Key result
High LDL-C/albumin ratio linked to ~216% higher mortality risk in stable CAD post-PCI.
Why the study?
The risk and all-cause mortality associated with the low-density lipoprotein cholesterol-albumin ratio (LAR) in stable CAD patients undergoing PCI remained unclear.
Does a high LDL-C-albumin ratio increase all-cause mortality in patients with stable coronary artery disease following percutaneous coronary intervention?
Cohort (n=198)
No
Does a high LDL-C-albumin ratio increase all-cause mortality in patients with stable coronary artery disease following percutaneous coronary intervention?
Hazard Ratio: 3.16 (95% CI 1.25–7.97)
Absolute Event Rate: 16% vs 6.8%
p-value: p=0.028
An elevated LDL-C-albumin ratio (≥ 32.5 mg/g) is a significant independent predictor of all-cause mortality in patients with stable coronary artery disease undergoing PCI, suggesting its utility for risk stratification.
LAR may refine post-PCI mortality risk assessment in stable CAD; hypothesis-generating and should not yet change practice.
Background Both low-density lipoprotein cholesterol (LDL-C) and albumin are well-established predictors of adverse outcomes in patients with stable coronary artery disease (CAD) who have undergone percutaneous coronary intervention (PCI). However, the risk and all-cause mortality (ACM) of the LDL-C-albumin ratio (LAR)—a composite index integrating these two parameters—remains unclear. Methods This study enrolled 198 consecutive patients with newly diagnosed stable CAD who underwent PCI at Shinonoi General Hospital between 2014 and 2017. The primary aim was to assess the risks related to high LAR levels and the association between LAR and ACM in this population. Results The association between the LAR and ACM was evaluated through multiple methods. Analyzed as a continuous variable, each 1 mg/g increase in LAR conferred a 6% higher adjusted risk of ACM (Hazard Ratio [HR] 1.06, 95% Confidence Interval [95% CI] 1.00–1.12, P = 0.035). When categorized into quartiles (Q1-Q4) based on LAR level, the highest LAR quartile (Q4) shows a statistically significant 3.72–4.01-fold increase in ACM risk (vs. Q1) after covariate adjustment, the risk is not linear across all groups but is concentrated in the top 25% of patients with the highest LAR values. This finding was reinforced by an inverse probability of treatment weighting (IPTW) model, which demonstrated that patients with a high LAR (≥ 32.5 mg/g) had a 3.16-fold greater risk of ACM than those with a low LAR (95% CI 1.25–7.97, P = 0.028). Four-year Kaplan-Meier analysis confirmed that the high LAR group had a significantly lower adjusted survival probability ( P = 0.017), with adjustments made for the same variables as those included in the IPTW analysis. In a separate analysis, LAR ≥ 32.5 mg/g is driven by elevated levels of atherogenic lipids (LDL-C, TC) and reduced serum albumin. Notably, the protective effect of male sex on high LAR-related risk requires further investigation. Conclusions High level LAR is associated with ACM in stable CAD patients following PCI, with a level above 32.5 mg/g distinguishing a high-risk subgroup that warrants closer clinical monitoring due to a significantly elevated risk of adverse outcomes.
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Huang et al. (2026) conducted a cohort in Stable coronary artery disease following percutaneous coronary intervention (n=198). High low-density lipoprotein cholesterol-albumin ratio (≥ 32.5 mg/g) vs. Low low-density lipoprotein cholesterol-albumin ratio (< 32.5 mg/g) was evaluated on All-cause mortality (HR 3.16, 95% CI 1.25-7.97, p=0.028). A high low-density lipoprotein cholesterol-albumin ratio (≥ 32.5 mg/g) was associated with a 3.16-fold higher risk of all-cause mortality compared to a low ratio in stable CAD patients after PCI.
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