Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High concentrations of serum lipoprotein(a) (Lp(a)) are associated with an increased risk of atherosclerotic vascular disease in the nontransplanted population. However, its relation with accelerated coronary artery disease (CAD) in cardiac transplant recipients has not been reported. We measured serum Lp(a) in 130 cardiac transplant recipients undergoing routine follow-up, which included annual coronary angiography. The median Lp(a) concentration in 33 patients with CAD was 71 mg/dl, which was significantly higher than the corresponding value of 22 mg/dL in the 97 patients without CAD (p = 0.0006). Multivariant analysis showed the serum Lp(a) value to be a higher significant risk factor for CAD irrespective of the other factors included in the regression analysis. Thus a high concentration of serum Lp(a) is an important, independent risk factor for the development of accelerated CAD in transplant recipients.
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PMID:Lipoprotein(a) and accelerated coronary artery disease in cardiac transplant recipients. 136 97

Lipoprotein(a) (Lp[a]) is a low density lipoprotein particle that contains plasminogen-like apolipoprotein(a). Recent studies suggest an association of Lp(a) with atherosclerotic vascular disease. We have studied the accumulation of Lp(a) in atherosclerotic arteries of monkeys with diet-induced atherosclerosis. Immunohistochemistry with monospecific Lp(a) antisera revealed striking accumulations of Lp(a) in atherosclerotic coronary artery lesions. There was no Lp(a) in the normal, nonatherosclerotic arteries. Analysis of paired tissue and serum samples from 17 male hyperlipoproteinemic monkeys revealed a significant correlation between aortic wall Lp(a) and serum Lp(a) levels. The serum cholesterol level failed to correlate with either aortic Lp(a) or serum Lp(a). These results add further evidence for the potential role of Lp(a) in the pathogenesis of atherosclerosis.
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PMID:Lipoprotein(a) in diet-induced atherosclerosis in nonhuman primates. 182 15

The last 25 years have witnessed an exponential increase of interest in the lipoprotein Lp(a). The structure of the gene encoding for its unique apo protein, Apo(a) has been determined resulting in possible structure/function relationships which may explain the close association between elevated levels of Lp(a) and atheromatous vascular disease. These findings may have profound therapeutic implications for the future treatment of the hyperlipidaemias and hypercholesterolaemia in particular.
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PMID:The Apo(a) gene: structure/function relationships and the possible link with thrombotic atheromatous disease. 215 25

With sensitive methods, the lipoprotein Lp(a) can be demonstrated in the serum of all human subjects, except patients with abetalipoproteinaemia. A high serum level of Lp(a) is considered as a risk factor for atherosclerotic vascular disease (coronary heart disease). The chemical and physical properties of Lp(a) are very similar to those of low density lipoproteins (LDL, Lp-B). In contrast to LDL, Lp(a) has an additional apolipoprotein, the specific Lp(a) antigen. From in vivo studies with 125I-labeled lipoproteins, the following conclusions can be drawn: 1. Lp(a) is not a metabolic product of other apolipoprotein B-containing lipoproteins. Apparently, Lp(a) is synthesized as a separate lipoprotein. 2. Lp(a) is not catabolized to other lipoproteins. Lp(a) leaves the plasma as an intact particle. 3. The fractional catabolic rate and the distribution between the intra- and extravascular compartment are similar for Lp(a) and LDL. 4. The serum level of Lp(a) is primarily determined by the synthetic rate and not by the catabolic rate.
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PMID:[Metabolism and clinical significance of lipoprotein Lp(a) (author's transl)]. 645 20

PURPOSE--To evaluate if the levels of lipoprotein (a) [Lp(a)], apolipoproteins (apo) A1, B and the lipid profile (LP) differ among heart transplantation (HT) patients, with coronary artery disease (CAD) and patients without CAD (NL) and if LP discriminates patients with graft vascular disease (GVD). METHODS--A hundred and seventy patients separated in 3 groups: I) HT [n = 43 46 +/- 15 years, 24 months (median) after transplantation], of these 28 were submitted to serial angiography after the first year of transplantation subgroups with GVD (n = 9) and without GVD (NGVD) (n = 19); II) CAD (n = 72, 48 +/- 6 years); III) NL (n = 45, 50 +/- 6 years). RESULTS--HT presented higher apo A1 levels than CAD and NL (1.5 +/- 0.5 vs 1.2 +/- 0.05 vs 1.1 +/- 0.06 g/l p < 0.05 respectively). Apo B was higher on CAD than in HT and NL (1.5 +/- 0.05 vs 1.2 +/- 0.07 vs 1.3 +/- 0.09 g/l p < 0.05). Lp (a) presented a trend to higher levels in HT and CAD than in NL [25(2-97), 24(1-130) and 15 (1-100) mg/dl, p = 0.05)]. However, when individually evaluated against NL Lp(a) levels were higher in HT and CAD (p = 0.019 and 0.03 respectively). LP did not differ between GVD and NGVD. CONCLUSION--Increased Lp(a) levels after transplantation might be related to the high prevalence of GVD. The LP did not discriminate GVD.
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PMID:[Lipoprotein (a), apolipoproteins and the lipid profile late after heart transplantation]. 760 29

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for vascular disease and a potential link between coagulation, lipoproteins, and the development of atherosclerosis. Its role in the vascular complications of patients with chronic renal disease is unclear. We review methodologic issues involved in measuring Lp(a), particularly as they relate to studies of patients with chronic renal disease. The accurate measurement of Lp(a) is difficult because all the commercially available assays are sensitive to apolipoprotein(a) isoform size, Lp(a) behaves like an acute phase reactant, and levels vary markedly among ethnic groups. The results of 12 studies that included data on median Lp(a) levels in controls and patients receiving renal replacement therapy were analyzed. Although there was variation among studies, most found elevated levels of Lp(a) in patients receiving hemodialysis (range of medians, 9.0 to 38.4 mg/dL) compared with controls (range of medians, 4.7 to 19.7 mg/dL). With the exception of one study, Lp(a) levels also were elevated in patients receiving continuous ambulatory peritoneal dialysis compared with controls and patients receiving hemodialysis. In one study, an elevated Lp(a) level in patients receiving hemodialysis correlated with subsequent development of vascular events. A separate study associated the occurrence of vascular access occlusion with Lp(a) level. Following renal transplantation, Lp(a) levels decreased in all four studies, which included data before and after transplantation. Although variability in results were seen, Lp(a) levels appear to be elevated in patients receiving renal replacement therapy. Renal transplantation at least partially reverses this effect. The variability in results is probably related to methodologic difficulties in measuring Lp(a) and failure to segregate ethnic groups in study design and analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein(a) levels in patients receiving renal replacement therapy: methodologic issues and clinical implications. 761 Dec 48

Numerous studies have shown lipoprotein (a) [Lp(a)] serum levels above 0.3 gL-1 to be a genetically determined and independent risk factor for atherosclerotic vascular disease. In this study of sera from 1009 patients attending our lipid clinics, multivariate regression analysis revealed an inverse correlation between the serum concentrations of triglycerides (TG) and Lp(a) (r = -0.31; P < 0.001) as determined by electroimmunodiffusion. This was not observed in 1237 controls from a random population. Detailed analysis of the frequency distribution of Lp(a) levels at different degrees of hypertriglyceridaemia (HTG) revealed a decreasing dosage effect of HTG on Lp(a) serum levels. In 60% of patients with TG > 9.12 mmol L-1, this effect led to undetectable serum Lp(a) levels. Dilution of hypertriglyceridaemic samples with normotriglyceridaemic sera containing high levels of Lp(a) revealed that analytical interference in part accounts for the decreasing effect of TG-rich lipoproteins on Lp(a). Re-evaluation of 45 hypertriglyceridaemic samples by enzyme immunoassay and immunoblotting revealed the presence of small amounts of Lp(a) in several samples which were considered to be free of Lp(a) upon electroimmunodiffusion. We conclude that TG-rich lipoproteins interfere with the quantification of Lp(a), at least by electroimmunodiffusion. However, HTG may also decrease Lp(a) plasma concentrations in vivo, possibly by increased clearance of TG-rich Lp(a).
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PMID:Effect of hypertriglyceridaemia on lipoprotein (a) serum concentrations. 762 17

Lipoprotein (a) [Lp(a)] has been recognized for nearly 30 years, and increasingly, associated with the processes of atherogenesis and thrombogenesis. Despite this, the physiological and pathological function (and factors that influence levels) of Lp(a) remain largely unknown. Most experimental evidence supporting the mechanisms of vascular disease, thrombogenesis and atherogenesis have been generated in vitro, and to date, no in vivo confirmation exists. There is also a lack of sound evidence for Lp(a) as a risk factor in prospective as opposed to case-controlled studies. A fuller understanding of Lp(a) is still required in the molecular biology of atherogenesis and thrombogenesis.
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PMID:Lipoprotein (a) and vascular disease: thrombogenesis and atherogenesis. 764 39

High concentrations of lipoprotein (a) (Lp(a)) are associated with an increased risk of atherosclerotic vascular disease. Lp(a) synthesis is mainly under genetic control but many endocrine disturbances may modulate Lp(a) plasmatic concentrations. There is no agreement upon Lp(a) variations in patients under a hypocaloric diet. This study was undertaken to assess this point in obese females subjected to a 1100 kcal/d diet. Ninety-two obese patients (42.4 +/- 10.4 yr old, BMI 33.9 +/- 5.6 kg/m2) came once a week as out patients during 9 weeks. Lp(a) concentrations distribution was highly skewed. The threshold Lp(a) concentration for a significant cardiovascular risk is estimated at 0.3 g/l. Concentrations above 0.3 g/l were found in 29/92 patients (31%). If the patients were distributed in 2 groups according to their Lp(a) values (< or = ou > 0.3 g/l), the BMI, total cholesterol or triglycerides were not different. There were no significant correlation between Lp(a) and age, total cholesterol or triglycerides. After 9 weeks BMI and total cholesterol values decreased (-1.6 +/- 3.4 kg/m2 and -0.17 +/- 0.68 mmol/l, respectively). Lp(a) concentrations were unchanged (0.3 +/- 0.3 vs 0.3 +/- 0.3 g/l). There were no significant correlation between Lp(a) variations and age, BMI or initial Lp(a) concentrations. No significant decrease of Lp(a) could be detected even in the sub-group of patients with initial concentrations of Lp(a) > 0.3 g/l or even in a sub-group with Lp(a) > 0.7 g/l (n = 7). Under our conditions, weight loss is not associated with a decrease of Lp(a) concentrations suggesting that in a given obese a single determination is enough to assess his Lp(a)-related atherosclerotic risk.
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PMID:[Lp(a) and weight loss in obese patients]. 767 9

The effect of a 17-kringle form of recombinant apo(a) [r-apo(a)] on in vitro fibrin clot lysis was studied. In these assays, fibrin clots were formed in the wells of microtiter plates, and lysis of the clots was monitored by measurement of the turbidity at 405 nm. The results indicate that r-apo(a) produces a dose-dependent antifibrinolytic effect in clots formed using either purified components or barium-adsorbed plasma. This effect was found to be independent of clot structure, since lysis of clots formed using both high and low concentrations of thrombin was prolonged by r-apo(a) to the same extent. The two components of the antifibrinolytic effect of r-apo(a) were determined to be (i) attenuation of tPA-mediated plasminogen activation (the major component) and (ii) inhibition of plasmin degradation of fibrin, although r-apo(a) did not directly attenuate plasmin activity, as measured by S-2251 hydrolysis. r-Apo(a) interfered most substantially with tPA-mediated activation of Glu-plasminogen and less substantially with tPA-mediated Lys-plasminogen activation and urokinase-mediated activation of plasminogen. In summary, we have demonstrated that apo(a) is able to attenuate fibrin clot lysis in vitro, primarily as a consequence of the interference by apo(a) with tPA-mediated Glu-plasminogen activation. These studies illuminate possible mechanisms by which Lp(a) may contribute to the development of vascular disease in vivo.
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PMID:Antifibrinolytic effect of recombinant apolipoprotein(a) in vitro is primarily due to attenuation of tPA-mediated Glu-plasminogen activation. 771 Oct 34


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