Key result
Elevated Lp(a) is linked to ~3.4-fold higher post-PCI hsTroponin T in ACS patients.
Why the study?
While lipoprotein(a) is a genetically determined and stable independent cardiovascular risk factor, its interaction with acute inflammatory responses and myocardial injury during ACS has not been fully elucidated.
Does elevated lipoprotein(a) correlate with increased inflammatory and myocardial injury biomarkers in acute coronary syndrome patients undergoing percutaneous coronary intervention?
Observational (n=281)
No
Does elevated lipoprotein(a) correlate with increased inflammatory and myocardial injury biomarkers in acute coronary syndrome patients undergoing percutaneous coronary intervention?
In ACS patients undergoing PCI, elevated Lp(a) is significantly associated with higher pre- and post-procedural hsTroponin T and hsCRP levels, indicating a greater acute inflammatory and myocardial injury burden.
Elevated Lp(a) may flag higher-risk ACS-PCI patients; leaves open whether lowering it reduces injury or inflammation.
Background 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. Purpose To investigate associations between Lp(a), demographic characteristics, risk factors, and biomarkers of myocardial necrosis in patients undergoing percutaneous coronary intervention (PCI) for ACS. Methods 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). Results 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). Conclusions 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.
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Horvath et al. (2026) conducted an observational in Acute coronary syndrome undergoing percutaneous coronary intervention (n=281). Elevated Lipoprotein(a) [Lp(a)] (highest quartile, median 162.7 nmol/L) vs. Lowest Lp(a) quartile (median 7.0 nmol/L) was evaluated on Biomarkers of myocardial necrosis (pre- and post-PCI hsTroponin T) and inflammation (hsCRP) (p=0.015 (pre-PCI hsTroponin T), 0.016 (post-PCI hsTroponin T), 0.0001 (hsCRP)). Elevated Lp(a) (Q4 vs Q1) in ACS-PCI patients was associated with higher post-PCI hsTroponin T (944 vs 279 ng/L, p=0.016) and hsCRP (9.2 vs 3.66 mg/L, p=0.0001).
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