Elevated lipoprotein(a) is associated with increased inflammatory and myocardial injury markers in acute coronary syndrome patients undergoing percutaneous coronary intervention
Oct 2026· European Heart Journal· Vol 47· 0 citations
TL;DR
The results indicate that elevated Lp(a) is associated with increased atherothrombotic burden in coronary syndrome, and a significant positive correlations between Lp(a) and both hsCRP and hsTroponin T were found.
Abstract
Lipoprotein(a) [Lp(a)] is recognized as an independent cardiovascular (CV) risk factor, with the ESC defining high risk at ›105 nmol/L. While Lp(a) is genetically determined and considered stable over time, its interaction with acute inflammatory responses and myocardial injury during acute coronary syndrome (ACS) has not been fully elucidated.
To investigate associations between Lp(a), demographic characteristics, risk factors, and biomarkers of myocardial necrosis in patients undergoing percutaneous coronary intervention (PCI) for ACS.
We determined Lp(a) levels, clinical and laboratory parameters in patients admitted to our institution over 18 months for ACS with PCI (n=281, STEMI: 154, NSTEMI: 75, UAP: 52).
Lp(a) showed non-normal distribution with median 20.8 nmol/L (IQR: 8.7-80.6). Sixty patients (21%) were in the high CV risk group based on ESC Lp(a) criteria. Patients were divided into quartiles based on Lp(a) levels (Q1 median: 7.0 nmol/L [IQR: 7.0-7.3] vs. Q4 median: 162.7 nmol/L [IQR: 113-213]). No significant differences were found in demographic parameters (hypertension, diabetes, smoking, prior ACS and stroke, statin use; p›0.05). Female sex showed a trend toward higher Lp(a) (p=0.1). Importantly, patient age did not differ significantly between the lowest and highest Lp(a) quartiles (Q1 median: 55 years [IQR: 48-67] vs. Q4 median: 58 years [IQR: 50-68], p=0.26). Both pre- and post-PCI hsTroponin T levels were significantly higher in the highest Lp(a) quartile (pre-PCI hsTroponin T: Q1 median: 146 ng/L [IQR: 27-797] vs. Q4 median: 580 ng/L [IQR: 111- 1288], p=0.015; post-PCI hsTroponin T: Q1 median: 279 ng/L [IQR: 70-1261] vs. Q4 median: 944 ng/L [IQR: 288-3215], p=0.016). Significant positive correlations were found between Lp(a) and both pre-PCI hsTroponin T (ρ=0.15, p‹0.05) and post-PCI hsTroponin T in the total population (ρ=0.17, p‹0.05). Similarly, hsCRP was significantly higher in the highest Lp(a) quartile (Q1 median: 3.66 mg/L [IQR: 1.33-9.4] vs. Q4 median: 9.2 mg/L [IQR: 3.7-37.8], p=0.0001), and a significant positive correlation was detected between Lp(a) and hsCRP (ρ=0.24, p‹0.05).
Twenty-one percent of ACS patients undergoing PCI in our cohort had Lp(a) levels exceeding the ESC-recommended high cardiovascular risk threshold. Significantly higher pre- and post-PCI hsTroponin and hsCRP levels were observed in patients with elevated Lp(a) in the upper quartile. These findings were corroborated by significant positive correlations between Lp(a) and both hsCRP and hsTroponin biomarkers. Our results indicate that elevated Lp(a) is associated with increased atherothrombotic and inflammatory burden in acute coronary syndrome, suggesting a potential role for Lp(a) assessment in risk stratification during the acute phase.
Elevated Lp(a) is independently associated with adverse cardiovascular outcomes after AMI, particularly HF, and measurement of Lp(a) may improve risk stratification after AMI and help identify patients at high risk of developing HF, including HFpEF.
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BACKGROUND
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