Lipoprotein(a) as a predictive marker of coronary artery calcification (CAC). The results from the STAR-Lp(a) cohort study.

Abstract Background Lipoprotein(a) [Lp(a)] concentration is an independent risk factor for cardiovascular disease, including atherosclerosis. Purpose The aim of the study was to assess the relationship between the elevated Lp(a) levels, and the risk of developing atherosclerosis assessed using coronary artery calcium (CAC) score. Methods The analysis was conducted among 553 primary prevention patients (65.7% women, the average age was 65.8±10.1 years) from the outpatient specialist care who underwent coronary computed tomographic angiography (CTA). This group accounted for 22.3% of all patients (n=2475) included in the registry. Lp(a) levels were assessed in three groups: <30 mg/dL (<75 nmol/l) (normal level), 30-50 mg/dL (75-125 nmol/l) (moderate cardiovascular risk) and >50 (>125 nmol/l) (high cardiovascular risk). Patients were divided into groups: with normal CAC score (CAC=0), with CAC 1-100 (presence of atherosclerotic), and those with CAC>100 (advanced atherosclerosis). Statistical analysis was performed using STATISTICA 13.1. Quantitative variables were known by providing descriptive statistics (mean and standard deviation [SD]). The chi-square test was used to assess the relationship between quantitative variables and Mann-Whitney and Kruskal Wallis in the case of qualitative variables. Pearson's correlation coefficient was used to measure correlation. To determine the effect of factors on the probability of occurrence CAC=0 a multivariate logistic regression model was built. P<0.05 was judged as significant. Results Positive significant correlation between CAC score and age was revealed (r=0.266, p<0.001). An analogous relationship was observed regarding to glucose level (r=-0.123, p=0.012). This was not observed for Lp(a). However, we showed a significant relationship between the level of Lp(a) and CAC score (r=0.113, p=0.009) (Fig. 1). Lp(a) levels increased with the CAC score increase. For every 10 mg/dL (25 nmol/l) of Lp(a), CAC score increases by 15.7±0.57 (p=0.006). The mean CAC among patients with normal Lp(a) level was 203.1 (±412.6) and respectively 206.6 (±460.1) in those with moderate cardiovascular risk and 335.6 (±784.9) for people with high risk (p=0.183). In the regression model the factors determining the absence of atherosclerosis (CAC=0; "power of zero") included female gender (OR = 4.05; 95CI: 2.48-6.59), age under 65 (OR = 0.31; 95CI: 0.07-1.34 for aged 40-65), and Lp(A)≤50 mg/dl (≤125 nmol/l) (OR=2.26; 95CI: 1.12-4.61). People with hypertension had a significantly lower odds of CAC=0 (OR=0.58; 95CI: 0.38-0.89). Conclusions The study showed a significant linear relationship between increased Lp(a) levels, and the progression of atherosclerosis expressed by the CAC score. Results confirm some existing recommendations that if an elevated Lp(a) level is found in a patient for primary prevention, a CT scan of the coronary arteries with assessment of the CAC score should be considered for more appropriate risk stratification.