequential versus standard citrate anticoagulation (micromol/L) were as follows: at the beginning, 143 +/- 65 versus 148 +/- 77 (not significant [NS]); after 2 h, 317 +/- 157 versus 354 +/- 111 (NS); at the end, 125 +/- 81 versus 405 +/- 133 (P < 0.01). Sequential anticoagulation reduces the final serum citrate concentration to predialysis level. It can be a good anticoagulation strategy for patients in whom the reduction of citrate load is desired.

Mildly elevated serum creatinine concentration was proposed to be a marker for increased risk of cardiovascular disease mortality. The aim of our prospective study was to evaluate a possible association between serum creatinine concentration and extent of coronary atherosclerosis together with conventional risk factors for atherosclerosis. Serum creatinine concentration was measured in 40 male patients without overt renal or ischemic renal disease (mean age 53 +/- 7 years) with stable or unstable angina undergoing routine coronary arteriography. The extent of coronary atherosclerosis was assessed by Gensini score. In univariate linear regression analysis Gensini score significantly correlated with serum concentrations of apolipoprotein AII (r=-0.3242, P<0.05) and creatinine (r=+0.3194, P<0.05), but not with serum concentrations of lipids (total, low- and high-density lipoprotein cholesterol, triglycerides), other apolipoproteins (apo B, apo AI), lipoprotein(a), autoantibodies to oxidatively modified low-density lipoprotein or age, weight and status of smoking, diabetes or hypertension. Multivariate linear regression analysis revealed that elevated serum creatinine was associated with the extent of coronary atherosclerosis independently of conventional risk factors for atherosclerosis. Mildly elevated serum creatinine was probably the marker of generalised vascular disease denoting early nephrovasculopathy in correlation with established atherosclerotic risk factors.

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The authors tested the hypothesis that lipoprotein lipase (LPL) gene expression and enzyme activity are increased in lung cancer tissue, as compared to adjacent, apparently healthy, lung tissue. Paired samples of lung cancer tissue and adjacent noncancer lung tissue were collected from 42 patients with resectable non-small cell lung cancer. LPL activity was higher in cancer tissue (1.9-fold median difference, P < .0001); however, LPL gene expression was higher in noncancer tissue (3.8-fold median difference, P < .0001). The higher LPL activity in lung cancer tissue provides a possible mechanism for increasing the supply of lipid nutrients to the tumor, necessary for tumor growth.