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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We determined the level of lipoprotein (a) [Lp(a)] in 1,266 healthy persons and established the reference value of Lp(a) in various groups of age and sex. The analysis of lipids in myocardial infarction survivors and stroke survivors suggest that increased Lp(a) is an independent risk factor in cardio-cerebrovascular diseases. The characteristics of abnormal lipids in cardio-cerebrovascular diseases are discussed.
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PMID:[Determination and clinical significance of lipoprotein(a) in cardio-cerebrovascular diseases]. 131 9

Elevated plasma levels of the lipoprotein Lp(a) are associated with increased risk for atherosclerosis and its manifestations, myocardial infarction, stroke and restenosis (for reviews, see refs 1-3). Lp(a) differs from low-density lipoprotein by the addition of the glycoprotein apolipoprotein(a), a homologue of plasminogen that contains many tandemly repeated units which resemble the fourth kringle domain of plasminogen, and single homologues of its kringle-5 and protease domain. As plasma Lp(a) concentration is strongly influenced by heritable factors and is refractory to most drug and dietary manipulation, the effects of modulating it are difficult to mimic experimentally. In addition, the absence of apolipoprotein(a) from virtually all species other than primates precludes the use of convenient animal models. Here we show that transgenic mice expressing human apolipoprotein(a) are more susceptible than control mice to the development of lipid-staining lesions in the aorta, and that apolipoprotein(a) co-localizes with lipid deposition in the artery walls.
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PMID:Atherogenesis in transgenic mice expressing human apolipoprotein(a) 146 21

The association between serum Lp(a) concentration, a risk factor for atherothrombotic disease, and other cardiovascular risk factors such as smoking, alcohol intake, hypertension, obesity, and indices of glycemic control is examined in a cohort of 313 elderly Chinese subjects (M = 160, mean age +/- SD = 68 +/- 11 year; F = 153, mean age +/- SD = 73 +/- 11). Although associations existed for the above risk factors and other serum lipid levels, there was no association with serum Lp(a) concentration in the overall population. Men with Lp(a) greater than or equal to 30 mg/dl had a higher mean age and blood pressure. A higher percentage of subjects with Lp(a) greater than or equal to 30 mg/dl had a family history of stroke, although the total number of those with a family history was too small to reach statistical significance. The lack of association with known modifiable cardiovascular risk factors is compatible with the conclusion that Lp(a) concentration is primarily under genetic control and therefore unlikely to be a modifiable risk factor.
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PMID:Association of serum lipoprotein(a) concentration with other cardiovascular risk factors in a Chinese population. 183 21

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL)-like lipoprotein particle recently described as a risk factor for premature coronary heart disease, stroke, and atherosclerosis. Structurally, Lp(a) is similar to LDL in that it has comparable lipid composition and contains apolipoprotein B-100 (apo B-100). In addition, Lp(a) contains the glycoprotein apolipoprotein(a) [apo(a)], which is disulfide-linked to apo B-100. The recent awareness of a striking correlation between atherosclerosis and concentrations of Lp(a) in plasma prompted our development of an accurate quantitative assay for plasma Lp(a), a monoclonal-antibody-based enzyme-linked immunosorbent assay for Lp(a) that is shown to be sensitive, precise, and highly specific. The response to several isoforms of Lp(a) is linear, and as many as 80 samples can be quantified on one plate. This easily performed assay is suitable for use in the clinical laboratory and for screening large populations.
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PMID:A monoclonal-antibody-based enzyme-linked immunosorbent assay of lipoprotein(a). 213 83

Lipoprotein(a) [Lp(a)] is a macromolecular complex found in human plasma that combines structural elements from the lipoprotein and blood clotting systems and that is associated with premature coronary heart disease and stroke. It is assembled from low-density lipoprotein (LDL) and a large hydrophilic glycoprotein called apolipoprotein(a) [apo(a)], which is homologous to the protease zymogen plasminogen. Plasma Lp(a) concentrations vary 1000-fold between individuals and represent a continuous quantitative genetic trait with a skewed distribution in Caucasian populations. Variation in the hypervariable apo(a) gene on chromosome 6q2.6-q2.7 and interaction of apo(a) alleles with defective LDL-receptor genes explain a large fraction of the variability of plasma Lp(a) concentrations. Though of high theoretical and practical interest, many aspects of the metabolism, function, evolution, and regulation of plasma concentrations of Lp(a) are presently unknown, controversial, or mysterious.
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PMID:The mysteries of lipoprotein(a). 253 Jun 31

To evaluate the role of lipoprotein(a) (Lp(a] in patients with cerebrovascular disease (CVD), lipid parameters were compared with a control group (CO). Additionally, the Lp(a) serum levels were investigated in a coronary artery disease (CAD) group. The CO was made up of 37 healthy persons (age: 54.5 +/- 7.7, 26 males and 11 females), the CVD group included 46 patients with sustained transient ischemic attack (TIA) prolonged reversible ischemic neurologic deficits (PRIND) and cerebral infarction (CI) (age: 53.6 +/- 9.7, 32 males and 14 females), and the CAD group was made up of 28 survivors of myocardial infarctions (age: 52.5 +/- 8.1, 18 males and 10 females). The median values of Lp(a) in CVD were significantly higher than in the CO (p less than 0.01) and did not differ significantly from the CAD. Total TC, HDL-C, TG, LDL-C and the ratio of LDL-C/HDL-C did not show any significant difference between the control and cerebrovascular disease group. For quantification of the vascular lesions of the carotid system, a Duplex Doppler score system was used. The score correlated with Lp(a) in patients between 40 to 65 years of age (r = 0.34, p less than 0.01). Thus, we conclude that Lp(a) is not only a risk factor for CAD but also for CVD.
Stroke
PMID:Lipoprotein(a) as a strong indicator for cerebrovascular disease. 294 94

The extensive homology between apolipoprotein(a) and plasminogen has led to the hypothesis that the increased risk for atherosclerosis, cardiac disease and stroke associated with elevated levels of apolipoprotein(a) may reflect modulation of fibrinolysis. We have investigated the role of apolipoprotein(a) on clot lysis in transgenic mice expressing the human apolipoprotein(a) gene. These mice develop fatty streak lesions resembling early lesions of human atherosclerosis. Pulmonary emboli were generated in mice by injection, through the right jugular vein, of a human platelet-rich plasma clot radiolabelled with technetium-99m-labelled antifibrin antibodies. Tissue plasminogen activator was introduced continuously via the right jugular vein. Clot lysis, determined by ex vivo imaging, was depressed in mice carrying the apolipoprotein(a) transgene relative to their sex-matched normal littermates. These results directly demonstrate an in vivo effect of apolipoprotein(a) on fibrinolysis, an effect that may contribute to the pathology associated with elevated levels of this protein.
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PMID:Antifibrinolytic activity of apolipoprotein(a) in vivo: human apolipoprotein(a) transgenic mice are resistant to tissue plasminogen activator-mediated thrombolysis. 758 43

A number of epidemiological studies have clearly shown that post-menopausal women on hormone therapy (which tends to simulate normal ovarian production) have a reduced risk of cardiovascular disease (coronary heart disease, stroke and thrombotic events). In fact most of the studies have involved equine oestrogen (Premarin) taken orally. The effects of oestrogens and the progestins depend on the type of administration (oral or percutaneous administration) and the variety of the drug chosen and finally is also dose dependent. The most favourable effect is obtained in normolipidaemic women with the combination of conjugated oestrogens given orally and a non-androgenic progestins. Such therapy is associated with an increase in HDL-cholesterol and a decrease in LDL-cholesterol. HDL subfraction analysis shows that HDL2 are the main species involved in this increase. The mechanism of action of oestrogens and progestins can be summarized as follows: oestrogens stimulate hepatic triglyceride secretion, inhibit the action of hepatic lipase, augment LDL breakdown via the cellular receptor apo B-E and may decrease LDL oxidability and Lp(a) levels. Although several points remain obscure, we may notice that most of studies show that the atherogenic profile of the women who are currently being treated tends to improve.
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PMID:[Substitutive hormonal treatment of menopause. Effects on lipoprotein metabolism]. 763 33

Two new important independent risk factors for coronary artery disease (CAD) have been identified: lipoprotein (a) [Lp(a)] and homocyst(e)ine. Both are associated with increased frequency of cardiovascular events, both coronary and peripheral. Measurement of these two factors should be considered in patients with symptomatic CAD, stroke, a strong family history (but low other conventional risk factors); in first degree relatives of those with very high Lp(a) or homocyst(e)ine levels; and in other individuals in whom the need for an aggressive treatment of metabolic risk factors is indicated. While treatment of high serum Lp(a) with drugs is difficult it appears from the epidemiological or clinical evidence that the additional risk due to Lp(a) can be drastically lowered by decreasing the patient's low density lipoprotein (LDL) cholesterol levels to below 3 mmol/L. The treatment of increased homocyst(e)ine can be easily accomplished by vitamin B6 or folic acid administration. Various analyses describing the value of positive tests for diagnosis of atherosclerosis indicate that overall risk evaluated by computer models from Framingham data, use of total: high density lipoprotein (HDL) cholesterol ratio and/or the National Cholesterol Education Program (NCEP) II guidelines are the best predictors of future cardiovascular events. The strategic aim for treatment regimens should be threefold: lower serum LDL cholesterol levels; decrease serum triglycerides (and triglyceride-rich lipoproteins); and increase HDL cholesterol. Niacin and statin drugs are the most cost effective means to achieve the former and niacin and fibrates to achieve the latter goal. Where target LDL cholesterol levels can be achieved with less expensive statin preparations their use may be economically advantageous.
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PMID:Lipoproteins and homocyst(e)ine as risk factors for atherosclerosis: assessment and treatment. 775 44

Most large studies of the blood parameters that act as risk factors for myocardial infarction, stroke and atherosclerosis have identified elevated circulating levels of lipoprotein(a) as an important risk factor. Lipoprotein(a) consists of an LDL particle that is covalently bound to the distinguishing protein component apolipoprotein(a). Ever since apolipoprotein(a) was cloned in 1987 and the marked sequence homology to plasminogen was noted, mechanisms for the atherogenic activity of lipoprotein(a), based on the competitive inhibition of plasminogen activity, have been proposed. However, with the availability of transgenic mice expressing both human apolipoprotein(a) and lipoprotein(a), recent studies have demonstrated that lipoprotein(a) acts to inhibit plasminogen activation in vivo. One consequence of this is reduced activation of the cytokine transforming growth factor-beta, an important regulator of vessel wall structure.
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PMID:Transforming growth factor-beta: the key to understanding lipoprotein(a)? 777 72


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