Plasma lipoprotein (a) and long-term all-cause mortality in myocardial infarction survivors: a cohort study

Abstract Background Elevated concentrations of lipoprotein (a) [Lp(a)] are a well-established risk factor for the development of coronary artery diseases and acute myocardial infarction (AMI). The objective of the present study was to analyze the association between plasma concentrations of Lp(a) and long-term all-cause mortality among individuals with a history of hospitalized AMI. Methods The analysis was based on data from 617 patients with a history of AMI recruited by the Augsburg Myocardial Infarction Registry and examined in a follow-up visit within the scope of the KORA Family Heart Study in 1996 and 1997 (median time between AMI and follow-up examination: 6.2 years). In addition, 545 siblings of the patients were included in the study and underwent examination. The examination included venous blood sampling and a patient interview. Plasma concentrations of Lp(a) were measured using a latex-enhanced immunoassay. Information on vital status was obtained in November 2025 in a comprehensive mortality follow-up [median follow-up time: 18.2 years (IQR: 10.8–27.7)]. Follow-up time was calculated from examination date to date of death or censoring. Kaplan-Meier curves were used to display estimated survival probability of Lp(a) high (≥ 50 mg/dL) and low (< 50 mg/dL) group. Multivariable adjusted Cox regression models with restricted cubic splines were used to analyze the association between Lp(a) concentrations and long-term all-cause mortality after AMI. Results Kaplan-Meier curves and log rank test (p value: 0.273) demonstrated no differences in long-term all-cause mortality between the high and low Lp(a) group. The multivariable adjusted Cox regression confirmed the absence of a significant association between Lp(a) concentrations and total mortality (HR for the high Lp(a) group: 1.04, 95%CI: 0.84–1.28, p value: 0.734). Several sensitivity analyses, including a mixed model on a sample including siblings of the AMI patients (HR for the high Lp(a) group: 1.09) and a more thoroughly adjusted model including additional potential confounders confirmed the results of the main model. Conclusions In this study, no association between elevated Lp(a) and long-term mortality was detected. Due to the observational character of the study, no conclusions about treatment of patients with elevated Lp(a) can be made and results must be regarded as exploratory and hypothesis generating.