Lipoprotein(a), Other Lipoproteins and Hemostatic Profiles in Patients with Ischemic Stroke: The Relation to Cardiogenic Embolism

Dahl, Tobias; Kontny, Frederic; Slagsvold, Carl-Erik; Christophersen, Bjørn O.; Abildgaard, Ulrich; Ødegaard, O.R.; Mørkrid, Lars; Dale, Jon

doi:10.1159/000016039

Cited by 29 publications

(17 citation statements)

References 41 publications

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“…Further studies are needed to confirm these results. Other studies have suggested that Lp(a) may be related to the increased stroke risk via coagulation markers of thrombosis rather than to risk factors associated with atherosclerosis [33]. We were unable to explore this pathway further due to limitations in our data collection.…”

Section: Discussionmentioning

confidence: 93%

Increased Stroke Risk and Lipoprotein(a) in a Multiethnic Community: The Northern Manhattan Stroke Study

et al. 2010

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Context: Elevated lipoprotein(a) [Lp(a)] is associated with ischemic stroke (IS) among Whites, but data is sparse for non-White populations. Objective: Using a population-based case-control study design with subjects from the Northern Manhattan Stroke Study, we assessed whether Lp(a) levels were independently associated with IS risk among Whites, Blacks and Hispanics. Design and Setting: Lp(a) levels were measured in 317 IS cases (mean age 69 ± 13 years; 56% women; 16% Whites, 31% Blacks and 52% Hispanics) and 413 community-based controls, matched by age, race/ethnicity and gender. In-person assessments included demographics, socioeconomic status, presence of vascular risk factors and fasting lipid levels. Logistic regression was used to determine the independent association of Lp(a) and IS. Stratified analyses investigated gender and race/ethnic differences. Results: Mean Lp(a) levels were greater among cases than controls (46.3 ± 41.0 vs. 38.9 ± 38.2 mg/dl; p < 0.01). After adjusting for stroke risk factors (hypertension, diabetes mellitus, coronary artery disease, cigarette smoking), lipid levels, and socioeconomic status, Lp(a) levels ≧30 mg/dl were independently associated with an increased stroke risk in the overall cohort (adjusted odds ratio, OR, 1.8, 95% confidence interval, CI, 1.20–2.6; p = 0.004). There was a significant linear dose-response relationship between Lp(a) levels and IS risk. The association between IS risk and Lp(a) ≧30 mg/dl was more pronounced among men (adjusted OR 2.0, 95% CI 1.1–3.5; p = 0.02) and among Blacks (adjusted OR 2.7, 95% CI 1.2–6.2; p = 0.02). Conclusion: Elevated Lp(a) levels were significantly and independently associated with increased stroke risk, suggesting that Lp(a) is a risk factor for IS across White, Black and Hispanic race/ethnic groups.

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Section: Discussionmentioning

confidence: 93%

Increased Stroke Risk and Lipoprotein(a) in a Multiethnic Community: The Northern Manhattan Stroke Study

et al. 2010

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“…D-dimer levels have been shown to be associated with cardioembolic strokes [4,6,7,8,9,10,12,14], yet their significance in acute stroke remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

D-Dimers Predict Stroke Subtype when Assessed Early

Isenegger¹,

Meier

Lämmle

et al. 2009

Cerebrovasc Dis

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Background:Early classification of ischemic stroke subtype is important for secondary stroke prevention and may guide further investigations. Methods: Levels of coagulation activation [fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT)] and fibrinolysis activation [plasmin-α₂-antiplasmin complex (PAP), D-dimers] markers were measured in 98 consecutive patients with a first-ever acute ischemic stroke admitted within 12 h after symptom onset. Results: Median age was 67 years and 44% were women. Median time from symptom onset to blood sampling was 4 h. Stroke subtype was classified as ‘cardioembolic’ (54%), ‘large-artery atherosclerosis’ (11%), ‘small-vessel disease’ (5%), ‘other determined’ (9%) or ‘undetermined etiology’ (20%). Patients with cardioembolic stroke suffered more often from coronary artery disease than patients with other stroke etiologies (40 vs. 22%, p = 0.019). There were no differences in age, sex, stroke severity, time to blood sampling, frequency of hypertension, diabetes mellitus or current smoking. D-dimers (medians) were higher in patients with cardioembolic strokes than in those with other etiologies (615 vs. 322 μg/l, p < 0.001). No differences in F1+2, FPA, TAT or PAP levels were found. After multivariate analysis, higher D-dimer levels remained independently associated with cardioembolic stroke (p = 0.022). When measured within 6 h, D-dimers below 300 μg/l excluded cardioembolic stroke with a sensitivity of 100% and a specificity of 52%. Conclusions: Low D-dimer levels in the first few hours make a cardioembolic stroke unlikely, and may be useful to guide further investigations. Other coagulation markers were not useful in differentiating between different stroke etiologies.

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“…Several studies demonstrate a role of Lp(a) as an important risk marker, partly independent of other risk markers, for the occurrence of an acute coronary syndrome and spontaneous, partly recurring, ischemic strokes and of venous thromboses and thromboembolism in children and adults [58,[90][91][92][93][94][95][96], while other investigations did not establish any relationship between the occurrence of thrombotic events or thromboembolism and the existence of an elevated Lp(a) plasma concentration [97][98][99]. Moreover, elevated Lp(a) plasma concentrations were measured in a number of studies performed in patients with early-stage or terminal kidney diseases and autoimmune diseases (antiphospholipid syndrome, systemic sclerosis, chronic thromboembolic pulmonary hypertension, rheumatoid arthritis and systemic lupus erythematosus), which fact supports the involvement of Lp(a) in the increased occurrence of thromboembolic events [100][101][102][103][104][105][106][107][108][109].…”

Section: Lp(a) In Hemostasismentioning

confidence: 99%

Lipoprotein(a) - Structure, Epidemiology, Function and Diagnostics of a Cardiovascular Risk Marker

Siekmeier¹,

Scharnagl²,

Kostner³

et al. 2008

TOCCHEMJ

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Decades after its first description by Berg 1963 lipoprotein(a) (Lp(a)) is an established risk marker of cardiovascular diseases which is independent from other risk markers. The main difference of Lp(a) compared to LDL is the apo(a) residue which is covalently bound to apoB. Apo(a) is a glycoprotein which underlies a large genetic polymorphism. The latter is caused by a variation of the kringle-IV-type-2 repeats of the protein which is characterized by a large structural homology to plasminogen. The Lp(a) plasma concentration in the population is highly skewed and determined to more than 90 % by genetic factors. In healthy subjects the Lp(a)-concentration is correlated to its synthesis and not to its metabolism. Plasma concentrations of Lp(a) are affected by different diseases (e.g. diseases of liver and kidney), hormonal factors (e.g. sexual steroids, glucocorticoids, thyroid hormones), individual and environmental factors (e.g. age, cigarette smoking) as well as pharmaceuticals (e.g. derivatives of nicotinic acid) and therapeutic procedures (lipid apheresis). However, even though a large number of studies on Lp(a) were performed up to now many details of its physiological function and regulation of plasma concentration are not yet understood. In addition, studies showed contradictory results because there were large differences of the included patients, use of not sufficiently validated tests as well as analysis of frozen samples. Aim of our review was to describe function and physiological regulation of Lp(a) as well as factors influencing its plasma concentration.

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Lipoprotein(a), Other Lipoproteins and Hemostatic Profiles in Patients with Ischemic Stroke: The Relation to Cardiogenic Embolism

Cited by 29 publications

References 41 publications

Increased Stroke Risk and Lipoprotein(a) in a Multiethnic Community: The Northern Manhattan Stroke Study

Increased Stroke Risk and Lipoprotein(a) in a Multiethnic Community: The Northern Manhattan Stroke Study

D-Dimers Predict Stroke Subtype when Assessed Early

Lipoprotein(a) - Structure, Epidemiology, Function and Diagnostics of a Cardiovascular Risk Marker

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