This study is the first to examine the link between IPI levels and the risk of CIN and clinical outcomes in patients having CAG and/or PCI. Higher IPI levels were independently associated with increased CIN risk, and baseline IPI levels predicted severe arrhythmia and AMI. These findings suggest that IPI could be a useful prognostic marker in this patient population.
CIN is a complication that often arises in patients undergoing CAG and/or PCI, with notable morbidity and lethality23. Its development is likely associated with factors such as immunity, oxidative stress, and inflammatory responses24. While the exact pathophysiological mechanism remains uncertain, it is hypothesized to involve the cytotoxicity of contrast agents on renal tubules, leading to aggravated renal vasoconstriction, endothelial dysfunction, renal medulla ischemia, and hypoxia, ultimately resulting in renal tubular cell injury and death. Our analysis of 3340 patients undergoing CAG and/or PCI revealed a clear relationship between IPI levels and the risk of CIN. Particularly, patients in the highest quartile of IPI levels, indicative of more severe inflammatory responses, demonstrated a significantly elevated risk of CIN (p < 0.001). This association persisted even after adjusting for baseline confounders, consistent with prior studies25. Additionally, factors such as endothelial dysfunction, oxidative stress, and renal vasoconstriction have been identified as potential contributors to CIN26. Furthermore, subgroup analysis indicated that PCI treatment and preoperative use of DAPT were protective against CIN, whereas preoperative CKD and diuretic use increased the risk. These findings are in line with existing research27,28, suggesting that PCI may improve renal hemodynamics, while diuretic use may exacerbate renal tubular toxicity. Identifying high-risk individuals is crucial for implementing targeted interventions.
An increasing body of research suggests that inflammation plays a crucial role in the development and destabilization of atherosclerotic plaques, highlighting its significance in CAD30–32. Our study, focusing on patients undergoing CAG and/or PCI, revealed a notable association between baseline levels of the IPI and postoperative MACE, including AMI and severe arrhythmia (p < 0.05). Specifically, patients in the highest quartile of IPI demonstrated the highest incidence of AMI, a finding that remained significant even after adjusting for baseline confounders (p < 0.001). Subsequent subgroup analysis identified hyperlipidemia and the extent of coronary artery involvement as independent risk factors for AMI, while preoperative DAPT emerged as a protective factor, consistent with previous studies25. The severity of the inflammatory response, as reflected by IPI levels, correlates with the magnitude of AMI, which is closely linked to immune-inflammatory responses and oxidative stress34. The intensity of the inflammatory response during AMI affects infarct size and subsequent ventricular remodeling35, serving as an indicator of AMI severity to some extent. Interestingly, while initially no difference in severe arrhythmia incidence was observed among patients with varying IPI levels (p > 0.05), this association became significant after adjustment (p < 0.001). Furthermore, subgroup analysis identified atrial fibrillation as an independent risk factor for severe arrhythmia in patients. However, existing research on the relationship between inflammation and arrhythmia risk presents conflicting conclusions36,37, likely due to variations in study populations and designs. Therefore, future studies with longer follow-up periods and larger, multicenter samples are needed to obtain more definitive evidence on the association between inflammatory factors and arrhythmias.
Coronary stent implantation is the primary method for revascularization in patients with CHD23. In-stent restenosis (ISR) is a significant postoperative complication that has attracted considerable attention. The pathogenesis of ISR is complex, involving vascular endothelial cell injury, excessive proliferation and migration of vascular smooth muscle cells (VSMC), in-stent intimal hyperplasia, in-stent thrombosis, and persistent vascular inflammation. Previous studies have reported that 17–32% of patients with stent implantation develop ISR, typically occurring 6 to 12 months after PCI38. However, existing research predominantly focuses on the long-term association between individual inflammatory factor levels and ISR, overlooking the exploration of the relationship between IPI levels and repeated revascularization. Our study findings indicate no significant association between IPI and repeated revascularization (p > 0.05). This contrasts with some prior research conclusions39, possibly due to population differences in inflammatory responses and the duration of inflammation persistence. Further investigations are necessary to clarify these inconsistencies and comprehensively understand the role of inflammation in ISR and repeated revascularization.
After nearly 1 year of follow-up in this study, a significant correlation was observed between IPI and the all-cause readmission rate. However, after adjusting for covariates, Cox regression analysis did not provide further evidence to support this relationship (p > 0.05). The study findings indicated that the risk of all-cause readmission in male patients was 1.3 times higher than that in female patients (p > 0.05), consistent with findings from other studies17. This could be attributed to the higher mortality rate and incidence of adverse cardiac events among elderly male patients post-PCI compared to females12. Additionally, elderly male patients tend to have higher rates of smoking, drinking, and being overweight compared to females. Furthermore, research by domestic scholars has shown that elderly male patients exhibit lower compliance with chronic disease treatment and medication than elderly female patients33, leading to a higher risk of all-cause readmission in male patients. Additionally, we observed significantly lower all-cause readmission rates among patients who underwent PCI compared to those who did not (p < 0.001). This highlights the importance of focusing on patients who do not receive PCI treatment and ensuring timely PCI intervention based on the disease condition.
Limitations
Our study has limitations. It's a single-center retrospective study, not multicenter. Future research should prioritize multicenter prospective studies for broader insights. Also, we lack long-term follow-up data, focusing mainly on short-term in-hospital prognosis. Lastly, IPI levels may change during hospitalization, so future studies should monitor them dynamically. Despite limitations, our study is the largest to date and the first to explore IPI levels' association with patient prognosis in coronary angiography and/or percutaneous coronary intervention.