Key result
Combined residual inflammatory and Lp(a) risk linked to ~47% higher MACE after AMI.
Why the study?
Do elevated Lp(a) and hs-CRP increase the risk of MACE and all-cause death in adults hospitalized for AMI with prior statin use?
Cohort (n=6,498)
Yes
Do elevated Lp(a) and hs-CRP increase the risk of MACE and all-cause death in adults hospitalized for AMI with prior statin use?
Answers are grounded in this paper and cite their sources.
In patients with AMI on prior statin therapy, elevated Lp(a) and hs-CRP are associated with increased MACE risk specifically in those with low admission LDL-C (< 2.6 mmol/L).
Background Patients can experience acute myocardial infarction (AMI) despite documented prior statin exposure, indicating persistent residual cardiovascular risk. The prognostic relevance of lipoprotein(a) [Lp(a)] and residual inflammation in this setting remains unclear. Methods This retrospective multicentre cohort study included 6,498 adults hospitalized for AMI with prior statin use. Baseline low-density lipoprotein cholesterol (LDL-C) at admission was used to stratify patients into low (< 2.6 mmol/L) and high (≥ 2.6 mmol/L) LDL-C groups. Residual risk profiles were defined by elevated Lp(a) (> 30 mg/dL), elevated high-sensitivity C-reactive protein (hs-CRP > 3 mg/L), or both. The primary outcomes were major adverse cardiovascular events (MACE) and all-cause death. Results Baseline characteristics differed across residual LDL-C strata and risk profiles. During a median follow-up of 5.71 years (IQR 4.38–7.27), restricted cubic spline analyses showed a significant association between Lp(a) and outcomes only in the low LDL-C group, whereby high residual inflammatory risk (adjusted hazard ratio [aHR] 1.53, 95% CI 1.24–1.88), high residual Lp(a) risk (aHR 1.44, 95% CI 1.11–1.87), and combined residual risk (aHR 1.47, 95% CI 1.16–1.86) were each associated with higher MACE risk. In the high LDL-C group, no significant residual risk category was associated with MACE. Irrespective of LDL-C status, residual inflammatory risk alone and combined residual risk were associated with increased risks of all-cause mortality and cardiovascular death. Sensitivity analyses suggested that a 30 mg/dL Lp(a) cut-off may be more informative in this cohort. Conclusions In patients with AMI despite documented prior statin exposure, the prognostic associations of residual inflammatory and Lp(a) risk appeared to differ across admission LDL-C strata, supporting the potential value of LDL-C–stratified residual risk assessment.
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Gu et al. (2026) conducted a cohort in Acute myocardial infarction with prior statin use (n=6,498). Elevated Lp(a) (> 30 mg/dL) and/or elevated hs-CRP (> 3 mg/L) vs. Low residual risk was evaluated on Major adverse cardiovascular events (MACE) and all-cause death (aHR 1.47, 95% CI 1.16-1.86). In AMI patients with prior statin use and low admission LDL-C, combined residual inflammatory and Lp(a) risk was associated with higher MACE risk (aHR 1.47; 95% CI 1.16-1.86).
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