Epidemiology
Lp(a) raises heart disease risk especially in men with high LDL cholesterol, the PRIME Study of 9133 men (Atherosclerosis 2002)
Original title: Lipoprotein (a) as a predictor of coronary heart disease: the PRIME Study
The PRIME Study, a prospective cohort of 9133 French and Northern Irish men aged 50-59 without prior coronary heart disease (CHD), measured Lp(a) at baseline and followed participants for 5 years, during which 288 had a CHD event. Lp(a) was a significant CHD risk factor overall (P<0.0006); the highest Lp(a) quartile carried 1.56 times the relative risk of CHD versus the lowest (95% CI 1.10-2.21). A significant interaction was found between Lp(a) and LDL cholesterol: the relative risk from Lp(a) at or above 33 mg/dL rose from 0.82 (95% CI 0.28-2.44) in men with the lowest LDL cholesterol quartile (below 121 mg/dL) to 1.58 (95% CI 1.06-2.40) in the highest quartile (above 163 mg/dL). The findings confirm Lp(a), measured independent of apo(a) size, predicts CHD, particularly myocardial infarction and angina, especially in men with high LDL cholesterol.
Original abstract
The association of an elevated level of lipoprotein (a) (Lp(a)) with the development of coronary heart disease (CHD) remains controversial. Lp(a) was investigated as a CHD risk factor in the PRIME Study, a prospective cohort study which included 9133 French and Northern Irish men aged 50-59 at entry, without a history of CHD and not on hypolipidaemic drugs. During a follow-up of 5 years, 288 subjects experienced at least one CHD event (myocardial infarction (MI), coronary death, angina pectoris). Lp(a) was measured by immunoassay in all subjects on fresh plasma obtained at entry. Traditional cardiovascular risk factors such as low-density lipoproteins (LDL)-cholesterol, HDL-cholesterol, triglycerides, the presence of diabetes, hypertension or smoking were determined. Logistic regression analysis was used to evaluate Lp(a) level as a CHD risk factor after controlling for the other risk factors. In addition, its possible interaction with LDL- and HDL-cholesterol levels was investigated. Lp(a) appeared a significant risk factor (P<0.0006) in the whole cohort without between-population interaction, even if the association was not statistically significant in the Belfast sample. The relative risk (RR) of CHD events in subjects with Lp(a) levels in the highest quartile was 1.5 times that of subjects in the lowest quartile (RR: 1.56; 95% confidence intervals (CIs): 1.10-2.21). A high Lp(a) level was a risk for MI, coronary death and angina pectoris. A significant interaction term between Lp(a) and LDL-cholesterol levels, however, was found. The relative CHD risk associated with a Lp(a) level > or =33 mg/dl in comparison with Lp(a) <33 mg/dl increasing gradually from 0.82 (95% CI: 0.28-2.44) in men with LDL-cholesterol in the lowest quartile (<121 mg/dl) to 1.58 (95% CI: 1.06-2.40) in the highest quartile (>163 mg/dl). In conclusion, Lp(a) increased the risk for MI and angina pectoris, especially in men with a high LDL-cholesterol level. This study which analyzed Lp(a) level using a measurement independent of apolipoprotein (a) size on fresh plasma, has confirmed utility of Lp(a) as a predictor of CHD.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.