👤 Bimmer E P M Claessen

Lipoprotein(a) [Lp(a)] is a potent, independent causal risk factor for coronary artery disease (CAD). This study aimed to assess the association between Lp(a) and the diagnosis, clinical presentation, and angiographic characteristics of obstructive CAD and occurrence of myocardial infarction (MI). We included 446 individuals with very high Lp(a) (>230 nmol/L) who underwent routine lipid profiling, matched 2:1 by age and sex using nearest-neighbor propensity matching to 223 controls with low Lp(a) (≤7 nmol/L). Kaplan-Meier analysis was used to assess CAD- and MI-free survival. Multivariable ORs were calculated for multivessel disease and the SYNergy Between percutaneous coronary intervention with TAXus and Cardiac Surgery-1 score. Median follow-up time, defined by age at last follow-up, was 60 years (Q1-Q3: 50-71). Individuals with very high Lp(a) had significantly lower event-free survival time for the diagnosis of obstructive CAD and occurrence of MI (P = 0.006 and P = 0.012, respectively). In multivariable analysis, Lp(a) was associated with multivessel CAD (adjusted OR: 1.43 [per 100 nmol/L]; 95% CI: 1.04-1.96; P = 0.028), but not with an intermediate or high SYNergy Between percutaneous coronary intervention with TAXus and Cardiac Surgery-1 score (adjusted OR: 1.28 [per 100 nmol/L]; 95% CI: 0.82-1.99, P = 0.279). Individuals with very high Lp(a) levels had a 2.4-fold higher risk of ST-segment elevation MI and a 15.9-fold higher risk of recurrent MI compared to those with low Lp(a). Very high Lp(a) is associated with earlier diagnosis of obstructive CAD and MI, predominantly ST-segment elevation MI. In addition, individuals with very high Lp(a) levels seem at a particular high risk of recurrent MI. Show less

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. 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). 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. 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. Show less