Effects of Lowering Elevated LDL Cholesterol on the Cardiovascular Risk of Lipoprotein(a)

Maher, Vincent; Brown, B. Greg; Marcovina, Santica M.; Hillger, Lynn A.; Zhao, Xue-Qiao; Albers, John J.

doi:10.1001/jama.1995.03530220037029

Cited by 245 publications

(69 citation statements)

References 27 publications

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“…Therapeutic lowering of LDL cholesterol by Ն10% was found to dilute the predictive value of high Lp(a) for coronary artery disease. 33 Finally, a recent study revealed high Lp(a) plasma concentrations to increase the risk of familial coronary artery disease only if the total/HDL cholesterol ratio was elevated. 34 Apparently, the interaction of Lp(a) with other lipoproteins triggers or enhances its atherosclerotic properties.…”

Section: Kronenberg Et Al Lp(a) Apo(a) Phenotype and Atherogenesismentioning

confidence: 99%

Role of Lipoprotein(a) and Apolipoprotein(a) Phenotype in Atherogenesis

et al. 1999

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Background-Experimental studies have suggested both atherogenic and thrombogenic properties of lipoprotein (a) [Lp(a)], depending on Lp(a) plasma concentrations and varying antifibrinolytic capacity of apolipoprotein(a) [apo(a)] isoforms. Epidemiological studies may contribute to assessment of the relevance of these findings in the general population. Methods and Results-This study prospectively investigated the association between Lp(a) plasma concentrations, apo (a) phenotypes, and the 5-year progression of carotid atherosclerosis assessed by high-resolution duplex ultrasound in a random sample population of 826 individuals. We differentiated early atherogenesis (incident nonstenotic atherosclerosis) from advanced (stenotic) stages in atherosclerosis that originate mainly from atherothrombotic mechanisms. Lp(a) plasma concentrations predicted the risk of early atherogenesis in a dose-dependent fashion, with this association being confined to subjects with LDL cholesterol levels above the population median (3.3 mmol/L). Apo(a) phenotypes were distributed similarly in subjects with and without early carotid atherosclerosis. In contrast, apo(a) phenotypes of low molecular weight emerged as one of the strongest risk predictors of advanced stenotic atherosclerosis, especially when associated with high Lp(a) plasma concentrations (odds ratio, 6.4; 95% CI, 2.8 to 14.9). Conclusions-Lp(a) is one of the few risk factors capable of promoting both early and advanced stages of atherogenesis.Lp(a) plasma concentrations predicted the risk of early atherogenesis synergistically with high LDL cholesterol. Low-molecular-weight apo(a) phenotypes with a putatively high antifibrinolytic capacity in turn emerged as one of the leading risk conditions of advanced stenotic stages of atherosclerosis.

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Section: Kronenberg Et Al Lp(a) Apo(a) Phenotype and Atherogenesismentioning

confidence: 99%

Role of Lipoprotein(a) and Apolipoprotein(a) Phenotype in Atherogenesis

et al. 1999

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“…pregnancy (7,(10)(11)(12)(13)(14), under the influence of drugs (19,25), oral contraceptives (17) and hormones (19,26,27), including gonadotropins (15,16). Results from animal studies (28) cannot be compared directly with results from humans (5) without due consideration of animal physiology.…”

Section: Resultsmentioning

confidence: 99%

Do Gonadotropins Influence Serum Lipoprotein(a) Concentrations? Observations on Children, Adolescents and Adults

Schumacher¹,

Weigert²,

Wood³

1996

CCLM

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Summary:Data from 7045 subjects were examined. The main groups consisted of the following in-and outpatients: 1414 neonates, 2554 children and adolescents (1336 males, 1218 females), 1209 women directly postpartum, 786 non-pregnant women and 1090 men aged between 18 and 100 years of age. Unless otherwise stated, persons were under medical observation or therapy.The results were obtained over a three-year period using an in-house immunolurninometric assay specific for apolipoprotein(a) using two polyclonal antibodies and a single lot of reagents to allow for comparability of results.Girls aged between 10 and 12 years of age had significantly higher serum lipoprotein(a) (median 124 mg/1) levels than boys (median 88 mg/1) of the same age (p < 0.05 -Mann-Wliitney U-test). Post-pubertal lipoprotein(a) concentrations were not significantly different from pre-pubertal levels. Between the ages of 0-9 and 13-17 years there were no statistically significant sex-linked differences in serum lipoprotein(a).In adults, lipoprotein(a) serum levels were significantly higher in women (median 163 mg/1) aged between 50 and 59 years, when compared with men (median 128 mg/1) of the same age group (p = 0.05 -Kruskal-Wallis one way ANOVA followed by the Nemenyi test).There was no significant difference in serum lipoprotein(a) concentrations between healthy women (median 91 mg/1), women direct postpartum (median 116 mg/1) and in-patient women (median 117 mg/1) aged between 18 and 41 years of age (p = 0.11-0.96). There was no correlation between maternal lipoprotein(a) and birth weight in mature newborns (r = -0.028-0.085).The results may indicate a direct influence of gonadotropins at puberty and during the menopause which cause an increase in serum lipoprotein(a) concentrations.

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“…A moderately above median concentration of Lp(a) (> 0.30 g/litre) is a conditional risk factor, which is dependent on the presence of high associated concentrations of low density lipoprotein, and is reduced with low density lipoprotein reduction 25 ; at progressively higher values it acts as an independent risk factor for the development of cardiovascular and cerebrovascular disease. 1 2 19 Given this association, any situation (such as the APR) in which Lp(a) concentrations might increase rapidly, even if only briefly, could influence both the interpretation of Lp(a) results and related decisions in clinical management, and could also contribute to an increased risk of vascular events.…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein (a) does not participate in the early acute phase response to training or extreme physical activity and is unlikely to enhance any associated immediate cardiovascular risk

Byrne¹,

Jagroop²,

Montgomery³

et al. 2002

Journal of Clinical Pathology

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Aims: To investigate the proposal that lipoprotein (a) (Lp(a)) contributes to the acute phase response and thus possibly to the acute cardiac risks associated with major physical effort. Methods/Results: Fit, healthy, British army recruits were reviewed at the beginning and the end of a 10 week programme of basic training concluding with an intense 48 hour military exercise. Final recruit assessment was staggered over the last week of training, giving rise to six recruit groups, with determination of Lp(a), C reactive protein (CRP), fibrinogen, albumin, and total creatine kinase values from 12 hours to five days after the final exercise. A clear acute phase response was seen following the final exercise, marked by a significant increase in circulating concentrations of fibrinogen and a reduction of albumin, and a trend with non-significant increases in CRP. Conclusion: Lp(a) did not behave as an early marker of the acute response. Previous reports may have been confounded by concurrent disease in older subjects and by late sampling. Lp(a) determination for cardiovascular risk profiling is not confounded by associated physical effort. It is also unlikely that the acute risks of major physical effort are enhanced by any process involving Lp(a).

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Effects of Lowering Elevated LDL Cholesterol on the Cardiovascular Risk of Lipoprotein(a)

Cited by 245 publications

References 27 publications

Role of Lipoprotein(a) and Apolipoprotein(a) Phenotype in Atherogenesis

Role of Lipoprotein(a) and Apolipoprotein(a) Phenotype in Atherogenesis

Do Gonadotropins Influence Serum Lipoprotein(a) Concentrations? Observations on Children, Adolescents and Adults

Lipoprotein (a) does not participate in the early acute phase response to training or extreme physical activity and is unlikely to enhance any associated immediate cardiovascular risk

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