作者
Benjamin Bay,R.J. Tanner,Michael C. Gao,Angelo Oliva,Samantha Sartori,Birgit Vogel,Mauro Gitto,Kenneth Smith,Francesca Maria Di Muro,Amit Hooda,Joseph Sweeny,Parasuram Krishnamoorthy,Pedro Moreno,Prakash Krishnan,George Dangas,Annapoorna Kini,Samin K. Sharma,Roxana Mehran
摘要
Abstract 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.