Lipoprotein(a): New insights into mechanisms of atherogenesis and thrombosis

Deb, Arjun; Caplice, Noel M.

doi:10.1002/clc.4960270503

Cited by 79 publications

(59 citation statements)

References 112 publications

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“…1 Lipoprotein(a) can enter into human atherosclerotic plaques, 6 and results from in vitro and animal studies implicate lipoprotein(a) in foam cell formation, smooth muscle cell proliferation, and plaque inflammation and instability. 2,7,8 Lipoprotein(a) has also been shown to bind proinflammatory oxidized phospholipids recently associated with coronary artery disease. 28 Lipoprotein(a) enters into and leaves the arterial wall by mechanisms similar to LDL 3,4 and appears to accumulate more at sites of arterial injury than LDL.…”

Section: Discussionmentioning

confidence: 99%

“…2,8 Most but not all prospective studies of lipoprotein(a) and risk of IHD have found positive associations, 10 -16,26,27 and levels of lipoprotein(a) have also been related to severity of coronary artery disease. 29 Our risk estimates are, however, higher than those detected in the majority of previous studies.…”

Section: Kamstrup Et Al Lipoprotein(a) and Myocardial Infarctionmentioning

confidence: 99%

“…1 Previous in vitro, animal, and epidemiological studies suggest that lipoprotein(a) could contribute to the development of atherosclerosis and/or thrombosis and thus myocardial infarction (MI) and ischemic heart disease (IHD). [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] However, the use of lipoprotein(a) as a risk factor for MI and IHD has not been implemented in clinical practice. Limitations of previous studies include measurements in long-term frozen samples, in which different lipoprotein(a) isoforms may degrade differently, 17 and lack of correction for regression dilution bias.…”

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confidence: 99%

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Extreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population

Benn²,

et al. 2008

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Background-Elevated lipoprotein(a) levels are associated with myocardial infarction (MI) in some but not all studies.Limitations of previous studies include lack of risk estimates for extreme lipoprotein(a) levels, measurements in long-term frozen samples, no correction for regression dilution bias, and lack of absolute risk estimates in the general population. We tested the hypothesis that extreme lipoprotein(a) levels predict MI in the general population, measuring levels shortly after sampling, correcting for regression dilution bias, and calculating hazard ratios and absolute risk estimates. Methods and Results-We examined 9330 men and women from the general population in the Copenhagen City Heart Study. During 10 years of follow-up, 498 participants developed MI. In women, multifactorially adjusted hazard ratios for MI for elevated lipoprotein(a) levels were 1.1 (95% CI, 0.6 to 1.9) for 5 to 29 mg/dL (22nd to 66th percentile), 1.7 (1.0 to 3.1) for 30 to 84 mg/dL (67th to 89th percentile), 2.6 (1.2 to 5.9) for 85 to 119 mg/dL (90th to 95th percentile), and 3.6 (1.7 to 7.7) for Ն120 mg/dL (Ͼ95th percentile) versus levels Ͻ5 mg/dL (Ͻ22nd percentile). Equivalent values in men were 1.5 (0.9 to 2.3), 1.6 (1.0 to 2.6), 2.6 (1.2 to 5.5), and 3.7 (1.7 to 8.0). Absolute 10-year risks of MI were 10% and 20% in smoking, hypertensive women aged Ͼ60 years with lipoprotein(a) levels of Ͻ5 and Ն120 mg/dL, respectively. Equivalent values in men were 19% and 35%. Conclusions-We observed a stepwise increase in risk of MI with increasing levels of lipoprotein(a), with no evidence of a threshold effect. Extreme lipoprotein(a) levels predict a 3-to 4-fold increase in risk of MI in the general population and absolute 10-year risks of 20% and 35% in high-risk women and men. (Circulation. 2008;117:176-184.)

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Section: Discussionmentioning

confidence: 99%

Section: Kamstrup Et Al Lipoprotein(a) and Myocardial Infarctionmentioning

confidence: 99%

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confidence: 99%

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Extreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population

Benn²,

et al. 2008

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“…Potential antithrombolytic activity has been proposed because of structural similarity with plasminogen the activity of which Lp(a) may oppose. 19 A recent editorial supported its role as a prothrombotic factor by pointing out that Lp(a) appears to be significantly associated with carotid artery occlusion but not plaque size. 20 On the contrary, there may be a stronger linkage between the kringle IV type 2 genotype and atherosclerotic stenosis in large arteries than with thrombosis in veins.…”

Section: Downloaded Frommentioning

confidence: 99%

Plasma Lipoprotein(a) Concentration Predicts Future Coronary and Cardiovascular Events in Patients With Stable Coronary Heart Disease

Nestel

Barnes

Tonkin

et al. 2013

ATVB

121

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L ipoprotein(a) (Lp(a)) is a recognized risk factor for coronary heart disease (CHD).1 Population studies and metaanalyses show association between Lp(a) levels and first-ever CHD events, but there is less evidence in patients with overt CHD and stable clinical symptoms. In a general population cohort (Copenhagen City Heart Study), the hazard ratio (HR) for future CHD reached a significant value of 1.9 between the 67th and 89th percentiles of Lp(a) concentration.2 Furthermore, as reported by Kamstrup et al, 3,4 risk rises most in those patients whose Lp(a) concentration is in the top decile. Causality was predicated on the basis of a strong genetic influence on the Lp(a) level through the kringle IV type 2 size polymorphism which had been shown also to associate with future myocardial infarction.2,4 In a meta-analysis of 36 prospective studies that yielded 9318 cases of nonfatal myocardial infarctions and CHD deaths, the risk ratio became significant above Lp(a) levels of ≈50 mg/dL. 5 For the 22 076 first-ever fatal or nonfatal cardiovascular disease (CVD) outcomes, the association with Lp(a) was broadly continuous but modest.6 These findings were consistent with preceding reports based on fewer studies that showed an average 1.7-fold increased risk for ischemic heart disease between the upper and lower thirds of the Lp(a) distribution. A recent very large 20-year prospective cohort study of 3467 blacks and 9851 whites showed a graded risk between Lp(a) concentration and incident CVD events which was significant only when the highest and lowest quintiles were compared with respective HRs of 1.35 and 1.27 for the 2 populations. 7 The importance of Lp(a) size polymorphisms had been appreciated for some time and summarized in a review of 36 studies that showed a doubling in CHD risk in the presence of the smaller rather than the larger isoforms (risk ratio of 2.08 for the smaller isoforms).8 By contrast, isoform size was not a predictor of future CHD events in a 12.3-year prospective study of the Framingham Offspring Cohort, although elevated Lp(a) levels were found to have independent significant associations with CHD in men but not in women.9 The © 2013 American Heart Association, Inc. Objective-Association between lipoprotein(a) (Lp(a)) level and a first-ever coronary (CHD) event is recognized. Less is evident in patients with overt CHD and stable symptoms in whom we investigated associations between Lp(a) and future events. Approach and Results-Relationships between Lp(a) concentration and CHD and cardiovascular disease outcomes during 6 years' median follow-up were evaluated in the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study. Lp(a) concentrations were measured in plasma from 7863 patients who had sustained a previous coronary event and been randomized to pravastatin or placebo. Lp(a) levels were categorized by lowest half, third quartile, 75th to 90th percentile, and highest decile. The prognostic value of Lp(a) on outcomes was assessed by fitting a Cox proportionalhazards mod...

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“…20 In CRF, besides other lipid abnormalities, there is significant increase in the level of serum Lp(a). 8 Dialysis therapy may increases Lp(a) 10 or decreases Lp(a) level.…”

Section: Discussionmentioning

confidence: 99%

Lipid profile and lipoprotein(a) in chronic renal failure patients with and without hemodialysis

Sharma¹,

Shah²,

Gorasia

et al. 2012

IJMEDPH

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Objectives: Chronic renal failure (CRF) is complicated by characteristic dyslipidemias. CRF patients on hemodialysis have abnormalities in lipid profile and have a high incidence of cardiovascular diseases. Lipoprotein(a) [Lp(a)] is now considered as a novel cardiovascular risk factor and its level is increased in CRF patients with and without hemodialysis. We sought to evaluate the pattern of lipid profile including Lp(a) level in CRF patients with and without hemodialysis. Methodology: Study were divided into 3 groups, Group-I: healthy controls (30), Group-II: CRF patients who never undergone hemodialysis (30) and Group-III: CRF patients on hemodialysis for more than 6 months (30). We obtained serum samples from patients in the morning after an overnight fast and were analysed for total cholesterol (TC), triglycerides (TGs), HDL, LDL, Lp(a) using standard colorimetric assays on fully automated analyzer. VLDL concentration was calculated using Friedewald's Formula. Results: Among the various parameters tested triglyceride and VLDL levels were significantly higher in group-II and III as compared to controls (p<0.01). HDL levels were significantly lower in group-II and III as compared to control (p<0.05). HDL level was found reduced in group-III as compared to Group-II (p<0.01). There was no significant change (p>0.05) observed in total cholesterol and LDL levels in between healthy controls and CRF patients with & without hemodialysis. Lp(a) levels were significantly higher in group-II and III as compared to controls (p<0.01) but the difference between Lp(a) levels in group-II and III was found insignificant (p>0.05). There was no significant difference (p>0.05) observed between Lp(a) levels and lipid profile in male and female patients in control group and in CRF patients with and without hemodialysis. Conclusions: This study demonstrated that CRF patients with and without hemodialysis are at greater risk of development of dyslipidemias, characterized by hypertriglyceridemia, elevated VLDL and Lp(a) levels and decreased HDL levels. Total cholesterol and LDL cholesterol levels remain normal or decreased in these patients. Both male and female patients of CRF with and without hemodialysis have dyslipidemias without any discrimination of sex and it is not attenuated by the hemodialysis process.

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Lipoprotein(a): New insights into mechanisms of atherogenesis and thrombosis

Cited by 79 publications

References 112 publications

Extreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population

Extreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population

Plasma Lipoprotein(a) Concentration Predicts Future Coronary and Cardiovascular Events in Patients With Stable Coronary Heart Disease

Lipid profile and lipoprotein(a) in chronic renal failure patients with and without hemodialysis

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