Epidemiology
Lp(a) at or above 30 mg/dL triples myocardial infarction risk in a 106-patient case-control study (Medicina (Kaunas) 2024)
Original title: Exploring the Relationship Between Lipoprotein (a) Level and Myocardial Infarction Risk: An Observational Study
In this case-control study of 64 patients with acute myocardial infarction (STEMI and NSTEMI) and 42 healthy controls, those with Lp(a) at or above 30 mg/dL had a threefold increased risk of AMI compared with those below that threshold, independent of cholesterol, smoking, and body weight. Elevated Lp(a) was present in 50% of AMI patients versus 28.57% of controls (p = 0.028). Multivariate analysis identified high Lp(a), low HDL-C, and obesity as significant independent AMI predictors, with the Lp(a)-AMI association consistent across subgroups and compounded by low HDL-C. The findings reinforce Lp(a) as an independent AMI risk factor warranting screening alongside traditional risk markers, with the authors calling for further study of Lp(a)-lowering therapies to reduce AMI incidence.
Original abstract
Background and Objectives: This observational study investigates the relationship between Lipoprotein (a) (Lp(a)) levels and the risk of acute myocardial infarction (AMI). This study aims to highlight the association of elevated Lipoprotein (a) levels with an increased atherogenic profile and the potential risk of AMI. Materials and Methods: We conducted a case-control study involving 106 individuals, including 64 AMI patients (both STEMI and NSTEMI) and 42 healthy controls. Comprehensive clinical and biochemical assessments, including Lp(a) measurements, were conducted. Results: Patients with Lp(a) levels ≥ 30 mg/dL had a threefold increased risk of AMI compared to those with lower levels, independent of traditional risk factors such as cholesterol, smoking, and body weight. Elevated Lp(a) was observed in 50% of AMI patients compared to 28.57% in controls (p = 0.028). Notably, a multivariate analysis identified high Lp(a) levels, low HDL-C levels, and obesity as significant independent predictors of AMI, indicating these factors may contribute to AMI risk more prominently than other conventional risk factors in patients with elevated Lp(a). Moreover, the association between Lp(a) and AMI risk was consistent across various patient subgroups, with low HDL-C further compounding the risk. Conclusions: Lp(a) is a significant independent risk factor for acute myocardial infarction; therefore, screening for Lp(a) levels can help identify high-risk individuals beyond traditional markers. Therapeutic approaches targeting Lp(a) may reduce AMI incidence. Future research should explore how Lp(a) promotes atherosclerosis and assess Lp(a)-lowering therapies to improve patient outcomes.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.