Lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular events but whether Lp(a) predicts early recurrence in patients with acute coronary syndromes (ACS) has not been well established. Recent evidence suggests that Lp(a) may only be predictive under conditions of elevated low-density lipoprotein cholesterol (LDL-C) or in the presence of pro-inflammatory genotypes (interleukin-1 [IL-1]). Participants enrolled in the the GENESIS-PRAXY multicenter prospective cohort: population underwent plasma Lp(a) measurement by rate nephelometry on an Immage system analyzer (Beckman-Coulter Inc., Fullerton, CA, USA) using an anti-Lp(a) antibody (Immage, Beckman-Coulter). In addition, a 7 single nucleotide polymorphisms (SNP) Lp(a) Genetic Risk Score (GRS) was calculated and pro-inflammatory IL-1 genotypes were also obtained. Cox regression models were constructed to evaluate the association between Lp(a) and the Lp(a) GRS with major adverse cardiovascular events (a composite of all-cause mortality, recurrent ACS and cardiac re-hospitalization) at 1 year with appropriate interaction terms for LDL-C and IL-1 SNPs. We included 939 patients with premature ACS (median age = 49 yrs, interquartile range 46-53 yrs; men = 66.9% ). Neither naturally log transformed Lp(a) or Lp(a) ≥ 50 mg/dL were associated with major adverse events (HR 1.02 per unit, 95% CI 0.89-1.17, p = 0.78; HR 0.77, 95% CI 0.52-1.14, p= 0.19, respectively). Similarly, the 7 SNP Lp(a) GRS was not predictive of major adverse events (HR 0.96, 95% CI 0.85-1.08, p = 0.49). Adjustment for age, sex, diabetes, BMI, GRACE score, hypercholesterolemia and multi-vessel disease status did not materially change these estimates. There was no significant interaction between high LDL-C or pro-inflammatory IL-1 SNP carrier status with Lp(a) levels in predicting recurrent events. In young ACS patients, Lp(a) or a 7 SNP Lp(a) GRS are not associated with major adverse events in the first year post-ACS irrespective of LDL-C or pro-inflammatory IL-1 genotypes.