Residual inflammation, but not cholesterol risk, was associated with an increased risk of MACE among statin-treated patients undergoing PCI.
Is residual inflammation or residual cholesterol risk associated with an increased risk of MACE in statin-treated patients undergoing PCI?
In statin-treated patients undergoing PCI, residual inflammation appears to be a more significant driver of future MACE than residual cholesterol risk.
Absolute Event Rate: 0% vs 0%
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 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.
Bay et al. (Thu,) reported a other. Residual inflammation, but not cholesterol risk, was associated with an increased risk of MACE among statin-treated patients undergoing PCI.