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1.
OBJECTIVES: Patients with elevated lipoprotein(a) [Lp(a)] and fibrinogen levels have an increased risk of coronary heart disease and adverse cardiovascular events. There is evidence that coronary plaque progression is linked to a higher risk for future cardiovascular events. BACKGROUND: There are no data demonstrating a relation between Lp(a), fibrinogen, and directly measured coronary plaque progression over time. METHODS: We performed a retrospective analysis of serial intravascular ultrasound (IVUS) studies of 60 left main stems (18 +/- 9 months apart) to evaluate plaque progression in relation to Lp(a) and fibrinogen levels and association with adverse cardiovascular events. RESULTS: There was a positive correlation between Lp(a) (r = 0.58; p < 0.0001), fibrinogen (r = 0.48; p < 0.0001), and changes in plaque-plus-media area. Patients with plaque progression (n = 41) had higher Lp(a) (30 +/- 26 mg/dl vs. 14 +/- 9 mg/dl; p < 0.0012) and fibrinogen (295 +/- 88 mg/dl vs. 240 +/- 72 mg/dl; p = 0.019) levels than patients with plaque regression (n = 19). Multivariate linear regression analysis showed Log Lp(a) (regression coefficient = 9.45; p = 0.0008) but not fibrinogen to be independently associated with plaque progression. A total of 19 patients suffered from adverse cardiovascular events; they had higher Lp(a) (44 +/- 30 mg/dl vs. 16 +/- 12 mg/dl; p < 0.0001) and fibrinogen (342 +/- 73 mg/dl vs. 248 +/- 76 mg/dl; p < 0.0001) levels. Multivariate logistic regression analysis showed Log Lp(a) (odds ratio 10.20, 95% confidence interval 2.36 to 44.13; p = 0.0019) and fibrinogen (odds ratio 1.01, 95% confidence interval 1.00 to 1.03; p = 0.018) were independently associated with adverse cardiovascular events. CONCLUSIONS: Serial IVUS showed a positive correlation between Lp(a) and fibrinogen levels and plaque progression. Lp(a), but not fibrinogen, remains independently associated with plaque progression. In addition, the present data suggest a considerable incremental value of Lp(a) in predicting cardiovascular risk.  相似文献   

2.
Subclinical hypothyroidism (SH) is being accepted as a condition that is associated with increased risk of cardiovascular disease. Restoration of euthyroidism might be involved in prevention of cardiovascular disease. Thus, we evaluated biochemical risk factors of 75 patients with SH without evidence of any other diseases before and after restoration of euthyroidism and compared to 27 healthy controls. Before and a mean of 18.2+/-4.4 weeks after restoration of euthyroidism, serum total and LDL cholesterol, lipoprotein (Lp) (a), total homocysteine (t-Hyc) and highly sensitive C-reactive protein (hsCRP) levels were analyzed. Pre-treatment levels of TSH (10.04+/-5.36 vs 1.74+/-1.1 mIU/l, p<0.05), total cholesterol (204+/-68 vs 179+/-26 mg/dl, p<0.05) and LDL cholesterol (129+/-50 vs 106+/-16 mg/dl, p<0.05) were significantly higher than controls while Lp (a), t-Hyc, and hsCRP levels were not different. None of these biochemical risk factors have improved after euthyroidism in patients with SH with average dose of 85+/-30 microg/day, when compared to pre-treatment levels. Only in a subgroup of patients (no. 30) with higher TSH levels (>10 mIU/l), did serum LDL cholesterol levels decrease significantly (139+/-38 vs 112+/-35 mg/dl, p<0.05). Lp (a), t-Hyc and hsCRP levels were not significantly different after treatment with levothyroxine therapy even in this subgroup of patients. We conclude that clinical management of SH does not contribute to prevention of cardiovascular disease in the short term, and monitoring risk factors of cardiovascular disease does not offer additional benefits for treating patients with SH.  相似文献   

3.
Patients with insulin dependent diabetes mellitus (IDDM) often suffer from cardiovascular diseases as renal failure occurs. Elevated albumin excretion rate (AER) is a predictive value of this event. Relations between AER, blood pressure, serum lipids and apoproteins concentrations in 100 patients with IDDM have been surveyed. Twenty one hypertensive patients (HT group) were compared to 21 patients without hypertension (n HT group), matched for sex, age, diabetes duration, and metabolic control, assessed by glycosylated haemoglobin. Comparison of both groups showed HT group had elevated systolic blood pressure (137 +/- 12 vs 126 +/- 20 mmHg; p less than .05), elevated diastolic blood pressure (80 +/- 7 vs 71 +/- 8 mmHg; p less than .001), increase in AER (27 range 3-4023 vs 6 range 2-51 mg/day; p less than .001), slightly elevated serum creatinine (95 +/- 32 vs 78 +/- 15 mumol/l; p less than .05). In HT group, serum lipid composition showed: raise in total cholesterol (251 +/- 43 vs 221 +/- 41 mg/dl; p less than 0.5), elevated apoprotein B (130 +/- 30 vs 99 +/- 21 mg/dl; p less than .001) elevated apoprotein B/apoprotein A1 ratio (.91 +/- .32 vs .66 +/- .27; p less than .001), elevated triglycerides (157 +/- 53 vs 98 +/- 43 mg/dl; p less than .005) and elevated LDL-cholesterol (170 +/- 42 vs 143 +/- 33 mg/dl; p less than .05). Levels of apoprotein A1 and HDL-cholesterol were not significantly different. Body mass index, daily insulin requirement and tobacco usage were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

4.
The prevalence of abnormalities of lipoprotein cholesterol and apolipoproteins A-I and B and lipoprotein (a) [Lp(a)] was determined in 321 men (mean age 50 +/- 7 years) with angiographically documented coronary artery disease and compared with that in 901 control subjects from the Framingham Offspring Study (mean age 49 +/- 6 years) who were clinically free of coronary artery disease. After correction for sampling in hospital, beta-adrenergic medication use and effects of diet, patients had significantly higher cholesterol levels (224 +/- 53 vs. 214 +/- 36 mg/dl), triglycerides (189 +/- 95 vs. 141 +/- 104 mg/dl), low density lipoprotein (LDL) cholesterol (156 +/- 51 vs. 138 +/- 33 mg/dl), apolipoprotein B (131 +/- 37 vs. 108 +/- 33 mg/dl) and Lp(a) levels (19.9 +/- 19 vs. 14.9 +/- 17.5 mg/dl). They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). On the basis of Lipid Research Clinic 90th percentile values for triglycerides and LDL cholesterol and 10th percentile values for HDL cholesterol, the most frequent dyslipidemias were low HDL cholesterol alone (19.3% vs. 4.4%), elevated LDL cholesterol (12.1% vs. 9%), hypertriglyceridemia with low HDL cholesterol (9.7% vs. 4.2%), hypertriglyceridemia and elevated LDL cholesterol with low HDL cholesterol (3.4% vs. 0.2%) and Lp(a) excess (15.8% vs. 10%) in patients versus control subjects, respectively (p less than 0.05). Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. Not applying a correction for beta-adrenergic blocking agents, sampling bias and diet effects leads to a serious underestimation of the prevalence of LDL abnormalities and an overestimation of HDL abnormalities in patients with coronary artery disease. However, 35% of patients had a total cholesterol level less than 200 mg/dl after correction; of those patients, 73% had an HDL cholesterol level less than 35 mg/dl.  相似文献   

5.
Serum lipoprotein (a) (Lp[a]) has been associated with coronary artery atherosclerosis. Its association with restenosis after percutaneous transluminal coronary angioplasty (PTCA) has not been previously studied. Serum levels of Lp(a), in addition to other lipoproteins, and their components using standard assays, were determined in subjects undergoing cardiac catheterization within 10 months after PTCA. Clinical (e.g., sex, diabetes, angina class) and angiographic (e.g., PTCA percent diameter reduction) factors were not different between the group without (diameter reduction less than 50%; group A) and the group with (diameter reduction greater than or equal to 50%; Group B) restenosis. Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B and Lp(a) were compared. Univariate predictors of restenosis were serum triglycerides (2.50 +/- 1.07 mmol/liter for group A vs 1.72 +/- 0.79 +/- mmol/litre for group B, p = 0.008), and Lp(a) (median: 7.0 mg/dl [range 0 to 44] for group A vs 19 mg/dl [range 1 to 120] for group B; p = 0.006). Stepwise logistic regression revealed the only significant independent predictor of restenosis to be serum Lp(a) (p = 0.018). Each quintile of Lp(a) was associated with a progressively higher risk of restenosis, with the highest quintile (40 to 120 mg/dl) having an odds ratio of 11 (95% confidence interval 9 to 13) compared with the lowest quintile (0 to 3.9 mg/dl) (p = 0.033). A serum Lp(a) of greater than 19 mg/dl was associated with an odds ratio of 5.9 (95% confidence interval 4.6 to 7.2) (restenosis rates of 58% in the group with 0 to 19 mg/dl and 89% in the group with 19 to 120 mg/dl; p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

6.
Lipoprotein(a) [Lp(a)] is a risk factor for coronary heart disease (CHD) in particular in association with high low density lipoprotein (LDL) cholesterol concentrations. Hypertriglyceridemia on the other hand has been found to be associated with low Lp(a) values. This observation could be confirmed in 851 patients of the outpatient lipid clinic. Lp(a) median levels were 2.7-fold higher in patients with triglycerides below 200 mg/dl as compared with patients expressing triglyceride levels above 200 mg/dl (19 vs 7 mg/dl, P < 0.0001). In contrast to these data apolipoprotein(a) [apo(a)] has been detected in triglyceride-rich lipoproteins (TRL). To find out whether the presence of apo(a) in TRL is determined by the concentration of these particles, apo(a) concentrations were measured in TRL in fasting plasma of ten hypertriglyceridemic patients and ten normal controls with Lp(a) serum levels above 25 mg/dl. The apo(a) concentration in TRL did not show statistically significant differences between controls and patients (2.0+/-0.9 vs 1.8+/-1.6 mg/dl). In the second part of the study apo(a) levels in TRL were measured before and after fat feeding in eight healthy volunteers. Again no significant differences were observed in the apo(a) concentrations of the d < 1.006 a ml fraction before and after fat feeding (1.03+/-1.06 vs 0.81+/-0.63 mg/dl). In summary, this study fails to show an association of apo(a) with TRL for different states of hypertriglyceridemia. This negative finding is shown for constant particle numbers but might not be true if the particle number in TRL increases.  相似文献   

7.
Previous studies have shown that serum concentrations of lipoprotein(a) [Lp(a)] are markedly different among different ethnic groups. We examined the serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol and Lp(a) in apparently healthy subjects aged 20-69 years in Japan (n = 865) and the Dominican Republic (n = 1,893). Dominicans had significantly lower levels of total cholesterol and HDL cholesterol than Japanese. The distribution of Lp(a) concentrations were markedly skewed towards low levels in both Japanese and Dominicans. However, the mean Lp(a) concentration in Dominicans was approximately 2 times higher than in Japanese (21.7 +/- 23.7 vs 12.3 +/- 15.9 mg/dl, p < 0.001). This is possibly because the majority of Dominicans are of mixed Negroid and European blood.  相似文献   

8.
BACKGROUND: The plasma concentration of lipoprotein (a) [Lp(a)] is associated with atherosclerotic and thrombotic vascular diseases. The aim of the present study was to evaluate the association between plasma Lp(a) concentration and in-stent restenosis. METHODS AND RESULTS: One hundred and 9 patients with successful elective coronary stent implantation underwent follow-up angiography at 24+/-6 weeks. Restenosis after stent implantation occurred in 38 patients. Univariate analysis showed that the reference diameter of the lesion was smaller in the restenosis group (2.93+/-0.29 mm) than in the no-restenosis group (3.21+/-0.43 mm) (p < 0.05). The lesion was longer in the restenosis group (14.2+/-5.3 mm) than in the no-restenosis group (11.6+/-4.9 mm) (p < 0.05). Plasma Lp(a) concentrations in the restenosis group (30.5+/-23.9 mg/dl) were higher than in the no-restenosis group (16.9+/-11.1 mg/dl) (p < 0.01). Other lipid concentrations were similar in both groups. Among the plasma Lp(a) concentrations, the rate of restenosis (71.4%) in the high Lp(a) group (> 40 mg/dl) (n = 14) was greater compared with the other groups: 33.3% in the intermediate Lp(a) group (10-40 mg/dl) (n = 54), and 24.4% in the low Lp(a) group (< 10 mg/dl) (n = 41) (p < 0.01). The late loss (0.57+/-0.53 mm) in the low Lp(a) group was significantly less than the other groups: 0.88+/-0.47 mm in the intermediate Lp(a) group, and 1.08+/-0.56 mm in the high Lp(a) group (p < 0.05). In a multivariate regression model, plasma Lp(a) concentration remained significant as an independent predictor of restenosis in patients undergoing stent implantation (p = 0.020 odds ratio (OR) 1.37 95%conficence interval (CI) 1.050-1.793), although the reference diameter (p = 0.025 OR 0.23 95%CI 0.061-0.830) and lesion length (p = 0.021 OR 1.12 95%CI 1.017-1.232) were related to stent restenosis. CONCLUSIONS: Plasma Lp(a) concentration is an independent predictor of stent restenosis.  相似文献   

9.
The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.  相似文献   

10.
Apolipoprotein AI and alcoholic liver disease   总被引:1,自引:0,他引:1  
A prospective study of apolipoprotein AI has been undertaken in 581 alcoholic patients and in 100 controls in order to describe the changes of apolipoprotein AI according to the different stages of the alcoholic liver disease, to correlate the changes to serum liver tests and to estimate its diagnosis and prognostic value. Results showed that apolipoprotein AI concentration is highly related to the degree of liver injury, reaching a maximum in patients with steatosis (229 +/- 90 mg per dl), beginning to decrease in patients with fibrosis (188 +/- 88 mg per dl) and reaching a minimum in patients with severe cirrhosis (91 +/- 46 mg per dl). Apolipoprotein AI had an independent and discriminative value for the diagnosis of fibrosis (p less than 0.001) vs. steatosis and for the diagnosis of cirrhotic vs. noncirrhotic fibrosis (p less than 0.001) or vs. acute alcoholic hepatitis without cirrhosis (p less than 0.001). Cirrhotic patients with apolipoprotein AI less than 100 mg per dl had a lower survival rate at 1 year (62 +/- 7%) than patients with greater value (80 +/- 6%; p less than 0.05), but this prognostic value disappeared in multivariate analysis when other known prognostic factors were taken into account.  相似文献   

11.
OBJECTIVE: The significance of dyslipidemia in subclinical hypothyroidism (SH) and the effect of thyroid substitution on lipids remain controversial. The present study aimed to assess the association of SH with lipid abnormalities and to quantify the effect of L-thyroxine therapy on serum lipid profiles. DESIGN: Serum lipid parameters of 66 patients with SH and 75 age- and sex-matched euthyroid controls were evaluated in a cross-sectional study. RESULTS: Patients with SH had higher total cholesterol (TC) (222+/-45 (s.d.) vs 190+/- 32 mg/dl), low-density lipoprotein cholesterol (LDL-C) (139+/-28 vs 118+/-39 mg/dl), apolipoprotein B (149+/-21 vs 139+/-18 mg/dl) and lipoprotein (a) (Lp(a)) (median 12.5 (0.8-101) mg/dl vs 7 (0.8-44) mg/dl) levels compared with euthyroid controls (P<0.05 for all comparisons). In a follow-up study including 37 patients with SH, all measurements were repeated after restoration of a euthyroid state with incremental doses of l-thyroxine. No significant changes in serum lipid profiles were observed except for a decrease in high-density lipoprotein cholesterol (59+/-15 to 55+/-14 mg/dl, P<0.05). However, patients with high pre-treatment TC (> or =240 mg/dl) showed a significant reduction in both TC (278+/-28 vs 257+/-36 mg/dl, P<0.05) and LDL-C (192+/-23 vs 173+/-28 mg/dl, P<0.01) levels. Similar but more pronounced changes were observed in a subgroup of patients with pre-treatment levels of TSH > or =10 microU/ml. Thyroid autoimmunity had no effect on either the baseline or the post-treatment lipid profile. CONCLUSION: Although patients with subclinical hypothyroidism exhibit increased levels of the atherogenic parameters (mainly LDL-C and Lp(a)), thyroid substitution therapy does not seem to significantly improve dyslipidemia in the whole group of patients.  相似文献   

12.
We examined the zinc status of 80 children with sickle cell disease (SCD) and 44 disease-free sibling controls aged 3 to 18 years. For both patients and controls, variations in serum zinc by age, type of hemoglobinopathy, and growth status were measured. The mean serum zinc concentration of patients was significantly lower than for controls (77.8 +/- 9.9 vs. 82.2 +/- 9.8 micrograms/dl, mean +/- 1SD, P less than .05). Serum levels of alkaline phosphatase (AP) and retinol-binding protein (RBP), two zinc-dependent proteins, were also lower among patients (AP: 171 +/- 66 vs. 243 +/- 97 IU/L, P less than .001; RBP: 1.92 +/- .9 vs. 2.77 +/- .9 mg/dl, P less than .001). Patients greater than or equal to 12 years of age (n = 34) had significantly lower zinc levels than those less than 12 years (74.5 +/- 8.4 vs. 80.3 +/- 10.3 micrograms/dl, P less than .01), and children with homozygous SCD (Hb SS, n = 55) had a more pronounced deficiency than those with a variant hemoglobinopathy (76.3 +/- 8.9 vs. 81.5 +/- 11.5, micrograms/dl, P less than .05). Patients classified as having "poor" growth (height-for-age less than 5th percentile, n = 24) had a lower serum zinc level than those with "normal" growth (72.8 +/- 8.0 vs. 79.8 +/- 10.0 micrograms/dl, P less than .01). Dietary intake data, body mass index, and serum total protein and albumin levels were similar for patients and controls, suggesting that zinc deficiency in SCD does not relate to inadequate dietary intake. The origin of low serum zinc levels in children with SCD is more likely to relate to factors such as increased urinary zinc excretion, chronic intravascular hemolysis, and/or zinc malabsorption.  相似文献   

13.
Elevated levels of lipoprotein(a) [Lp(a)] have been associated with an increased risk of ischemic heart disease (IHD), and higher levels of Lp(a) are associated with lesions of significantly greater severity. We have examined Lp(a), total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) levels in patients with IHD including those with normal coronary arteries with vasospastic angina. The study population consisted of 206 patients (166 males and 40 females) who underwent diagnostic coronary angiography for known IHD. Twenty-eight patients had effort angina, 36 rest angina, 8 unstable angina and 134 old myocardial infarction. IHD patients were categorized as zero vessel disease (0VD), single vessel disease (SVD) and multi-vessel disease (MVD). To investigate the relationship between atherosclerosis and IHD, these patients were further divided into 3 groups based on angiographic findings. Eighteen patients had entirely normal coronary arteries (normal group), 24 discretely diseased coronary arteries (discrete group) and 80 diffusely diseased coronaries (diffuse group). The results were compared with those obtained from 50 healthy individuals. Lp(a) levels for IHD patients (12.4 mg/dl) were significantly higher than those of controls (7.1 mg/dl, p < 0.05). However, there were no statistical differences between 0VD (13.1 mg/dl) and MVD (12.8 mg/dl). Similarly, no statistical differences of Lp(a) values were found among the normal group (13.3 mg/dl), discrete group (12.0 mg/dl) and diffuse group (12.9 mg/dl). Mean levels of HDL-C in 0VD (51.3 +/- 13.5 mg/dl) were significantly higher than those of SVD (42.9 +/- 11.5 mg/dl, p < 0.05). However, no significant differences were observed between controls (59.5 +/- 15.3 mg/dl) and 0VD (51.3 +/- 13.5 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

14.
Plasma apolipoproteins in patients with multi-infarct dementia   总被引:12,自引:0,他引:12  
We examined 27 elderly patients with multi-infarct dementia developed on the basis of cerebral arteriosclerosis. The levels of plasma cholesterol and triglyceride in the patients were 177 +/- 48 and 91 +/- 27 mg/dl (mean +/- SD), respectively. Despite normal plasma lipid levels, the patients had significantly higher plasma apo B (102 +/- 30 vs. 82 +/- 21 mg/dl for controls, P less than 0.01) and lower plasma apo A-I levels (104 +/- 25 vs. 130 +/- 22 mg/dl for controls, P less than 0.01) than the controls. Isoelectric focusing of apo E showed a 2-fold higher relative frequency for the epsilon 4 allele in patients than in Japanese controls (20.8 vs. 8.6-11.7% of total, P less than 0.05). The patients with phenotypes of E4/4 (n = 1) and E4/3 (n = 8) had higher plasma cholesterol levels than those with E3/3 (n = 15) (196 +/- 45 vs. 169 +/- 43 mg/dl). The results indicate that the patients had abnormalities in plasma lipoprotein metabolism and this may contribute to the development of cerebral arteriosclerosis.  相似文献   

15.
Because we had found that ethanol interacts with retinol, we investigated whether it also affects its precursor, beta-carotene. In 14 baboons fed ethanol (50% of total energy) for 2 to 5 yr with a standard amount of beta-carotene (one 200-gm carrot/day), levels of beta-carotene were much higher than in controls fed isocaloric carbohydrate, both in plasma (122.5 +/- 30.9 nmol/dl vs. 6.3 +/- 1.4 nmol/dl; p less than 0.005) and in liver (7.9 +/- 1.1 nmol/gm vs. 1.8 +/- 0.5 nmol/gm; p less than 0.001). Even 20 days after withdrawal of the carrots, plasma beta-carotene levels remained higher in alcohol-fed baboons than in controls (10.1 +/- 3.8 nmol/dl vs. less than 0.1 nmol/dl). Next, the diet was supplemented with beta-carotene beadlets: in four pairs of baboons given a low dose of beta-carotene (3 mg/1,000 kcal), plasma levels were significantly higher in alcohol-fed animals than in controls, even when expressed per cholesterol (although the latter increased with alcohol intake). Seven pairs of animals were given a higher dose (30 mg/1,000 kcal) of beta-carotene for 1 mo, followed, in four pairs, by 45 mg for another month. On cessation of beta-carotene treatment, plasma levels decreased more slowly in the alcohol-fed baboons than in the controls. Percutaneous liver biopsy specimens revealed that liver concentrations of beta-carotene correlated with plasma levels but were higher in the alcohol-fed baboons than in the control baboons, whereas the beta-carotene-induced increase in liver retinoids was lower (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

16.
This study in 352 asymptomatic middle-aged Brazilian men demonstrated that serum uric acid increases linearly with an increasing number (0 to >/=3) of metabolic risk factors (5.78 +/- 1.1, 6.14 +/- 1.0, 6.27 +/- 1.1, and 6.79 +/- 1.3, p <0.001). In patients who had >/=3 metabolic risk factors, there was a higher prevalence of serum uric acid in the highest quartile (7.2 to 10.3 mg/dl) than in the lowest quartile (2.6 to 5.4 mg/dl, 35% vs 12%, p <0.001). Mean serum levels of uric acid were higher in those who had an abnormal ratio of >/=3 for triglyceride to high-density lipoprotein (suggesting insulin resistance) than in those who had a normal ratio (6.6 +/- 1.2 vs 5.87 +/- 1 mg/dl, p <0.001).  相似文献   

17.
Although the serum lipoprotein fraction Lp(a) has been associated with coronary artery atherosclerosis, its relationship to narrowing of saphenous vein grafts has not previously been elucidated. We therefore measured serum Lp(a) levels in 167 symptomatic patients undergoing cardiac catheterization who had had coronary artery bypass surgery 0.7 to 14.3 years earlier. Lp(a), total cholesterol, and total triglyceride levels were compared with the degree of saphenous vein graft stenosis to test for any association. Serum Lp(a) levels were significantly associated with the degree of stenosis of saphenous vein grafts (r = .24, p = .002). Mean Lp(a) levels (mg/dl) in the 135 patients with stenosis were almost double (32.0 +/- 32.7, mean +/- SD) those in the 32 patients with no graft stenosis (16.7 +/- 22.6; p = .002). Graft stenosis was not associated with previous myocardial infarction, hypertension, obesity, diabetes, or smoking. Serum cholesterol levels (mg/dl) were slightly higher in the stenosis group (251.3 +/- 69) than in the no-stenosis group (231.8 +/- 48.8), but the difference was of borderline significance (p = .06). A stepwise increase in mean Lp(a) was found in groups of patients with increasing vein graft stenosis. At a serum Lp(a) level of 31.6 mg/dl or above, 92% of the patients demonstrated vein graft stenosis. Thus, patients with elevated Lp(a) levels have an increased risk of developing saphenous vein graft stenosis after coronary bypass surgery.  相似文献   

18.
OBJECTIVES: This study sought to determine the effect of lipoprotein(a), or Lp(a), levels and apolipoprotein(a), or apo(a), sizes on endothelial function and to explore ethnic differences in their effects. BACKGROUND: Although high levels of Lp(a) have been shown to confer increased cardiovascular risk in Caucasians, its significance in non-Caucasian populations is uncertain. The pathogenic role of the apo(a) component of Lp(a) is also unclear. METHODS: The relationship of Lp(a) levels and apo(a) sizes to endothelial function was examined in a multiethnic cohort of 89 healthy subjects (age 42 +/- 9 years; 50 men, 39 women) free of other cardiac risk factors. Endothelium-dependent, flow-mediated dilation (FMD) and endothelium-independent, nitrate-induced dilation (NTG) were assessed by ultrasound imaging of the brachial artery. RESULTS: Plasma Lp(a) levels were lowest in Caucasians (18.3 +/- 21.1 mg/dl, n = 40); intermediate in Hispanics (30.2 +/- 30.5 mg/dl, n = 21); and highest in African Americans (68.8 +/- 46.0 mg/dl, n = 28). Lipoprotein(a) levels were found to correlate inversely to FMD (r = -0.33, p < 0.005) but not to NTG (r = 0.06, p = 0.60). This association remained significant after adjusting for gender (p = 0.002). In addition, subjects with small apo(a) size of 相似文献   

19.
A prospective study (June 1988-December 1989) of all patients admitted with ascites due to cirrhosis was undertaken: Biochemical and immunological factors which may have significance in the development of spontaneous bacterial peritonitis were determined. Among 56 patients (44 males and 12 females) SBP developed in 16% of the group. No age differences were found and the etiology of the cirrhosis was mainly alcoholic. Patients with SBP had lower alpha-2 globulin concentrations: 0.43 +/- 0.12 vs. 0.60 +/- 0.18 g/dl (p less than 0.05) and a lower prothrombin time: 41 +/- 13% vs. 69.5 +/- 13 vs. 69.5 +/- 21% (p less than 0.001). Patients with SBP had also lower ascitic fluid total protein 0.99 +/- 0.4 vs. 1.64 +/- 1.1 g/dl (p less than 0.01) as well as lower alfa-2 globulin: 0.065 +/- 0.012 vs. 0.096 +/- 0.067 g/dl (p less than 0.05); beta globulin, 0.11 +/- 0.047 vs. 0.2 +/- 0.17 g/dl (p less than 0.05); gamma globulin, 0.32 +/- 0.1 vs. 0.52 +/- 0.4 g/dl (p less than 0.05); IgG, 275 +/- 157 vs. 477 +/- 335 g/dl (p less than 0.05); C3, 9.2 +/- 3.2 vs. 17 +/- 13 mg/dl (p less than 0.01) and C4, 2.83 +/- 1.5 vs. 4.66 +/- 3.9 mg/dl (p less than 0.05) than patients without this complication.  相似文献   

20.
We investigated alterations of serum levels of Lp(a) and lipid profiles in type 2 diabetic patients and their normoglycemic first-degree relatives to evaluate the potential genetic association among these subjects. Serum Lp(a), triglycerride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), and low density lipoprotein (LDL-C) levels were analyzed in 62 type 2 diabetic patients and 67 normoglycemic first-degree relatives from 29 type 2 diabetic pedigrees, and 45 healthy controls without family histories of diabetes. Dyslipidemia was observed in diabetics and their normoglycemic first-degree relatives. While higher serum TG levels were observed in both type 2 diabetics and their first-degree relatives than those in controls, higher TG levels in diabetics were found when compared with those in first-degree relatives. Meanwhile, lower serum HDL-C levels were observed in both type 2 diabetic patients and their first-degree relatives than those in controls. No significant difference of serum TC and LDL-C levels was found among the three groups. On the other hand, we did not observe significant differences of serum Lp(a) levels between type 2 diabetic patients and normoglycemic first-degree relatives, nor were any significant differences observed between diabetic patients and healthy controls (24.6+/-19.9 vs. 25.8+/-21.2, and 21.3+/-20.5 mg/dl). Although the average serum Lp(a) levels were similar in all subgroups, we did observe a positive correlation of Lp(a) between type 2 diabetic patients and their offspring (r=0.448, P<0.01), suggesting a potential genetic control for Lp(a) levels in type 2 diabetics families.  相似文献   

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