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Biomedical subjects

M Ahotupa

Publications and source records attributed to M Ahotupa.

At least 19 recordsLinked to original sources

Successful weight maintenance preserves lower levels of oxidized LDL achieved by weight reduction in obese men.

OBJECTIVE: We studied the association between weight maintenance, oxidized low-density lipoprotein (ox-LDL) and other lipoproteins in obese men. METHODS: A 2-month weight reduction phase (WRP) with a very-low-energy diet was followed by a 6-month weight maintenance period and an unsupervised 2-year follow-up. Ninety men entered and 68 (76%) completed the study. Subjects were analyzed as one group and after division into two subgroups: 20 most successful men in maintaining the lost weight (subgroup 1) and the remaining (n=48) men (subgroup 2). Ox-LDL was measured by quantifying the amount of conjugated dienes in LDL particles. RESULTS: The mean (+/-s.d.) weight reduction at the end of the WRP (n=68) was 14% (confidence interval (CI) 12.9-14.7%, 14.5+/-4.2 kg, P<0.001). Ox-LDL decreased by 22% (CI 16.9-28.1, 12.3+/-15.4 micromol/l, P<0.001). At the end of the 2-year follow-up, the regain in weight from the end of the WRP was 11% (CI 9.0-12.4, 9.6+/-6.2 kg, P<0.001). The regain in ox-LDL was 30% (CI 18.7-41.2, 8.2+/-15.4 micromol/l, P<0.001). In subgroup 1 vs 2, the respective regains were 3% (CI 0.9-4.2, 2.2+/-3.0 kg, P=0.006) vs 14% (CI 12.7-15.6, 12.9+/-4.0 kg, P<0.001) regarding weight and 9% (2.0+/-6.9 micromol/l, P=NS) vs 39% (CI 23.7-53.9, 11.2+/-17.2 micromol/l, P</=0.001) in ox-LDL. CONCLUSION: The favorable changes seen in ox-LDL particles and serum lipids during weight reduction could be maintained by keeping the weight reduced, which may indicate decreased risk of atherosclerosis. But weight regain causes a resurge of ox-LDL.

Adult↗

Decreased large artery distensibility in borderline hypertension is related to increased in vivo low-density lipoprotein oxidation.

The present study tested the hypothesis that reduced arterial elasticity seen in hypertension is related to increased oxidation of LDL. Fifteen men with borderline hypertension (BHT), with blood pressure values classified as high normal (systolic blood pressure 130-140 mmHg or diastolic blood pressure 85-89 mmHg) were included. The control group comprised 22 men with normal blood pressure values (<135/80 mmHg) matched for age, body size and LDL-cholesterol level. Distensibility of aorta was measured using magnetic resonance imaging, and distensibility of the common carotid artery using ultrasound. Baseline LDL diene conjugation was used as a marker for ox-LDL. Aortic and carotid distensibilities were lower in the BHT men than in controls (1.4 +/- 0.6 vs. 1.9 +/- 0.6%/10 mmHg, p<0.05 for aortic distensibility; 2.9 +/- 0.9 vs. 3.6 +/- 0.6%/10 mmHg, p<0.05 for carotid distensibility). Ox-LDL was significantly higher in the BHT men than in controls (44 +/-15 vs. 28 +/- 8 micromol/L, p<0.01). In univariate analysis, ox-LDL associated with aortic distensibility (r=-0.43, p<0.05). In multivariate analysis, the differences in distensibilities between the groups disappeared when the values were adjusted for ox-LDL. These data show decreased arterial elasticity and increased LDL oxidation in young men with borderline hypertension, and suggest that oxidative modification of LDL particles may play a pathophysiological role in the development of reduced arterial distensibility in hypertension.

Adult↗

Oxidized LDL and thickness of carotid intima-media are associated with coronary atherosclerosis in middle-aged men: lower levels of oxidized LDL with statin therapy.

We investigated the relation between serum lipids including oxidized LDL and the severity of coronary atherosclerosis. Serum lipids and oxidized LDL was measured in 62 men (33-66 years), who underwent diagnostic coronary angiography and sonography to measure the carotid intima-media thickness. LDL oxidation was found in chemical analyses to be due to conjugated fatty acids in cholesteryl esters and triglycerides. Regression analysis indicated that the carotid intima-media thickness and the ratio of LDL diene conjugation to LDL cholesterol (the ox-LDL:LDL ratio) were the only factors associated independently with the severity of coronary atherosclerosis. The patients with multi-vessel disease who did not use lipid lowering therapy had a 50% thicker carotid intima media (P = 0.030) and a 41% higher ox-LDL:LDL ratio (P = 0.020) than patients with normal vessels. Further, patients with multi-vessel disease on statin therapy had a 24% lower ox-LDL:LDL ratio than the subjects with multi-vessel disease who did not use lipid lowering drugs (P = 0.027), although the concentration of LDL cholesterol did not differ between the groups. This study supports the hypothesis that lipid oxidation plays a role in the development of atherosclerosis.

Adult↗

Reduced myocardial flow reserve relates to increased carotid intima-media thickness in healthy young men.

Increased carotid artery wall thickness and lipoprotein oxidation are key early events in atherosclerosis. To test the hypothesis that reduced myocardial flow reserve is a marker of subclinical atherosclerosis, we examined the relationships between flow reserve and carotid artery intima-media thickness (IMT) in young men free from coronary heart disease. Basal and dipyridamole stimulated coronary blood flow was measured using positron emission tomography (PET) in 55 healthy men aged 36+/-4 years. Myocardial flow reserve was calculated as the ratio of stimulated flow to basal flow. The mean carotid artery IMT was measured using high-resolution ultrasound. Oxidised LDL was measured as baseline LDL diene conjugation. Myocardial flow reserve decreased across the quartiles of increasing IMT (P=0.006), and was 5.2+/-1.9 in the lowest quartile for IMT and 3.7+/-1.2 in the highest (P=0.04, I vs. IV quartile). In univariate analysis, oxidised LDL correlated inversely with flow reserve (r=-0.35, P=0.01) and directly with IMT (r=0.51, P<0.001). The association between flow reserve and IMT remained significant (P< or =0.01) in multivariate regression model including age, blood pressure, left ventricular mass, ox-LDL, total cholesterol, HDL-cholesterol and triglycerides as covariates. These data support the concept that reduced myocardial flow reserve reflects subclinical atherosclerosis in asymptomatic subjects, and suggest that increased lipoprotein oxidation is directly related to early structural and functional atherosclerotic vascular changes.

Adult↗

No evidence for the in vivo activity of aromatase-inhibiting flavonoids.

Measurements of the aromatase-inhibiting and antioxidative capacities of flavonoids in vitro showed that slight changes in flavonoid structure may result in marked changes in biological activity. Several flavonoids such as 7-hydroxyflavone and chrysin (5,7-dihydroxyflavone) were shown to inhibit the formation of 3H-17beta-estradiol from 3H-androstenedione (IC(50)<1.0 microM) in human choriocarcinoma JEG-3 cells and in human embryonic kidney cells HEK 293 transfected with human aromatase gene (Arom+HEK 293). Flavone and quercetin (3,3',4',5,7-pentahydroxyflavone) showed no inhibition (IC(50)>100 microM). None of the requirements for optimal antioxidative capacity (2,3-double bond with 4'-hydroxy group, 3-hydroxyl group, 5,7-dihydroxy structure and the orthodihydroxy structure in the B-ring) is relevant for the maximum inhibition of aromatase by flavonoids. After oral administration to immature rats at a dose of 50 mg/kg body weight, which considerably exceeds amounts found in daily human diets, neither aromatase-inhibiting nonestrogenic flavonoids, such as chrysin, nor estrogenic flavonoids, such as naringenin and apigenin, induced uterine growth or reduced estrogen- or androgen-induced uterine growth. The inability of flavonoids to inhibit aromatase and, consequently, uterine growth in short-term tests may be due to their relatively poor absorption and/or bioavailability.

Androstenedione↗

Reduced oxidized low-density lipoprotein after weight reduction in obese premenopausal women.

BACKGROUND: Several studies support the hypothesis that oxidation of low-density lipoprotein (LDL) promotes atherogenesis. Obesity is one of the risk factors of atherosclerosis, but it is not known whether obesity is related to LDL oxidation. OBJECTIVE AND DESIGN: We investigated the effect of weight reduction and subsequent weight maintenance program on LDL oxidation in 77 obese premenopausal women (BMI 29-46 kg/m(2)). Another group of seven obese women served as a control group. Oxidized LDL was measured as baseline concentration of conjugated dienes in LDL lipids (ox-LDL). The weight reduction was performed in 12 weeks, using a very-low-energy diet. RESULTS: The mean weight loss was 13 kg (92 vs 79 kg). During weight reduction, the concentration of LDL cholesterol decreased by 11%, the concentration of ox-LDL decreased by 40%, and the ratio of ox-LDL to LDL by 33%. The concentration of LDL antioxidant capacity (LDL-TRAP) decreased by 8%, but the decrease was caused by the decrease in LDL. The concentration of LDL, ox-LDL or LDL-TRAP did not change in the control group. The weight reduction correlated with the decrease of ox-LDL. During the subsequent 9 month weight maintenance programme, the concentrations of serum LDL (10%), ox-LDL (11%), LDL-TRAP (29%), and the ratio of LDL-TRAP to LDL (21%) decreased. CONCLUSION: This study strengthens the evidence that the risk of atherogenesis is influenced favourably by weight reduction in obese women. This risk reduction is associated with a reduced oxidation of LDL.

Adult↗

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia.

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.

Adult↗

Oxidative stress and AP-1 activity in tamoxifen-resistant breast tumors in vivo.

BACKGROUND: Most breast cancers, even those that are initially responsive to tamoxifen, ultimately become resistant. The molecular basis for this resistance, which in some patients is thought to involve stimulation of tumor growth by tamoxifen, is unclear. Tamoxifen induces cellular oxidative stress, and because changes in cell redox state can activate signaling pathways leading to the activation of activating protein-1 (AP-1), we investigated whether tamoxifen-resistant growth in vivo is associated with oxidative stress and/or activation of AP-1 in a xenograft model system where resistance is caused by tamoxifen-stimulated growth. METHODS: Control estrogen-treated, tamoxifen-sensitive, and tamoxifen-resistant MCF-7 xenograft tumors were assessed for oxidative stress by measuring levels of antioxidant enzyme (e.g., superoxide dismutase [SOD], glutathione S-transferase [GST], and hexose monophosphate shunt [HMS]) activity, glutathione, and lipid peroxidation. AP-1 protein levels, phosphorylated c-jun levels, and phosphorylated Jun NH(2)-terminal kinase (JNK) levels were examined by western blot analyses, and AP-1 DNA-binding and transcriptional activities were assessed by electrophoretic mobility shift assays and a reporter gene system. All statistical tests are two-sided. RESULTS: Compared with control estrogen-treated tumors, tamoxifen resistant tumors had statistically significantly increased SOD (more than threefold; P=.004) and GST (twofold; P=.004) activity and statistically significantly reduced glutathione levels (greater than twofold; P<.001) and HMS activity (10-fold; P<.001). Lipid peroxides were not significantly different between control and tamoxifen-resistant tumors. We observed no differences in AP-1 protein components or DNA-binding activity. However, AP-1-dependent transcription (P=.04) and phosphorylated c-Jun and JNK levels (P<.001) were statistically significantly increased in the tamoxifen-resistant tumors. CONCLUSION: Our results suggest that the conversion of breast tumors to a tamoxifen-resistant phenotype is associated with oxidative stress and the subsequent antioxidant response and with increased phosphorylated JNK and c-Jun levels and AP-1 activity, which together could contribute to tumor growth.

Animals↗

Reduced mildly oxidized LDL in young female athletes.

We investigated the effect of physical activity and sports participation on LDL oxidation in vivo and on lipid risk factors in 183 teenage girls (9-15 years): 64 gymnasts, 61 runners, and 58 controls. Oxidized LDL was measured as baseline levels of conjugated dienes in LDL lipids (ox-LDL). The gymnasts had a 15% lower ratio of LDL conjugated dienes to LDL cholesterol (ox-LDL:LDL ratio, P = 0.0052) compared to controls, and the difference persisted when the body mass index was included as a covariate (ANCOVA, P = 0.013). Also, the gymnasts had a 12% higher ratio of HDL cholesterol to total cholesterol than the controls (ANCOVA, P = 0.046). There were no differences in the other common lipid risk factors between the groups. The ox-LDL:LDL ratio correlated negatively with HDL cholesterol (r = -0.23, P=0.0021) and with physical activity METs (multiples of resting metabolic rate) (r = -0.21, P=0.0040). Our study strengthens the evidence that the atherogenic risk is influenced favourably by physical exercise and sporting activities as early as in adolescents. This risk reduction is associated with lower mildly oxidized LDL in adolescent girls.

Adolescent↗

Increased arterial intima-media thickness and in vivo LDL oxidation in young men with borderline hypertension.

We used borderline hypertension as a model for prehypertension to examine the early influences of elevated blood pressure on subclinical atherosclerosis, lipoprotein oxidation, and cardiac adaptation. Healthy men (age 37+/-4 years) were classified prospectively into 2 groups on the basis of having either borderline hypertension (systolic 130 to 140 mm Hg or diastolic 85 to 89 mm Hg, n=16) or normal (<130/85 mm Hg, n=22) blood pressure values during the previous 2 years. The groups were matched for age, body size, and serum cholesterol levels. High-resolution ultrasound was used to measure intima-media thickness (IMT) of the carotid and brachial arteries, cardiac dimensions, and brachial artery endothelial function. Baseline low-density lipoprotein (LDL)-diene conjugation was measured as an estimate of in vivo LDL oxidation (ox-LDL). Compared with normotensive controls, men with borderline hypertension had higher IMT of the carotid artery (0.58+/-0.06 versus 0.75+/-0.07 mm, P<0.001) and IMT of the brachial artery (0.45+/-0.05 versus 0.57+/-0.07 mm, P<0.001), and increased levels of ox-LDL (29+/-9 versus 47+/-17 mol/L, P<0.001), but similar endothelial function. Left ventricular mass was similar in both groups, but there were significant differences in left ventricular geometry. In multivariate analyses, the predictors of carotid IMT were 24-hour systolic blood pressure (P<0.001) and ox-LDL (P=0.10). The current study demonstrates evidence of increased subclinical atherosclerosis and ox-LDL in borderline hypertension. These results are consistent with the idea that enhanced ox-LDL may be one of the pathophysiological events related to development of atherosclerosis in men with borderline elevated blood pressure.

Adult↗

Hydroxymatairesinol, a novel enterolactone precursor with antitumor properties from coniferous tree (Picea abies).

The potential for the extraction of the plant lignan hydroxymatairesinol (HMR) in large scale from Norway spruce (Picea abies) has given us the opportunity to study the metabolism and biological actions of HMR in animals. HMR, the most abundant single component of spruce lignans, was metabolized to enterolactone (ENL) as the major metabolite in rats after oral administration. The amounts of urinary ENL increased with the dose of HMR (from 3 to 50 mg/kg), and only minor amounts of unmetabolized HMR isomers and other lignans were found in urine. HMR (15 mg/kg body wt po) given for 51 days decreased the number of growing tumors and increased the proportion of regressing and stabilized tumors in the rat dimethylbenz[a]anthracene-induced mammary tumor model. HMR (50 mg/kg body wt) did not exert estrogenic or antiestrogenic activity in the uterine growth test in immature rats. HMR also showed no antiandrogenic responses in the growth of accessory sex glands in adult male rats. Neither ENL nor enterodiol showed estrogenic or antiestrogenic activity via a classical alpha- or beta-type estrogen receptor-mediated pathway in vitro at < 1.0 microM. HMR was an effective antioxidant in vitro.

4-Butyrolactone↗

Partial resistance of low density lipoprotein to oxidation in vivo after increased intake of berries.

BACKGROUND AND AIM: The health-promoting effects of fruit- and vegetable-based diets are known to be associated with their antioxidative components. We found in our preliminary in vitro laboratory tests that extracts of many common Finnish edible berries are potent scavengers of peroxyl radicals and inhibitors of lipid peroxidation. We therefore designed the current study to evaluate both the long-term (8 weeks) and short-term (5 hours) effects of increased intake of three berries on antioxidant potential and lipid peroxidation. METHODS AND RESULTS: Healthy 60-year-old men were randomized to berry, supplement and control groups (20 men in each group). The berry group ate, in addition to their normal diet, a 100 g portion of deep-frozen berries (bilberries, lingonberries, or black currants) daily for 8 weeks. The other groups ingested daily 100 mg of alpha-tocopherol and 500 mg of ascorbic acid (supplement group) or 500 mg of calcium gluconate (control group). In the short-term experiment 6 men ate 80 g of each of the three berries in one go. Serum ascorbate concentrations increased significantly in both the berry and the supplement group. Serum alpha-tocopherol levels and the antioxidant potential (TRAP) in low density lipoprotein (LDL) increased in the supplement group only. In the berry group, slightly lowered LDL diene conjugation (p = 0.074) and slightly increased total serum TRAP (p = 0.084) values were observed. No changes were found in these measures in the supplement or the control group. In the short-term experiment, LDL TRAP showed a small increase (about 10%, p = 0.039) during five hours after the intake of 240 g berries. CONCLUSIONS: The effects of consumption of berries on antioxidant potential and diene conjugation in LDL particles in vivo appear to be small.

Antioxidants↗

Constantly low HDL-cholesterol concentration relates to endothelial dysfunction and increased in vivo LDL-oxidation in healthy young men.

To test the hypothesis that low HDL-C concentration interferes with vascular endothelial function and lipoprotein oxidation, we measured endothelium-dependent flow mediated dilatation (FMD, %) of the brachial artery in young men (n=20) classified prospectively into two groups on basis of having either low or high HDL-C concentration over the past 2 years. As an estimate of in vivo low-density lipoprotein oxidation (ox-LDL), we measured LDL diene conjugation. FMD was present in the group with high HDL-C concentration, but impaired in the group with low HDL-C (5.5+/-3.2 vs 0.2+/-1.2%, P<0. 001). The group with high HDL-C level had significantly lower levels of ox-LDL compared to low HDL-C group (18.0+/-1.8 vs 22.9+/-4.4, P</=0.01). In all subjects, FMD correlated with HDL-C (r=0.59, P=0. 006), HDL(2)-C (r=0.62, P=0.004) and ox-LDL (r=-0.56, P=0.013) but not with HDL(3)-C (r=0.16, P=0.52). We conclude that constantly low HDL-C concentration is related with endothelial dysfunction and increased oxidative stress in healthy young men, consistent with the idea that HDL particles may protect endothelium and inhibit the oxidation of LDL. These findings may offer insight into increased atherosclerosis associated with low HDL-C levels.

Adult↗

Association of low-density lipoprotein oxidation to abnormal electrocardiographic late potentials.

In vivo oxidation of low-density lipoprotein is shown to be significantly related to another risk factor for coronary atherosclerosis, abnormal electrocardiographic late potentials, in clinically healthy pilots. Because both of these variables have been also associated with cardiac arrhythmogenic action, together they may improve the identification of patients at risk of ventricular tachyarrhythmias.

Action Potentials↗

Nitecapone inhibits myeloperoxidase in vitro and enhances functional performance after 8 h of ischemia in experimental heart transplantation.

Nitecapone (NC) has been shown to have beneficial effects on the functional recovery of rat hearts in Langendorff-preparation. The present study was executed to evaluate the effect of NC on preservation of grafts in heart transplantation and the role of NC in the inhibition of granulocyte infiltration. Donor hearts were perfused and stored at +4 degrees C for 8 h in either Ringer solution in the control-group (C-group, n = 26) or in NC (50 microM) added Ringer solution (NC-group, n = 18). The heterotopic heart transplantation was performed. The rats in both groups were killed at either 10 min or 60 min after release of the aortic clamp and tissue samples were obtained for antioxidative capacity, myeloperoxidase activity, and lipid peroxidation measurements. In vitro studies were performed using sodium azide or nitecapone to inhibit myeloperoxidase (MPO) activity of isolated human leukocytes. A total of 61% of the grafts began to beat in the NC-group, compared to 46% in the control group. Using an arbitrary scale of functional performance, only 33% (4/12) of the grafts were classified as well functioning in the control group, compared to 82% (9/11) in the NC-group (P<0.05). MPO activity was equal in both groups after 10 min but significantly lower after 60 min in the NC-group as compared to the control group (P<0.05). In vitro studies demonstrated that NC inhibits 50% of purified MPO activity at a concentration of 10 microM. NC did not significantly affect lipid peroxidation or the preservation of endogenous antioxidants. Since NC inhibited myeloperoxidase both in vitro and in vivo, it seems that the positive effects of NC on graft preservation may be mediated via the inhibition of granulocyte infiltration.

Animals↗

Baseline diene conjugation in LDL lipids: an indicator of circulating oxidized LDL.

The wide acceptance of the diene conjugation-method in monitoring low-density lipoprotein (LDL) oxidation ex vivo has led to development of an assay, which measures the amount of baseline diene conjugation (BDC) in circulating LDL, and is an indicator of oxidized LDL in vivo. The LDL-BDC assay is based on precipitation of serum LDL with buffered heparin, and spectrophotometric determination of baseline level of conjugated dienes in lipids extracted from LDL. Compared to existing methods for oxidized LDL, LDL-BDC is fast and simple to perform. Chemical studies by HPLC and NMR have verified that LDL-BDC is a specific indicator of circulating mildly oxidized LDL. Validity of the assay is further indicated by strong correlation with the titer of autoantibodies against oxidized LDL. Clinical studies have shown that LDL-BDC is closely related to coronary, carotid, and brachial atherosclerosis. Moreover, several independent studies have demonstrated surprisingly strong associations between LDL-BDC and known atherosclerosis risk factors (obesity, physical inactivity, hypertension, diabetes, and arterial functions). Indeed, these studies seem to indicate that as an indicator of the risk of atherosclerosis LDL-BDC clearly exceeds sensitivity and specificity of the common lipid markers of atherosclerosis. It is concluded that LDL-BDC is a promising candidate in search for methods for the evaluation of in vivo LDL oxidation and the risk of atherosclerosis.

Arteriosclerosis↗

Large-artery elastic properties in young men : relationships to serum lipoproteins and oxidized low-density lipoproteins.

Measures of arterial elasticity have been proposed as surrogate markers for asymptomatic atherosclerosis. We investigated the relations of serum lipoproteins, oxidized low-density lipoprotein (ox-LDL), and familial hypercholesterolemia (FH) to arterial elasticity among young men. As a marker of arterial elasticity we measured compliance in the thoracic aorta by using magnetic resonance imaging and in the common carotid artery by using ultrasound. LDL diene conjugation was used as a marker of ox-LDL. In study I, 25 healthy men (aged 29 to 39) were classified into 2 extreme groups according to previously measured high-density lipoprotein cholesterol to total cholesterol ratio (HDL-C/TC ratio). In study II, the healthy men were used as controls for 10 age matched asymptomatic patients with FH. In healthy men, the group with low HDL-C/TC ratio had decreased carotid artery compliance (2. 3+/-0.4% versus 1.9+/-0.5%/10 mm Hg, P=0.034). In univariate analysis, the compliance of the carotid artery associated with ox-LDL (r =-0.49, P=0.016) and HDL-C/TC ratio (r=0.41, P=0.040). In multivariate regression analyses, ox-LDL was the only independent determinant for compliance of the carotid artery (P=0.016). Aortic elasticity was not related to standard lipid variables, but the compliance of the ascending aorta associated with ox-LDL (r=-0.44, P=0.030). In FH patients, arterial elasticity was similar to that in controls. We conclude that elasticity of the common carotid artery is affected by serum lipid profile in young men. The current study demonstrates for the first time an in vivo association between ox-LDL and arterial elasticity suggesting that oxidative modification of LDL may play a role in the alteration of arterial wall elastic properties.

Adult↗