Key result
A 50% increase in baseline serum legumain was associated with a higher risk of cardiovascular death, spontaneous MI, or stroke (HR 1.13; 95% CI 1.04-1.21; P=0.0018), but not in the fully adjusted model.
Why the study?
Legumain is increased in patients with atherosclerosis, but its causal role in atherogenesis and cardiovascular disease remains unclear.
Are serum legumain levels associated with clinical outcomes in patients with acute coronary syndrome?
Cohort (n=4,883)
Are serum legumain levels associated with clinical outcomes in patients with acute coronary syndrome?
Hazard Ratio: 1.13 (95% CI 1.04–1.21)
p-value: p=0.0018
Baseline legumain levels are associated with adverse cardiovascular outcomes in ACS patients, but this association is attenuated after full multivariable adjustment, while higher levels at 1 month may be associated with a decreased risk of stroke.
Baseline legumain elevation associated with CV events only in partially adjusted models; leaves open its independent prognostic value in ACS.
Background The cysteine protease legumain is increased in patients with atherosclerosis, but its causal role in atherogenesis and cardiovascular disease is still unclear. The aim of the study was to investigate the association of legumain with clinical outcome in a large cohort of patients with acute coronary syndrome. Methods and Results Serum levels of legumain were analyzed in 4883 patients with acute coronary syndrome from a substudy of the PLATO (Platelet Inhibition and Patient Outcomes) trial. Levels were analyzed at admission and after 1 month follow‐up. Associations between legumain and a composite of cardiovascular death, spontaneous myocardial infarction or stroke, and its individual components were assessed by multivariable Cox regression analyses. At baseline, a 50% increase in legumain level was associated with a hazard ratio (HR) of 1.13 (95% CI, 1.04–1.21), P =0.0018, for the primary composite end point, adjusted for randomized treatment. The association remained significant after adjustment for important clinical and demographic variables (HR, 1.10; 95% CI, 1.02–1.19; P =0.013) but not in the fully adjusted model. Legumain levels at 1 month were not associated with the composite end point but were negatively associated with stroke (HR, 0.62; 95% CI, 0.44–0.88; P =0.0069), including in the fully adjusted model (HR, 0.57; 95% CI, 0.37–0.88; P =0.0114). Conclusions Baseline legumain was associated with the primary outcome in patients with acute coronary syndrome, but not in the fully adjusted model. The association between high levels of legumain at 1 month and decreased occurrence of stroke could be of interest from a mechanistic point of view, illustrating the potential dual role of legumain during atherogenesis and acute coronary syndrome. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00391872.
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Gregersen et al. (2020) conducted a cohort in Acute coronary syndrome (n=4,883). Serum legumain levels was evaluated on Composite of cardiovascular death, spontaneous myocardial infarction or stroke (HR 1.13, 95% CI 1.04-1.21, p=0.0018). A 50% increase in baseline serum legumain was associated with a higher risk of cardiovascular death, spontaneous MI, or stroke (HR 1.13; 95% CI 1.04-1.21; P=0.0018), but not in the fully adjusted model.
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