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Lipoprotein a Cholesterol, Lp(a)

Lipoprotein (a) is a modified form of LDL to which another glycoprotein, termed apolipoprotein (a), is covalently bound. It contributes to atherogenic risk by multiple mechanisms that include inhibition of fibrinolysis, increased cholesterol deposition in the arterial wall, and enhanced oxidation of LDL cholesterol. The evidence linking Lp(a) levels and the risk of coronary disease is strongest for middle aged white men. Higher Lp(a) levels have been consistently observed in white and Asian groups with vascular disease, but not in African Americans.

Environmental and racial factors may modulate Lp(a) concentrations. Levels are higher in Africans, African Americans, postmenopausal women and patients with hypercholesterolemia. Lp(a) levels are increased in renal insufficiency, in the nephrotic syndrome, after kidney transplantation, and in patients undergoing hemodialysis or peritoneal dialysis. Levels can increase dramatically after coronary ischemia and surgery because Lp(a) is an acute phase reactant. Lp(a) fluctuates during hormonal changes that occur in patients with diabetes mellitus, estrogen therapy, and pregnancy. Lower levels are seen in individuals with higher estrogen or androgen levels, cirrhosis, and alcoholism. Exercise and low fat diets do not significantly lower Lp(a).

Measurement of Lp(a) provides only modest assistance to the physician caring for patients at risk of coronary artery disease. Lp(a) is an independent but relatively weak predictor of coronary artery disease in unselected populations, but is a powerful predictor of premature CAD, especially in patients with concomitant hypercholesterolemia. Lp(a) testing should be reserved for individuals with premature myocardial infarction and a relatively normal risk factor profile, a strong family history of premature atherosclerosis not explained by other dyslipidemias, or patients with refractory hypercholesterolemia. Estrogen replacement therapy is the first line treatment for postmenopausal women and nicotinic acid is the first choice for men. The goal for pharmacologic therapy for white populations is a Lp(a) level of less than 30 mg/dL. Intra-individual variability is 15%.

Estrogen and progestin have been found to lower Lp(a) levels in postmenopausal women. The Heart and Estrogen/progestin Replacement Study (HERS) determined the relationships among treatment with estrogen and progestin, plasma Lp(a) levels and subsequent coronary heart disease in 2763 postmenopausal women with coronary artery disease (JAMA2000;283:1845-52). Ninety two percent of women were White and 8% were African American. Women were divided into quartiles based on Lp(a) level at enrollment. Increased baseline Lp(a) levels among women in the placebo arm of the study were associated with subsequent coronary heart disease, death or nonfatal myocardial infarction. Women in the third and fourth quartiles of baseline Lp(a) level had an increased relative risk compared to women in the lowest quartile.

Quartile

Lp(a) mg/dL

Relative Risk

1

0 – 7.0

1.00

2

7.1 – 25.3

1.01

3

25.4 – 54.9

1.31

4

55 - 236

1.54

Estrogen and progestin therapy reduced mean Lp(a) levels by 15 mg/dL for women in the third and fourth quartiles and reduced the risk of secondary coronary events by 15 to 20%.

This data suggests that Lp(a) is an independent risk factor for recurrent coronary heart disease in postmenopausal women and that treatment with estrogen and progestin lowers Lp(a) levels. Estrogen and progestin therapy appears to have a more favorable effect in women with high initial Lp(a) levels than in women with low levels.

Recently, two pediatric studies linked elevated Lp(a) levels to childhood venous thromboembolism. A recent study evaluated the role of Lp(a) as a risk factor for venous thrombosis in adults (Blood, 96: 3364-3368, 2000). A total of 685 consecutive subjects with a history of venous thromboembolism (men and women, aged 11-77) were screened for prothrombotic risk factors, including Lp(a), and compared with 266 age- and sex-matched healthy controls. Elevated Lp(a) levels >30 mg/dL were present in 20% of the patients and 7% of the controls, and were associated with a 3.2-fold increased risk of thrombosis. An increased risk of thrombosis was even seen for Lp(a) levels >20 mg/dL (2.2-fold increased risk), compatible with a concentration-dependent risk starting at Lp(a) levels within the normal range. In this study, Factor V Leiden (the most common hereditary prothrombotic risk factor) was associated with a 5.7-fold increased risk of thrombosis. Coexistence of Lp(a) >30 mg/dL with factor V Leiden was found in 7% of the patients, and only 0.8% of controls, and the combination was associated with a 9.8-fold increased risk of venous thromboembolism.

These findings suggest that Lp(a) elevation is a frequent and independent risk factor for venous thromboembolism. Furthermore, elevated Lp(a) levels may contribute to the thrombotic risk associated with factor V Leiden and other hereditary or acquired prothrombotic risk factors, compatible with the widely accepted concept that venous thrombosis is a multicausal disorder.

Reference range is:

Population

Reference Range

African American

22-74 mg/dL

Caucasian

6-34 mg/dL

Specimen requirement is one SST tube of blood.

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