https://doi.org/10.1007/s00392-025-02625-4
1Universitätsklinikum Essen Klinik für Kardiologie und Angiologie Essen, Deutschland
Background: Although lipoprotein(a) (Lp(a)) is a causal genetic risk factor for atherosclerotic cardiovascular disease, the precise impact of Lp(a) itself on the severity of the CAD in patients presenting with acute myocardial infarction remains uncertain.
Purpose: We aimed to clarify the association between Lp(a) levels and the severity of coronary artery disease in acute myocardial infarction (AMI) patients.
Methods: The present analysis we included patients with acute myocardial infarction (AMI) from the longitudinal Essen Coronary Artery Disease (ECAD) registry of consecutive patients undergoing coronary angiography with percutaneous revascularization therapy at the West German Heart and Vascular Center between 2004 and 2019. Lp(a) was quantified at hospital admission using a particle-enhanced immunonephelometric method. Baseline clinical characteristics were compared among patients with normal vs. elevated Lp(a) levels (≥30 mg/dL). The incidence of death due to any cause was evaluated during follow-up. Cox regression analysis was used to determine the association between Lp(a) and all-cause mortality, adjusting for age, sex, LDL-cholesterol, smoking status, diabetes, systolic blood pressure, and family history of premature cardiovascular disease.
Results: Among 996 patients (mean age 64.4 ± 13.1 years, 77.8% male), median Lp(a) was 16 (7; 56) mg/dL and 376 (26.5%) patients had elevated Lp(a)-levels. Patients with elevated Lp(a) had comparable age and sex distribution as patients with normal Lp(a) (64.3±12.8 years vs. 63.9±13.5 years, p=0.64, 77.6% vs. 78.2% male, p=0.88, for patients with normal vs. elevated Lp(a), respectively). Patients with elevated Lp(a) had higher BMI (26.1±4.1 vs. 29.3±5.9, p=0.035) and were less frequently active smokers (34.5% vs. 24.3%, p=0.0085). Other risk factors including LDL-cholesterol levels were not significantly different among groups. Patients with Lp(a) concentrations ≥ 30 mg/dL exhibited a higher prevalence of multi-vessel disease compared to those with lower levels (non-obstructive CAD: 14.4% vs. 12.3%, 1-vessel CAD: 35.8 vs. 26.7%, 2-vessel CAD: 26.6 vs. 26.2%, 3-vessel CAD: 23.2% vs. 34.8%, p<0.0001). Similarly, patients with elevated Lp(a) faced higher percentile of troponin levels at admission (47.9 [23.8; 77.3] vs. 57.0 [29.1; 77.4], p=0.033).
During a median follow-up 2.7 [0.6; 6.2] years, 167 patients (16.8 %) died. In multivariable Cox regression analysis, elevated Lp(a) was not associated with an increased risk of all-cause mortality (Hazard ratio (HR): 0.87, [95% confidence interval (CI): 0.63; 1.20] p=0.39).
Conclusions: In a longitudinal registry cohort of patients with AMI undergoing invasive coronary angiography, elevated Lp(a) was associated with a higher prevalence of multi-vessel coronary artery disease and higher troponin levels at admission. These differences did not convert into an impaired mid-term survival following the AMI.