Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lp(a) was found to represent an independent risk factor of extracranial carotid atherosclerosis (CA). Here we report on an investigation with 808 subjects randomly selected from stroke patients as well as from asymptomatic subjects. Serum levels of Lp(a), total cholesterol (TC), HDL-C and the ratios of TC/HDL-C and LDL-C/HDL-C correlated highly significantly with the carotid score using a univariate test. Performing a discriminant analysis, the following ranking was obtained: Lp(a), HDL-C, LDL-C/HDL-C. Evaluation of the vessel wall elasticity in 746 subjects revealed Lp(a) to be the only highly significant parameter. Thus, Lp(a) has to be taken into consideration when establishing a risk profile of CA.
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PMID:Cerebrovascular disease and Lp(a): its role in atherosclerotic plaque formation and vessel wall elasticity of the carotid arteries. 818 43

Apolipoprotein (a) [Lp(a)] phenotypes of 69 myocardial infarction survivor and 56 stroke patients were reported and compared to those of 190 healthy Chinese. The results revealed that the distributions of apo(a) phenotype frequency in patients with cardio-cerebrovascular disease (CCVD) were different from those of controls. The frequency of the phenotypes S1 and S2 were remarkably higher in patients than in controls within the same single-band apo(a) phenotype. Moreover, the Lp (a) serum concentrations in CCVD patients were significantly higher than in controls within the same single-band apo (a) phenotype. The apo (a) phenotype analysis of two pedigrees were shown as a typical autosomal dominant inheritance.
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PMID:Apolipoprotein (a) phenotypes in cardio-cerebrovascular diseases. 819 80

We quantified serum lipoprotein(a) [Lp(a)] in 1266 healthy persons and established the reference value of Lp(a) in groups of age and sex. The Lp(a) in myocardial infarction (MI) survivors, stroke and primary hypertension patients were determined in comparison with that of age-matched normal controls. Moreover, cholesterol, triglyceride, HDL-cholesterol, apo Al and apo B were measured. The Lp(a) concentrations were not correlated with other lipids in normal controls and patients. Our results suggest that increased Lp(a) is an independent risk factor for MI and stroke patients. The total detective rate of abnormal lipids in MI and stroke patients was as high as 50% and 53.8% (Lp(a) excluded) as well as 65.7% and 64.9% (Lp(a) included) respectively.
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PMID:Increased lipoprotein (a) as an independent risk factor for cardiovascular and cerebrovascular diseases. 822 8

Serum lipoprotein(a) [Lp(a)] concentrations were investigated in 155 Japanese children aged 5 years. The frequency distribution of Lp(a) concentrations was highly skewed and ranged from 1 to 109 mg/dL. The mean and median values of Lp(a) were 16.5 mg/dL (s.d. 17.3 mg/dL) and 12 mg/dL. The incidence of Lp(a) concentrations > or = 30 mg/dL was significantly high in children with total cholesterol > or = 200 mg/dL, not including the case of familial hypercholesterolaemia. Log Lp(a) values showed an inverse correlation with bodyweight and body mass index. No significant differences in Lp(a) levels could be seen between the groups according to the presence or absence of coronary heart disease and cerebral vascular accident in family histories. The results suggest that Lp(a) in Japanese children aged 5 years was essentially the same as that in adults. Further study may be needed to disclose the factors that influence Lp(a) concentration in childhood.
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PMID:Serum lipoprotein(a) in healthy Japanese children 5 years of age. 837 21

Lipoprotein(a) (Lp[a]) is a newly recognized risk factor for the development of coronary heart disease and stroke in human beings; however, the mechanisms by which Lp(a) increases the risk of coronary heart disease remain unclear. The purpose of this study was to examine the effects of Lp(a) on the occurrence of occlusive arterial thrombosis. Occlusive arterial thrombus formation was examined in 18 cynomolgus monkeys with high plasma Lp(a) concentrations (> 35 mg/dL, n = 6), intermediate Lp(a) concentrations (20-25 mg/dL, n = 6), and low Lp(a) concentrations (< 12 mg/dL, n = 6). A Goldblatt clamp was positioned around the left common carotid artery to produce a stenotic segment, and the artery was pinch-injured with needle holders. A 20-MHz Doppler velocity crystal, placed distal to the stenosis/injury site, was used to detect cyclic flow reductions (indicative of transient thrombosis) or permanent cessation of flow velocity (indicative of more stable occlusive thrombosis). All monkeys with high Lp(a) concentrations developed permanent cessation of flow, whereas only one of six arteries from low-Lp(a) monkeys developed permanent cessation of flow (p < 0.05). Arteries from monkeys with intermediate Lp(a) concentrations developed pronounced cyclic reductions of flow but did not progress to permanent cessation of flow. There were no differences in plasma von Willebrand factor activity among the three groups. Immunohistochemical analysis of the damaged arterial segments indicated incorporation of Lp(a) into the adventitia, media, and intima of arteries from monkeys with low and high plasma Lp(a) concentrations, as well as the presence of an occlusive thrombus in arteries that developed permanent cessation of flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Occlusive arterial thrombosis in cynomolgus monkeys with varying plasma concentrations of lipoprotein(a). 846 90

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic vascular disease. Several studies have described a correlation between high Lp(a) plasma levels and coronary heart disease, stroke, and peripheral atherosclerosis. In healthy individuals Lp(a) plasma concentrations are almost exclusively controlled by the apolipoprotein(a) [apo(a)] gene locus on chromosome 6q2.6-q2.7. More than 30 alleles at this highly polymorphic gene locus determine a size polymorphism of apo(a). There exists an inverse correlation between the size (molecular weight) of apo(a) isoforms and Lp(a) plasma concentrations. Average Lp(a) levels are high in individuals with low molecular weight isoforms and low in those with high molecular weight isoforms. Mean Lp(a) plasma levels are elevated over controls in patients with renal disease. Patients with nephrotic syndrome exhibit excessively high Lp(a) plasma concentrations, which can be reduced with antiproteinuric treatment. The mechanism underlying this elevation is unclear, but the general increase in protein synthesis caused by the liver due to high urinary protein loss is a likely explanation. Patients with end-stage renal disease (ESRD) also have elevated Lp(a) levels. These are even higher in patients treated by continuous ambulatory peritoneal dialysis than in those receiving hemodialysis. Lipoprotein(a) concentrations decrease to values observed in controls matched for apo(a) type following renal transplantation. This clearly demonstrates the nongenetic origin of Lp(a) elevation in ESRD. Both the increase in ESRD and the decrease following renal transplantation are apo(a) phenotype dependent. Only patients with high molecular weight phenotypes show the described changes in Lp(a) levels. In patients with low molecular weight types the Lp(a) concentrations remain unchanged during both phases of renal disease. As in the general population, Lp(a) is a risk factor for cardiovascular events in ESRD patients. In this patient group the apo(a) phenotype seems to be equally or better predictive of the degree of atherosclerosis than is Lp(a) concentration. Further prospective studies will be necessary to confirm these observations. Whether Lp(a) also plays a key role in the pathogenesis and progression of renal diseases needs further study. Controversial data on the role of the kidney in Lp(a) metabolism result from insufficient sample sizes of several studies. Due to the broad range and skewed distribution of Lp(a) plasma concentrations, large study groups must be investigated to obtain reliable results.
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PMID:Lipoprotein(a) in renal disease. 876 31

In this cross-sectional study we compared the abilities of lipoprotein(a) [Lp(a)], plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (TPA) to discriminate between individuals with and without a history of stroke from among subjects in a metabolic ward. A total of 210 subjects (108 men and 102 women; mean age, 63.8 years; range, 31 to 86 years) provided plasma and DNA samples for the study. Of these, 51 men and 50 women had a history of ischemic stroke. The 109 subjects without a history of stroke were compared with those with such a history for major risk factors for ischemic events. Mean plasma TPA and PAI-1 levels significantly (P < .001) discriminated among subjects younger than 70 years with a history of stroke. The mean plasma Lp(a) level of stroke subjects (21.9 mg/dL) did not differ significantly from that of control subjects (15.2 mg/dL). However, among individuals < 70 years old, Lp(a) plasma levels > 50 mg/dL were more common among stroke patients (8 with versus 1 without, P < .01 by chi 2 test). A molecular variation in the 5' flanking region of the apo(a) gene that has been related to elevated Lp(a) plasma levels (G/A-914) was not strongly correlated with circulating levels of Lp(a), nor did Lp(a) levels correlate with a polymorphism of the apo(a) gene (G/A-21), which is strongly linked (P < .001) to the G/A-914 variation. In this setting, the relation between Lp(a) and cerebral ischemia appears to be limited to individuals below 70 years with elevated (> 50 mg/dL) plasma levels of the lipoprotein.
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PMID:Plasma lipoprotein(a) levels in subjects attending a metabolic ward. Discrimination between individuals with and without a history of ischemic stroke. 854 12

The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. Observations were made on the distribution of Lp(a), Lp(a) and other risk factors for cerebral infarction and these were statistically analyzed, primarily by multiple logistic regression analysis. The diagnosis of these cases was based on the Classification of Cerebrovascular Diseases III of the National Institute of Neurological Disorders and Stroke. The following results were obtained. 1) Lipoprotein (a) (1) Lp(a) did not show a normal distribution with the curve showing a gradual declining slope to the right. It was therefore considered not appropriate in our analysis to use as a means or standard deviation. (2) The 25th percentile, 50th percentile, and 75th percentile of the control group were 5.0 mg/dl, 11.0 mg/dl, and 22.4 mg/dl, respectively. In studying the distribution in these percentile ranges by subtypes of infarction, an increase in cases showing values greater than the median of the control group was observed in asymptomatic lacunar infarction, lacunar infarction, and atherothrombotic infarction, when compared to the control group. In asymptomatic lacunar infarction and lacunar infarction in particular, Lp(a) showed a significantly higher value compared to the control group. (3) However, by multiple logistic regression analysis to adjust for age and sex, Lp(a) did not show a significant odds ratio for asymptomatic lacunar infarction, lacunar infarction and atherothrombotic infarction. 2) Various serum lipids and other parameters (1) The various serum lipids did not show any involvement in asymptomatic lacunar infarction. However, involvement of HDLC and Apo A-I in lacunar infarction and atherothrombotic infarction was observed with the odds ratios in lacunar infarction being 4.2 with a confidence interval of 2.9-9.4 and 4.7 with a confidence interval of 2.2-10.1, and the odds ratios in atherothrombotic infarction being 3.1 with a confidence interval of 1.1-9.0 and 9.6 with a confidence interval of 3.0-30.5, respectively. (2) Involvement of diabetes mellitus in asymptomatic lacunar infarction and lacunar infarction was small, but a strong involvement in atherothrombotic infarction was observed with the odds ratio being 4.3 with a confidence interval of 1.2-16.2. (3) Involvement of hypertension in asymptomatic lacunar infarction and lacunar infarction was observed with the odds ratios being 2.6 with a confidence interval of 1.4-5.2 and 5.6 with a confidence interval of 2.4-13.0, respectively, but the involvement in atherothrombotic infarction was low. The foregoing results indicated that there was no involvement of Lp(a) as a risk factor for any type of cerebral infarction, unlike its involvement in coronary heart diseases. Only blood pressure was involved as a risk factor for asymptomatic lacunar infarction, but for lacunar infarction not only blood pressure but also HDLC and Apo A-I were involved as risk factors. HDLC, Apo A-I, and diabetes mellitus were involved as risk factors for atherothrombotic infarction, but the involvement of hypertension was minimal.
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PMID:Lipoprotein(a) and other risk factors for cerebral infarction. 856 15

"Silent" lacunar stroke, often found in the elderly, has been proposed as a predisposing condition for clinically overt stroke. However, the risk factors related to this condition have not been studied thoroughly. We conducted brain magnetic resonance imaging and measured the levels of fibrinogen, molecular markers of coagulation activation [prothrombin fragment 1 + 2 (F1 + 2)] and endothelial cell damage [von Willebrand factor (vWF) and thrombomodulin], and lipid profiles including lipoprotein (a) [Lp(a)] in 178 asymptomatic, high-risk, Japanese subjects aged 44 to 93 years. We also studied 32 symptomatic patients with lacunar stroke (symptomatic lacunar group). The prevalence of silent lacunar stroke increased with age up to 85 years but decreased with age in those 85 years old and older. Of the 160 elderly subjects ( > or = 60 years) 84 (53%) had > or = 1 lacunar infarcts (silent lacunar group) and the remaining 76 were considered as the nonlacunar group. Fibrinogen and F1 + 2 levels in the silent lacunar group were significantly higher than those in the nonlacunar group (P < .01). Mean Lp(a) levels and the prevalence of subjects with an Lp(a) level > 30 mg/dL were significantly higher in the symptomatic lacunar group than the nonlacunar group (P < .05), whereas these levels in the silent lacunar group were intermediate to those of the other two groups. When we further classified the silent lacunar group into three subgroups based on the number of lacunes (few lacunes, 1 or 2; moderate number of lacunes, 3 or 4; and numerous lacunes, > or = 5), levels of Lp(a), F1 + 2, vWF, and thrombomodulin were significantly higher and Lp(a) levels > 30 mg/dL more common in the numerous-lacune than in the few-lacune subgroup. We conclude that silent lacunar stroke is often found in asymptomatic, high-risk, elderly Japanese patients and that silent multiple lacunar stroke is associated with hypercoagulability, endothelial cell damage, and high Lp(a) levels.
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PMID:'Silent' cerebral infarction is associated with hypercoagulability, endothelial cell damage, and high Lp(a) levels in elderly Japanese. 864 Apr

Lipoprotein(a) (Lp[a]) consists of a LDL-particle and an apolipoprotein(a) which is related to plasminogen. The physiological function of Lp(a) is largely unknown, but the clinical effects are well known: high plasma concentrations of Lp(a) correlate with a high risk for atherosclerosis independently from other risk factors. This was shown in several studies for coronary heart disease, stroke and peripheral atherosclerosis. Lp(a) has a special position within other risk factors because of the strict genetic control of the plasma concentrations by the apo(a) gene locus on chromosome 6q2.6-2.7. Studies which doubt this relationship have to be considered sceptically. Recent investigations with genetic markers confirm that Lp(a) is a risk factor for atherosclerotic vascular diseases.
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PMID:[Lipoprotein(a)--atherogenic waste product of evolution?]. 865 Sep 38


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