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

We studied apolipoprotein (a) (apo(a)) phenotypes of 69 myocardial infarction survivors and 56 stroke patients, and compared them with those of 190 healthy Chinese. The distribution of apo(a) phenotype frequency in cardio-cerebrovascular disease patients was different from those of controls. The frequency of the phenotypes B, S1 and S2 in patients was remarkably higher than that in controls within the same single-band apo(a) phenotype. Moreover, the Lp(a) serum concentrations in CCVD patients were significantly higher than those in controls within the same single-band apo(a) phenotype.
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PMID:[Apolipoprotein (a) phenotypes of patients with myocardial infarction]. 778 Aug 20

We measured fasting serum lipids, lipoproteins, apolipoproteins and lipoprotein(a) [Lp(a)] in 49 Caucasian patients with transient ischaemic attacks undergoing carotid angiography. The severity of extracranial cerebrovascular disease was assessed visually by a highly reproducible grading system that focused on the internal carotid artery and carotid bifurcation. Compared with a healthy reference group, patients had significantly higher serum concentrations of: total cholesterol (mean +/- SD), 6.2 +/- 1.6 vs. 5.6 +/- 1.0 mmol/l, p = 0.02; apolipoprotein B, 1.4 +/- 0.5 vs. 1.2 +/- 0.3 g/l, p = 0.03; triglyceride [geometric mean(95% CI)], 2.02(1.75-2.32) vs. 1.66(0.67-4.06) mmol/l, p = 0.03; and Lp(a), 0.33(0.26-0.42) vs. 0.17(0.40-0.76) g/l, p < 0.001. Regression analysis showed that of the lipoprotein-related variables, only Lp(a) was significantly related to the severity of carotid artery disease (p = 0.04) in the patients; this association remained significant after adjusting for age, sex, blood pressure, and a history of stroke. Serum Lp(a) concentration was significantly higher in patients with carotid artery disease severity score above the median value of the sample population compared with those below the median: 0.45 vs. 0.24 g/l (95% CI for difference 0.35-0.88), p = 0.01. Elevated serum Lp(a) is a significant determinant of the extent of carotid atherosclerosis and may be useful in identifying patients most at risk of stroke.
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PMID:Lipoprotein(a) as a determinant of the severity of angiographically defined carotid atherosclerosis. 779 86

Although both mean lipoprotein(a) [Lp(a)] concentration and national stroke prevalence estimates are consistently higher in American blacks than in whites, no information exists on the relationship of Lp(a) and stroke prevalence in African-Americans. Associations of Lp(a) with stroke or transient ischemic attack (TIA) are addressed in this report for 15,160 participants--4160 blacks and 11,000 whites--in the Atherosclerosis Risk in Communities (ARIC) Study. Lp(a) was measured in ARIC as its total protein component by double-antibody enzyme-linked immunosorbent assay (ELISA) for apo(a) detection. Self-reported stroke/TIA history was assessed as part of a standardized questionnaire, and resulted in age-adjusted stroke/TIA prevalences of 3.0% in blacks (n = 120) and 2.0% in whites (n = 222). Overall, mean Lp(a) protein levels were markedly higher for blacks than for whites (160.5 versus 81.6 micrograms/mL, respectively), and were statistically significantly higher among individuals reporting stroke/TIA history for both races (191.3 versus 159.6 micrograms/mL in blacks; 100.6 versus 81.2 micrograms/mL in whites). Multivariable logistic regression analysis for the association of Lp(a) protein with stroke/TIA status yielded a prevalence odds ratio (OR) (95% confidence intervals) of 1.17 (1.05, 1.30) overall (based on one standard deviation difference, 108.2 micrograms/mL, in Lp[a] protein). Race-specific ORs, after adjustment for the same covariates, were equivalent for blacks [OR = 1.17 (0.99, 1.39)] and whites [OR = 1.19 (1.04, 1.36)]. These data suggest that Lp(a) is an independent risk factor for stroke/TIA in both blacks and whites, and that the relative risk of stroke/TIA associated with Lp(a) protein does not vary by race.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein(a) as a correlate of stroke and transient ischemic attack prevalence in a biracial cohort: the ARIC Study. Atherosclerosis Risk in Communities. 798 41

The relation of serum total homocysteine and lipoprotein(a) (Lp(a)) with the incidence of atherosclerotic disease was investigated among 7424 men and women aged 40-64 years free of atherosclerotic disease at baseline in 1977. During the 9-year follow-up, 134 male and 131 female cases with either myocardial infarction or stroke were identified. For each case a control subject was selected belonging to the same sex and 5-year age group. Serum samples collected in 1977 were stored at -20 degrees C and analyzed in 1991. The mean serum homocysteine concentration of male cases and controls was 9.99 mumol/l and 9.82 mumol/l at baseline and that of female cases and controls 9.58 mumol/l and 9.24 mumol/l, respectively. The median serum Lp(a) concentration of male cases and controls was 73 mg/l and 108 mg/l and that of female cases and controls 113 mg/l and 91 mg/l, respectively. The differences between cases and controls were not statistically significant. There was also no significant association between either homocysteine or Lp(a) and atherosclerotic disease, myocardial infarction or stroke in logistic regression analyses. The odds ratios varied from 1.00 to 1.26 for homocysteine and from 0.81 to 1.06 for Lp(a). The results of this prospective population-based study do not support the hypotheses that serum homocysteine or Lp(a) are risk factors for atherosclerotic disease. The lack of association between serum homocysteine and atherosclerotic disease may be due to the exceptionally low gene frequency predisposing to homocysteinemia in Finland.
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PMID:Relation of serum homocysteine and lipoprotein(a) concentrations to atherosclerotic disease in a prospective Finnish population based study. 801 11

We compared possible factors leading to symptomatic and asymptomatic reinfarcts in 207 patients an average of 2.1 years after their index atherothrombotic stroke presenting with small subcortical infarcts. Symptomatic reinfarcts were mostly small infarcts in the perforating artery regions associated with angiographic evidence of atherosclerosis of parent arteries (large-artery disease), a high hematocrit, elevated fibrinogen and Lp(a) levels. They occurred with insufficient inhibition of platelet aggregability in patients receiving antiplatelet medication. In contrast, many asymptomatic reinfarcts were small perforator infarcts not associated with large-artery disease or cortical infarcts, and occurred in the absence of hematologic risk markers, and in spite of sufficient inhibition of platelet aggregability.
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PMID:Comparison of symptomatic and asymptomatic reinfarctions after small subcortical stroke. 803 39

Elevated levels of lipoprotein(a) (Lp(a)) in the plasma are a risk factor for coronary artery disease and stroke. Plasma Lp(a) concentrations are highly heritable and predominantly determined by the liver-specific apolipoprotein(a) (apo(a)) gene. In this report we show by deletion analysis that sequences from -98 to +130 of the apo(a) gene are sufficient to direct liver-specific transcription. DNase I protection analysis of this region using HepG2 nuclear extracts revealed six major protein-binding sites, designated A to F. A mutation within footprint C, situated in the 5'-untranslated region of the gene, resulted in a marked reduction of luciferase expression from a reporter construct to 12% of wild type. This was not due to a decrease in mRNA stability. Gel mobility shift assays demonstrated that site C binds hepatocyte nuclear factor 1 alpha (HNF-1 alpha), and overexpression of HNF-1 alpha in HepG2 cells resulted in a significant stimulation of transcription from this promoter fragment. Mutation of footprint B resulted in a 2-fold enhancement of transcription. These results show that positive regulation of transcription of the apo(a) gene is dependent on the binding of HNF-1 alpha to a regulatory element situated downstream of the mRNA start site, and suggest that an as yet unidentified protein may negatively regulate apo(a) transcription by binding to a discrete sequence within the 5'-untranslated region.
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PMID:Apolipoprotein(a) gene transcription is regulated by liver-enriched trans-acting factor hepatocyte nuclear factor 1 alpha. 805 Oct 57

Several studies have demonstrated that atherosclerotic complications are the major cause of morbidity and mortality in hemodialysis patients. High lipoprotein(a) [Lp(a)] plasma concentrations are an independent risk factor for atherosclerosis. Patients with end-stage renal disease (ESRD) have elevated plasma concentrations of Lp(a), which are not explained by size variation at the apolipoprotein(a) [apo(a)] gene locus. The aim of our study was to investigate whether Lp(a) concentrations and/or apo(a) phenotypes are predictive of the degree of atherosclerosis in the extracranial carotid arteries in ESRD patients. Of 167 patients, 108 showed atherosclerotic plaques (65%). Univariate analysis showed that the plaque-affected group was significantly older and had a higher frequency of angina pectoris, previous myocardial infarction, or cerebrovascular accident. Furthermore, this group included significantly more patients with low-molecular-weight apo(a) isoforms (26.9% versus 8.5%, P < .005) and had significantly higher mean Lp(a) plasma concentrations (29.3 +/- 31.0 versus 19.7 +/- 25.7 mg/dL, P < .05). Lp(a) plasma concentration increased significantly with the number of affected arterial sites, from 19.7 mg/dL in patients without plaques to 40.1 mg/dL in patients with seven or eight affected sites. In patients with low-molecular-weight phenotypes, significantly more arterial sites were affected (3.62 versus 2.08, P < .001). Multivariate regression analysis showed that age, angina pectoris, and the apo(a) phenotype were the only significant predictors of the degree of atherosclerosis. We conclude that, besides age, the apo(a) phenotype is the best predictor of carotid atherosclerosis in ESRD patients and may be used for assessment of general atherosclerosis risk in this patient group.
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PMID:Apolipoprotein(a) phenotypes predict the risk for carotid atherosclerosis in patients with end-stage renal disease. 806

Cerebrovascular accident (CVA) is an important predictor of survival in patients with chronic renal failure (CRF). Although serum lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerosis in the general population and Lp(a) levels are increased in patients with CRF, the relationship between increased Lp(a) and CVA has not been clarified in patients with CRF. We therefore determined the association between serum Lp(a) levels and the risk of CVA in a retrospective study of 105 patients with CRF. Lp(a) was measured by ELISA in 31 patients with CVA and 74 patients without CVA. The median Lp(a) concentration of the patients with CVA was significantly higher than that of patients without CVA (38 vs 23 mg/dl: p < 0.001). Logistic regression analysis determined that elevated serum Lp(a) concentration (relative risk ratio: 1.041, p < 0.005), hypertension (relative risk ratio: 9.747, p < 0.05) and smoking (relative risk ratio: 4.554, p < 0.05) were risk factors for CVA. In contrast, serum total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, gender underlying condition of renal disease and duration of hemodialysis were not associated with an increased risk of CVA. These results suggest that Lp(a) is a risk factor for clinical events attributable to CVA in patients with CRF.
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PMID:[Lipoprotein (a) is a risk factor for cerebrovascular accident in patients with chronic renal failure]. 807 23

We report apolipoprotein(a) (apo(a)) phenotypes of 69 myocardial infarction survivors and 56 stroke patients, and compare them with those of 190 healthy Chinese. The results indicate that the distribution of apo(a) phenotype frequency in cardio-cerebrovascular disease patients is different from those of controls. The frequency of the phenotypes B, S1 and S2 in patients is remarkably higher than those in controls within the same single-band apo(a) phenotype. Moreover, the Lp(a) serum concentrations in CCVD patients are significantly higher than those in controls within the same single-band apo(a) phenotype. The apo(a) phenotype analyses of two pedigrees are shown as a typical autosomal dominant inheritance.
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PMID:Apolipoprotein(a) phenotypes in cardio-cerebrovascular diseases. 818 26

Lipoprotein(a) (Lp(a)) is a risk factor for clinically manifest coronary heart disease (CHD) and cerebrovascular disease in Caucasian and in Asian populations. The role of Lp(a) as a risk factor in blacks has not been described, despite the markedly higher levels of Lp(a) and excess CHD and stroke prevalence observed in middle-aged blacks compared with whites. Further, little information exists on the association of Lp(a) and asymptomatic atherosclerosis in any race or gender group. In this report, 15,700 middle-aged black and white participants in the Atherosclerosis Risk in Communities (ARIC) Study had complete B-mode ultrasound scans of their extracranial carotid arteries. Of the 13,384 individuals with complete B-mode data at the carotid bifurcation, those with mean carotid bifurcation intima-media wall thickness at or above the 90th percentile of the population distribution (approximately 1.2 mm) were considered to have carotid atherosclerosis. Lp(a) was measured as its total protein content by double-antibody ELISA for apo(a) detection. Blacks in this study had mean Lp(a) protein values that were twice as high as those of whites (168.9, 147.1, 86.6, and 75.1 micrograms/ml for black females, black males, white females, and white males, respectively). For all race and gender groups, Lp(a) protein concentrations were higher among individuals with carotid atherosclerosis than for those without. From these cross-sectional data, we conclude that Lp(a) protein is a risk factor for preclinical atherosclerosis as well as for clinically manifest cardiovascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein(a) as a risk factor for preclinical atherosclerotic disease in a biracial cohort: the Atherosclerosis Risk in Communities (ARIC) Study. 818 41


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