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Residual cholesterol and inflammatory risk in statin-treated patients undergoing percutaneous coronary intervention†
Benjamin Bay1,2, Richard Tanner1,3, Michael Gao1
1Center for Interventional Cardiovascular Research and Clinical Trials, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1030, New York, NY 10029-6574, USA.
Insights
For patients on statin therapy undergoing percutaneous coronary intervention (PCI), residual inflammation, not cholesterol, significantly increases the risk of major adverse cardiovascular events (MACE). This highlights inflammation as a key target for improving outcomes post-PCI.
Area of Science:
- Cardiology
- Biomarkers
- Interventional Cardiology
Background:
- Elevated LDL-cholesterol and inflammation (high-sensitivity C-reactive protein) are linked to cardiovascular risk.
- Limited data exists on the comparative impact of residual cholesterol and inflammatory risk in statin-treated patients post-percutaneous coronary intervention (PCI).
Purpose of the Study:
- To investigate the independent and combined effects of residual cholesterol and inflammatory risk on major adverse cardiovascular events (MACE) in patients undergoing PCI while on statin therapy.
Main Methods:
- Analysis of 15,494 patients undergoing PCI from 2012-2022.
- Stratification based on LDL-cholesterol (≥70 vs <70 mg/dL) and high-sensitivity C-reactive protein (≥2 vs <2 mg/L) levels.
- Primary endpoint: MACE (all-cause mortality, myocardial infarction, stroke) at 1 year post-PCI.
Main Results:
- Residual inflammatory risk, isolated or combined with cholesterol risk, was associated with significantly higher MACE rates.
- Patients with residual inflammatory risk had a 1.8-fold higher risk of MACE (aHR: 1.78).
- Isolated residual cholesterol risk showed no independent association with MACE (aHR: 1.01).
Conclusions:
- Residual inflammation, rather than residual cholesterol, is a significant predictor of MACE in statin-treated patients after PCI.
- Inflammatory markers warrant close monitoring and targeted management in this patient population to reduce cardiovascular events.
Background And Aims:
Elevated LDL-cholesterol levels and inflammation, as assessed by high-sensitivity C-reactive protein, correlate with cardiovascular risk. However, data on the relative impact of residual LDL-cholesterol and inflammatory risk among statin-treated patients undergoing percutaneous coronary intervention (PCI) is lacking. Hence, this study aimed to investigate the impact of residual cholesterol/inflammatory risk in patients on statin therapy undergoing PCI.
Methods:
From 2012 to 2022, patients at a tertiary centre undergoing PCI were analysed. Patients were stratified according to LDL-cholesterol (≥70 vs <70 mg/dL) and high-sensitivity C-reactive protein (≥2 vs <2 mg/L) levels: no residual cholesterol or inflammatory risk, residual cholesterol risk, residual inflammatory risk, and combined residual cholesterol and inflammatory risk. Patients presenting with acute myocardial infarction, cancer, no statin treatment at admission, or high-sensitivity C-reactive protein levels >10 mg/L were excluded. The primary endpoint was major adverse cardiovascular events (MACEs), defined as the composite of all-cause mortality, spontaneous myocardial infarction, and stroke 1 year after the index PCI.
Results:
A total of 15 494 patients were included. After 1-year follow-up, individuals with isolated residual inflammatory risk had the highest MACE rate (5.1%), followed by patients with combined cholesterol and inflammatory risk, no residual risk, and isolated residual cholesterol risk. After multivariable Cox regression analysis, patients with residual inflammatory risk had a 1.8-fold higher risk for MACE (adjusted hazard ratio: 1.78, 95% confidence interval 1.36-2.33, P < .001) compared with those with no residual cholesterol or inflammatory risk. This was similar in patients with combined residual cholesterol and inflammatory risk (adjusted hazard ratio: 1.56, 95% confidence interval 1.19-2.04, P = 0.001). Of note, no independent association of isolated residual cholesterol risk (adjusted hazard ratio: 1.01, 95% confidence interval .76-1.35, P-value = .920) with MACE was noted (P-trend across all groups <.001).
Conclusions:
Among statin-treated patients undergoing PCI, residual inflammation but not cholesterol risk was associated with an increased risk of MACE during follow-up.
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