Approximately 20% of the population has elevated circulating levels of lipoprotein(a) (Lp[a]), one of the most robust predictors of cardiovascular disease risk. This is particularly true for women.
Many female patients with "normal" traditional risk factors or low atherosclerotic cardiovascular disease (ASCVD) risk scores may harbor high risk related to elevated levels of Lp(a).
A retrospective, cross-sectional study of consecutive female patients presenting to Heart Centers for Women was performed. Discordance between low-density lipoprotein cholesterol (LDL-C) and Lp(a) was determined. The ASCVD risk and Reynolds Risk Score models A (RRS-A) and B (RRS-B) were calculated, and level of agreement in patients meeting treatment threshold (≥7.5% for ASCVD, ≥10% for RRS-A and RRS-B) were compared.
Among 713 women, 290 (41%) had elevated Lp(a); however, LDL-C and Lp(a) were weakly correlated (r = 0.08). Significant discordance was observed between abnormal LDL-C and Lp(a) levels (McNemar P = 0.03). There was moderate correlation between RRS-A and ASCVD risk (r = 0.71, P < 0.001), and Bland-Altman plot showed diminished correlation with increased risk. More patients met treatment threshold by ASCVD risk estimation, but nearly 1 out of 20 patients met treatment threshold by RRS-A but not ASCVD score.
There is high prevalence of elevated Lp(a) among women presenting to Heart Centers for Women. Although traditional risk markers such as elevated LDL-C or high ASCVD risk may be absent in some women, elevated Lp(a) may identify patients who may benefit from aggressive risk-factor modification and pharmacologic therapy.
Lipoprotein(a) [Lp(a)] appears to be a risk factor for coronary heart disease (CHD) in men. The role of Lp(a) in women, however, is less clear.
We examined the ability of Lp(a) to predict CHD in a population-based case-control study of women 65 years of age or younger who lived in the greater Stockholm area. Subjects were all patients hospitalized for an acute CHD event between February 1991 and February 1994. Control subjects were randomly selected from the city census and were matched to patients by age and catchment area. Lp(a) was measured 3 months after hospitalization by use of an immunoturbidometric method (Incstar) calibrated to the Northwest Lipid Research Laboratories (coefficient of variation was < 9%). Of the 292 consecutive patients, 110 (37%) were hospitalized for an acute myocardial infarction, and 182 were hospitalized (63%) for angina pectoris. The mean age for both patients and control subjects was 56 +/- 7 years. Of participants, 74 patients (25%) and 84 control subjects (29%) were premenopausal. The distributions of Lp(a) were highly skewed in both patients and control subjects, with a range from 0.001 to 1.14 g/L. Age-adjusted odds ratio for CHD in the highest versus the lowest quartile of Lp(a) was 2.3 (95% confidence interval [CI], 1.4 to 3.7). After adjustment for age, smoking, education, body mass index, systolic blood pressure, total cholesterol, triglycerides, and HDL, the odds ratio was 2.9 (95% CI, 1.6 to 5.0). The odds ratios were similar when myocardial infarction and angina patients were compared with their respective control subjects. The odds ratios were 5.1 (95% CI, 1.4 to 18.4) and 2.4 (95% CI, 1.3 to 4.5) in premenopausal and postmenopausal women, respectively.
These results suggest that Lp(a) is a determinant of CHD in both premenopausal and postmenopausal women.
2013 Feb;61(2):99-106. doi: 10.1016/j.jjcc.2012.09.009. Epub 2012 Nov 17.
BACKGROUND AND PURPOSE:
Lipoprotein (Lp) (a) is a neglected element of the blood lipid profile. It is now recognized as a determinant of coronary heart disease progression and its role in atherosclerosis and its ability to induce thrombosis make it potentially important in the course of normal and complicated pregnancies. Pregnancy involves a major transformation of metabolism to sustain fetal growth. Multiple studies have been conducted on Lp(a) in pregnancy, and it is timely to synthesize and evaluate this evidence.
We reviewed the MEDLINE database for all articles published concerning "lipoprotein a" and "pregnancy" from May 2003 to May 2012. A previous comprehensive review assessed the literature up to May 2003.
We critically analyzed 14 studies detailing the effect of complications in pregnancy on Lp(a) profile, and subsequent pregnancy outcomes where available. Studies evaluating the normal metabolic response to pregnancy, pregnancies complicated by pre-eclampsia and intra-uterine growth restriction were reviewed.
A substantial mass of data has accumulated describing Lp(a) changes in pregnancy. The diversity of study design limits the ability to draw broad-ranging conclusions, but brings into focus the important questions remaining, which we discuss.