Göttinger Risiko-, Inzidenz- und Prävalenzstudie (GRIPS)

Cremer, P.; Nagel, Dorothea; Labrot, Barbara; Muche, Rainer; Elster, Harald; Mann, Horst; Seidel, D.

doi:10.1007/978-3-642-76323-6

Cited by 26 publications

(16 citation statements)

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“…Isoform ( ) size was expressed as the number of kringle 4 K4 repeats. 11.2%, P -0.05 , while there were no differences between ( ) SA patients and controls. The median apolipoprotein a -isoform ( ) size was 26 K4.…”

contrasting

confidence: 55%

Serum Lipoprotein(a) Concentrations and Apolipoprotein(a) Isoforms: Association with the Severity of Clinical Presentation in Patients with Coronary Heart Disease

Katsouras

Karabina

Tambaki

et al. 2001

European Journal of Cardiovascular Prevention & Rehabilitat

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Objective The aim of this study was to investigate the possible ( ) [ ( )] associations between lipoprotein a Lp a concentrations or ( ) apolipoprotein a isoforms and the mode of clinical presentation ( ) ( of coronary heart disease CHD acute thrombotic event or ) not .Methods A total of 131 CHD patients and 71 age-and ( gender-matched individuals without known CAD free of ) symptoms of heart disease were enrolled in the study. CHD patients were classified into patients with a history of an acute ( ) coronary syndrome ACS, n = 94 and patients with stable ( ) () angina SA, n = 37 . Lp a levels were measured with an ELISA ( ) method, whereas apolipoprotein a isoform analysis was ( ) performed in all patients and 33 controls by electrophoresis in 1.5% SDS-agarose gels followed by immunoblotting. Isoform ( ) size was expressed as the number of kringle 4 K4 repeats. ( ) [ Results ACS patients had higher Lp a plasma levels 21.9 ( ) ] ( 0.8-84.1 mg / dl and a greater proportion of elevated G 30 ) ( ) ( ) mg / dl Lp a concentrations 25.5% compared with SA [ ( ) patients 9.2 0.8-50.5 mg / dl, P -0.01 and 10.8%, ] [ ( ) P -0.05 and controls 8.0 0.8-55.0 mg / dl, P -0.01 and ] 11.2%, P -0.05 , while there were no differences between ( ) SA patients and controls. The median apolipoprotein a -isoform ( ) size was 26 K4. In 17 10% patients we could not detect any ( ) apolipoprotein a isoform bands by immunoblotting. ACS ( patients had a higher proportion of isoforms -26 K4 low ) ( molecular weight than SA patients 56/ 85 vs. 12/ 33, ) ( ) P -0.005 and controls 10/ 29, P -0.005 .Conclusions CAD patients with a history of ACS have higher ( ) Lp a plasma levels and a significantly higher proportion of low ( ) molecular weight apolipoprotein a isoforms compared with patients with SA or to controls.

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contrasting

confidence: 55%

Serum Lipoprotein(a) Concentrations and Apolipoprotein(a) Isoforms: Association with the Severity of Clinical Presentation in Patients with Coronary Heart Disease

Katsouras

Karabina

Tambaki

et al. 2001

European Journal of Cardiovascular Prevention & Rehabilitat

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“…At presence there is little or no treatment for diminishing lipoprotein(a) levels in blood (with the exception of the HELP apheresis) but there is a need for the early recognition of children at risk of developing atherosclerotic disease due to abnormally high levels of lipoprotein(a). Even for adults, the recommended upper limits of lipoprotein(a) (14) have been accepted without sufficient investigation or statistical analysis.…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein(a) Concentrations in Cord and Capillary Blood from Newborns and in Serum from In-Patient Children, Adolescents and Adults

Schumacher¹,

Keßler²,

Meier³

et al. 1994

CCLM

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Investigations have been made up.on the distribution of lipoprotein(a) concentrations in cord and capillary blood from newborns and in serum from in-patient children and adults. Full-tenn neonates (n = 123), children aged l month to 16 years (n = 331) and adults aged between 17 and 88 years (n = 252) of age were included in the study.Lipoprotein(a) was determined using an immunoluminometric assay and a single lot of reagents. The assay had an effective measuring ränge of 1-800 mg/1. Lipoprotein(a) could be measured either in cord or capillary blood in the majority of cases. Problems arose in isolated cases, in each of which there was a large concentration difference in lipoprotein(a) between mother and child. The correlation data was: r = 0.897, n = 37, log (capillary blood) = 0.874 log (cord blood) + 0.165. The median lipoprotein(ä) concentrations in cord and capillary blood were 13.9 and 10.2 mg/1 respectively.Mediän lipoprotein(ä) concentrations increased from birth up until the 6th decade (159 mg/1), decreasing to 95 mg/1 düring the 9th decade of life. In mature newborns, the median lipoprotein(a) concentrations correlated with gestational age.The distribution of Hpoprotein(a) concentrations in serum is skewed throughout life, the ratio mean/median being 2.07 at birth, 2.71 in children and 2.72 in adults. The percentage of children with lipoprotein(a) concentrations above 250 mg/1 was 23.0 (male) and 23.8 (femäle). The corresppnding figures for adults was 38.2 for males and 28.2 for females respectively. In the group of newborns 27.7 percent had concentrations above 25 mg/1.There was ho significant difference between median lipoprotein(a) concentrations after delivery in 80 healthy mothers aged 17-35 years (92.5 mg/1) and 51 age matched in-patients (104 mg/1). Adult males had significantly higher median serum lipoprotein(a) concentrations than adult females (p < 0.05, males 144 mg/1, females 89 mg/1).

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“…In contrast, a number of retrospective studies have shown that high circulating levels of this lipoparticle are associated with a high risk for cardiovascular and cerebrovascular diseases in young adults (<60 years old). Recent prospective studies have confirmed these observations (41)(42)(43)(44)(45) (Table 1). It is now well recognized that the circulating concentration of Lp(a) is mainly regulated by the apo(a) gene (46).…”

Section: Genetic Polymorphism and Functional Heterogeneity Of Lp(a)mentioning

confidence: 54%

“…Positive correlation Göteborg Study (41) (N = 776; 26/109) British United Provident Association (N = 21520; 229/1145) Study (43) Lipid Research Clinics (44) (N = 3806; 233/390) Göttingen Study (42) (N = 5471; 214/5124) Framingham Heart Study (45) (N = 1340; 169/1171) play different affinities for fibrin as a function of their size; this finding suggests that the variable number of kringles in apo(a) influences its ability to bind to fibrin (51). Thus, isoforms of low molecular mass showing the highest affinity for fibrin are the best competitor for plasminogen and are epidemiologically related to a higher cardiovascular risk (49)(50)(51) …”

Section: No Correlationmentioning

confidence: 99%

Structural basis for the pathophysiology of lipoprotein(a) in the athero-thrombotic process

Anglès-Cano

1997

Braz J Med Biol Res

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Lipoprotein Lp(a) is a major and independent genetic risk factor for atherosclerosis and cardiovascular disease. The essential difference between Lp(a) and low density lipoproteins (LDL) is apolipoprotein apo(a), a glycoprotein structurally similar to plasminogen, the precursor of plasmin, the fibrinolytic enzyme. This structural homology endows Lp(a) with the capacity to bind to fibrin and to membrane proteins of endothelial cells and monocytes, and thereby to inhibit plasminogen binding and plasmin generation. The inhibition of plasmin generation and the accumulation of Lp(a) on the surface of fibrin and cell membranes favor fibrin and cholesterol deposition at sites of vascular injury. Moreover, insufficient activation of TGF-ß due to low plasmin activity may result in migration and proliferation of smooth muscle cells into the vascular intima. These mechanisms may constitute the basis of the athero-thrombogenic mode of action of Lp(a). It is currently accepted that this effect of Lp(a) is linked to its concentration in plasma. An inverse relationship between Lp(a) concentration and apo(a) isoform size, which is under genetic control, has been documented. Recently, it has been shown that inhibition of plasminogen binding to fibrin by apo(a) is also inversely associated with isoform size. Specific point mutations may also affect the lysine-binding function of apo(a). These results support the existence of functional heterogeneity in apolipoprotein(a) isoforms and suggest that the predictive value of Lp(a) as a risk factor for vascular occlusive disease would depend on the relative concentration of the isoform with the highest affinity for fibrin. Correspondence

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Göttinger Risiko-, Inzidenz- und Prävalenzstudie (GRIPS)

Cited by 26 publications

References 0 publications

Serum Lipoprotein(a) Concentrations and Apolipoprotein(a) Isoforms: Association with the Severity of Clinical Presentation in Patients with Coronary Heart Disease

Serum Lipoprotein(a) Concentrations and Apolipoprotein(a) Isoforms: Association with the Severity of Clinical Presentation in Patients with Coronary Heart Disease

Lipoprotein(a) Concentrations in Cord and Capillary Blood from Newborns and in Serum from In-Patient Children, Adolescents and Adults

Structural basis for the pathophysiology of lipoprotein(a) in the athero-thrombotic process

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