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Lipoprotein(a) as a determinant of coronary heart disease in young women
K Orth-Gomér1, M A Mittleman, K Schenck-Gustafsson
1National Institute for Psychosocial Factors and Health, Karolinska Institute, Stockholm, Sweden. Kristina.Orth-Gomer@phs.ki.se
Insights
Lipoprotein(a) [Lp(a)] is a significant risk factor for coronary heart disease (CHD) in women. Elevated Lp(a) levels increase the likelihood of developing CHD in both premenopausal and postmenopausal women.
Area of Science:
- Cardiovascular Medicine
- Lipidology
- Preventive Cardiology
Background:
- Lipoprotein(a) [Lp(a)] is a recognized risk factor for coronary heart disease (CHD) in men.
- The association between Lp(a) and CHD risk in women remains less defined.
Purpose of the Study:
- To investigate the predictive value of Lp(a) for CHD in women.
- To determine if Lp(a) is an independent risk factor for CHD in different menopausal statuses.
Main Methods:
- A population-based case-control study was conducted in Stockholm.
- 292 women hospitalized for acute CHD events and matched controls were analyzed.
- Lp(a) levels were measured using an immunoturbidometric method.
Main Results:
- Elevated Lp(a) levels were associated with an increased risk of CHD in women.
- The age-adjusted odds ratio for CHD in the highest vs. lowest Lp(a) quartile was 2.3.
- After adjusting for multiple risk factors, the odds ratio increased to 2.9.
- Odds ratios were 5.1 for premenopausal women and 2.4 for postmenopausal women.
Conclusions:
- Lipoprotein(a) is a significant determinant of coronary heart disease in women.
- Lp(a) is a valuable biomarker for predicting CHD risk across all menopausal stages in women.
Background:
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.
Methods And Results:
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.
Conclusions:
These results suggest that Lp(a) is a determinant of CHD in both premenopausal and postmenopausal women.