Does Lp(a) lipoprotein inhibit the fibrinolytic system ?

Halvorsen, Sigrun; Skjønsberg, Ole Henning; Berg, Kåre; Ruyter, R.; Godal, H. C.

doi:10.1016/0049-3848(92)90080-t

Cited by 33 publications

(16 citation statements)

References 20 publications

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“…In our own studies (Halvorsen et al 1992), we found no influence of purified Lp(a) lipoprotein on plasminogen activation by tPA in the presence of fibrin, in an in vitro model. Addition of Lp(a) lipoprotein to whole blood did not reduce fibrin degradation following standardized coagulation.…”

mentioning

confidence: 58%

High Lp(a) lipoprotein level in maternal serum may interfere with placental circulation and cause fetal growth retardation

1994

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We report on a woman with an Lp(a) lipoprotein level above the 99th centile of the population distribution of concentrations, who at the age of 43 had had deep vein thrombosis causing a pulmonary embolus and whose brother, who also had a very high level, had suffered a cerebral infarction at the age of 43. She had given birth to three children, all with very low birth weight, one of whom died when 3 months old. The placentas had been small and ischemic. The concurrence of a very high Lp(a) lipoprotein level, familial thromboembolic disease and recurrent placental ischemia with delivery of children with low birth weight suggests the possibility that a very high Lp(a) lipoprotein concentration may predispose to placental insufficiency, presumably arising from pathological changes in maternal uterine vessels in the placental bed. If confirmed, a very high Lp(a) lipoprotein level may be a factor to consider in women who have repeated pregnancies with placental insufficiency and who give birth to children with low birth weight.

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confidence: 58%

High Lp(a) lipoprotein level in maternal serum may interfere with placental circulation and cause fetal growth retardation

1994

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“…Lipoprotein(a), an LDL like lipoprotein, competes with plasminogen for fibrin binding in vitro, and therefore may relate atherosclerosis to thrombosis (14)(15)(16)(17). Although some studies report an association between lipoprotein(a) levels and fibrinogen concentrations, most investigators failed to find any relation between lipoprotein(a) and factors of the haemostatic or fibrinolytic system (62)(63)(64). Also in the present study, the increases in lipoprotein(a) levels in both groups and the increases in fibrinogen levels in the male group at the end of the training programme were not correlated.…”

Section: Discussionmentioning

confidence: 99%

Regular Physical Activity and Changes in Risk Factors for Coronary Heart Disease: A Nine Months Prospective Study

Ponjee¹,

Janssen²,

Hermans³

et al. 1996

CCLM

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This study reports the non-acute effects of a long-term training programme of increasing intensity on some cardiovascular risk factors and the interrelation between these risk factors. Twenty sedentary men and 14 sedentary women were trained 3 to 4 times a week for nine months. After 36 weeks all individuals ran a half marathon run. The W max , weight, body mass index, systolic and diastolic blood pressure were recorded. The concentrations of fibrinogen, tissue plasminogen activator, plasminogen activator inhibitor, triacylglycerols, total cholesterol, LDL cholesterol, HDL cholesterol and lipoprotein(a) were measured. The training programme induced a median increase in W raax of 12% in the male group (from 226 to 251.5 Watt) and of 18% in the female group (from 160 to 188.5 Watt). These increases in W max did not correlate with any other property under investigation in this study. Blood pressure was not altered, but body weight and body mass index were significantly decreased in the male group (from 74.6 to 72.2 kg and from 23.1 to 22.0 kg/m 2 , respectively) at the end of the training programme and decreased non-significantly in the female group (from 63.0 to 60.7 kg and from 21.6 to 21.5 kg/m 2 , respectively). In the male group total cholesterol, low density lipoprotein cholesterol and triacylglycerols decreased significantly under the influence of the training sessions. Furthermore, in both groups, a great decrease in plasma plasminogen activator inhibitor concentrations was noticed: in men from 22.5 · 10 3 AU/1 to 4.5 · 10 3 AU/1 and in women from 18.7 · 10 3 AU/1 to 5.1 · 10 3 AU/1. However, the changes in the lipid and fibrinolytic quantities were not correlated with each other. Initial total cholesterol, LDL cholesterol and triacylglycerol levels correlated significantly with systolic blood pressure, while diastolic pressure was correlated to tissue plasminogen activator. Since tissue plasminogen activator also was significantly related to triacylglycerols, a trias existed between primary risk factors like blood pressure, lipid levels and fibrinolysis. In contrast, the changes in these properties under the influence of physical training were not interrelated. Median serum lipoprotein(a) concentrations were significantly increased in both men and women five days before the half marathon run: from 32 mg/1 to 39 mg/1 in men, and from 65 mg/1 to 125.5 mg/1 in women. Concomitantly, median fibrinogen concentrations were significantly elevated in men (from 2.32 g/1 to 3.10 g/1) and non-significantly in women (from 2.62 g/1 to 2.93 g/1), although no correlation existed between the changes in these properties.In conclusion, the nine months exercise programme increased the aerobic fitness in both men and women as indicated by the W max increase. This improvement coincided but was not correlated with beneficial changes in several anthropometric, lipid and fibrinolytic properties. Improvement in the risk factors under investigation was more pronounced in men than in women. The changes in lipid and haemostasis propert...

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“…Most clinical studies have failed to demonstrate that high levels of Lp(a) decrease systemic fibrinolysis (36,37). To date there is no definitive evidence that Lp(a) interferes with plasminogen binding and activation in vivo.…”

Section: Antifibrinolytic Activity Of Apolipoprotein(a) In Vivomentioning

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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Does Lp(a) lipoprotein inhibit the fibrinolytic system ?

Cited by 33 publications

References 20 publications

High Lp(a) lipoprotein level in maternal serum may interfere with placental circulation and cause fetal growth retardation

High Lp(a) lipoprotein level in maternal serum may interfere with placental circulation and cause fetal growth retardation

Regular Physical Activity and Changes in Risk Factors for Coronary Heart Disease: A Nine Months Prospective Study

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

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