Epidemiology
Lp(a) tracks with subclinical coronary disease in low-risk ageing endurance athletes, but does not explain their higher CAD prevalence, Master@Heart study finds (Eur J Prev Cardiol 2025)
Original title: The Role of Lipoprotein(a) in Predicting Coronary Artery Disease Among Ageing Endurance Athletes and Healthy Controls
The Master@Heart study included 558 men aged 45-70 without known cardiovascular risk factors, 191 lifelong athletes, 191 late-onset athletes, and 176 healthy controls, all undergoing coronary CT angiography, to test whether Lp(a) predicts subclinical coronary artery disease in this generally low-risk but CAD-prone population. Elevated Lp(a) (above 125 nmol/L, present in 76 participants, 13.6%) was significantly associated with a coronary calcium score in the age-specific top quartile (OR 1.80, P = 0.049) and with one or more mixed plaques (OR 1.76, P = 0.046); continuous Lp(a) was also significantly associated with calcium score above 100 (OR 1.03, P = 0.045) and top-quartile calcium (OR 1.04, P = 0.014). Lp(a) levels and prevalence of elevated Lp(a) were similar across the three groups (P = 0.586 and P = 0.724), and no interaction was found between Lp(a) and exercise history in predicting CAD. Lp(a) independently flags subclinical coronary disease in this low-conventional-risk population but does not explain why lifelong athletes have more CAD than controls.
Original abstract
Aims: Ageing endurance athletes have a higher prevalence of coronary artery disease (CAD) on coronary CT angiography (CCTA) than healthy controls, despite similarly low conventional cardiovascular risk. The predictive value of lipoprotein(a) [Lp(a)] for CAD in these low-risk individuals remains unclear.
Methods: The Master@Heart study included 558 men (aged 45-70 years) without known cardiovascular risk factors: 191 lifelong athletes, 191 late-onset athletes, and 176 healthy controls. CCTA assessed coronary artery calcification (CAC) and plaques. The association between Lp(a) and subclinical CAD was assessed using logistic regression analysis to estimate odds ratios (ORs), adjusted for cardiovascular risk factors. Lp(a) was analysed dichotomously (<125 vs. >125 nmol/L) and continuously (per 10 nmol/L increase).
Results: 76 participants (13.6%) had elevated Lp(a) levels (>125 nmol/L). Elevated Lp(a) was significantly associated with age-specific CAC percentile≥75 (OR 1.80, p=0.049) and ≥1 mixed plaque (OR 1.76, p=0.046). Other CAD measures all tended to be more prevalent in those with elevated Lp(a). In the continuous analysis, Lp(a) was significantly associated with CAC>100 (OR 1.03, p=0.045), CAC percentile≥75 (OR 1.04, p=0.014), and ≥1 mixed or non-calcified plaque (OR 1.03, p=0.029).Lp(a) and prevalence of elevated Lp(a) were similar across lifelong athletes, late-onset athletes, and controls (p=0.586 and p=0.724, respectively). No significant interaction was found between Lp(a) and the exercise groups in predicting CAD.
Conclusions: Lp(a) is independently associated with subclinical CAD in ageing endurance athletes and healthy controls, despite similarly low conventional cardiovascular risk. Lp(a) does not explain the higher CAD prevalence in lifelong athletes compared to controls, but may enhance risk stratification in this low-risk population.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.