Acute-phase versus post-stabilisation lipoprotein(a) levels in patients with acute myocardial infarction: a paired analysis

Introduction Lipoprotein(a) [Lp(a)] is a genetically determined lipid particle associated with residual cardiovascular risk and its measurement is recommended at least once in adulthood. Although recent evidence suggests that Lp(a) should ideally be measured outside acute inflammatory states, it is still frequently assessed during hospitalisation for acute coronary syndromes. However, evidence remains limited regarding whether acute-phase measurement during acute myocardial infarction (AMI) differs meaningfully from delayed testing. Purpose To compare Lp(a) concentrations measured during the acute phase of MI with values obtained after clinical stabilisation, and to characterise the clinical profile of the studied cohort. Methods A retrospective analysis was conducted at a tertiary centre, comparing Lp(a) levels obtained during hospitalisation with results from the first outpatient visit ≥6 weeks post-infarction. Paired samples were analysed using a paired t-test. Clinical, angiographic, and laboratory data were collected, including lipid profile, inflammatory markers, cardiac biomarkers and left ventricular ejection fraction (LVEF). Results A total of 89 patients were included (mean age 59 ± 13 years; 81% male). Most of them presented with STEMI (71%), Killip class I (67%) and single-vessel disease (49%); 97% underwent PCI and 82% achieved complete revascularisation. LVEF remained stable from hospitalisation to follow-up (46.4 ± 9.1% vs 46.1 ± 7.5%). LDL-C fell markedly (122 ± 47 to 53 ± 22 mg/dL), as did total cholesterol, triglycerides, hs-TnI, NT-proBNP and C-reactive protein, all with p<0.001 (as shown in Table 1). In contrast, Lp(a) rose significantly from the acute to stable phase (53.0 ± 44.7 to 66.2 ± 61.3 mg/dL; p = 0.002), without notable changes in haematological or renal parameters, suggesting biological stability despite the acute stress. Conclusion In patients with AMI, Lp(a) levels measured during the acute phase are significantly lower than those obtained after clinical stabilisation. These findings support measuring Lp(a) outside the acute phase to ensure accurate cardiovascular risk stratification. Nevertheless, given that Lp(a) is genetically determined and the observed variation is modest, post-acute measurements remain appropriate for long-term prognostic assessment.