With the acceleration of population aging, the burden of cardiovascular diseases is also increasing. Among them, ST-segment elevation myocardial infarction (STEMI) poses a significant challenge to human health (1). Percutaneous coronary intervention (PCI) is currently the main treatment for STEMI patients, but 15%–35% of patients develop contrast-induced acute kidney injury (CI-AKI) after PCI (2). Evidence suggests that STEMI is one of the key factors contributing to the increased incidence of CI-AKI and the need for dialysis, which may be related to the hemodynamic instability, neuroendocrine activation, and intense inflammatory response in STEMI patients (3, 4). Although CI-AKI is associated with poor prognosis, there is currently a lack of specific clinical drugs and interventions for preventing CI-AKI (5). Therefore, early identification of high-risk populations and active prevention of CI-AKI is crucial.

Although PCI successfully restores coronary epicardial blood flow, more than half of STEMI patients still experience coronary microcirculatory dysfunction (CMD) (6, 7). The index of microcirculatory resistance (IMR) is the “gold standard” for quantitatively measuring coronary microcirculatory dysfunction (8, 9). However, the additional procedure time, increased procedural costs, and the requirement for maximal hyperemia may hinder its use in clinical practice. This is particularly true in STEMI patients undergoing primary PCI, as it further increases patient risk. In recent years, coronary angiography-derived index of microcirculatory resistance (caIMR) has been extensively validated for accuracy and is widely used to assess CMD (10–12). Compared to traditional IMR, caIMR does not require pressure wires or adenosine, making it safer and more convenient. Previous studies have shown that CMD in STEMI patients significantly impacts prognosis (7, 13, 14). Notably, in one study, Thrombolysis in Myocardial Infarction (TIMI) was identified as an independent predictor of CI-AKI after PCI in STEMI patients (15). Additionally, nicorandil has been shown to effectively prevent CI-AKI, likely through its beneficial effects on microcirculation (16–18). To date, the relationship between IMR and CI-AKI remains unclear. This study aims to explore the relationship between caIMR and CI-AKI following primary PCI in STEMI patients.

To our knowledge, this is the first study on the relationship between CMD and CI-AKI. The main findings of this study are as follows: first, elevated caIMR is an independent risk factor for the development of CI-AKI after PCI in STEMI patients; second, there is a linear dose-response relationship between caIMR and CI-AKI; and third, integrating caIMR significantly improves the risk model for CI-AKI.

CI-AKI is characterized by kidney dysfunction occurring within 48–72 h after the administration of contrast agents (23). Although recent evidence suggests that the risk of CI-AKI may have been overestimated, an important prerequisite is the potential exclusion of high-risk patients (24). Numerous studies have shown that CKD patients are less likely to undergo coronary angiography or PCI due to concerns about worsening kidney function (25, 26). In our study, 10.6% of patients still developed CI-AKI. Given the relationship between CI-AKI and poor outcomes (27, 28), and the limited pharmacological treatment options (29), identifying additional risk factors and optimizing risk stratification are essential.

Despite the successful restoration of epicardial coronary flow in STEMI patients via PCI, more than half of STEMI patients still experience myocardial reperfusion injury due to the presence of coronary microcirculatory dysfunction (CMD) (6, 7). In our study, there were 277 (37.2%) patients whose caIMR was greater than 25 U. The reason why CMD is at a relatively low level may be that all the patients included in our study have a TIMI flow grade of 3. Current clinical tools for assessing CMD include cardiac magnetic resonance imaging (CMR) and the index of microcirculatory resistance (IMR). While CMR is non-invasive, its use is limited by indications and high costs, meaning that not all STEMI patients undergo this examination (30). IMR, although the “gold standard” for evaluating microcirculatory dysfunction, requires a pressure-temperature sensing wire and induced maximal hyperemia, which limits its routine clinical application, especially in STEMI patients undergoing primary PCI (8, 9). Recently, caIMR, as an alternative to traditional IMR, has been widely used for prognosis stratification in STEMI patients (10–12). There is a significant correlation (R = 0.782, P < 0.001) and consistency (Bias = −0.398, SD of Bias = 11.96) between caIMR and traditional IMR (10). Given its simplicity and safety, caIMR is particularly beneficial in STEMI patients. In a previous study, Çınar et al. demonstrated that TIMI was independently associated with CI-AKI in STEMI patients undergoing primary PCI and provided better predictive value for CI-AKI than traditional risk factors (15). Nicorandil, a commonly used drug for improving microcirculatory dysfunction, has been shown in prior studies to effectively prevent CI-AKI, whether administered intravenously or orally (16–18). Consistent with these findings, our study identified elevated caIMR as an independent risk factor for the development of CI-AKI after PCI in STEMI patients, and we found a linear dose-response relationship between caIMR and CI-AKI. Given the established relationship between CMD and poor prognosis in STEMI patients, our findings appear to be well-founded. Previous studies have shown that CMD in STEMI patients is associated with larger infarct sizes, worse left ventricular remodeling, and intense inflammatory response, which play an important role in the mechanism of CI-AKI (3, 4, 7, 13, 14). Additionally, AKI is closely associated with endothelial dysfunction (31). It is known that endothelial dysfunction is also an important mechanism of CMD. Therefore, systemic endothelial dysfunction may be a potential mechanism underlying the relationship between caIMR and CI-AKI. In our study, ROC analysis showed that caIMR is a strong predictor of CI-AKI, outperforming FBG, LVEF, and NT-proBNP, aligning with the previous study (15). In previous studies, a threshold value of 25 U for either caIMR or traditional IMR has been proposed for diagnosing microcirculatory dysfunction (8, 9, 32, 33). Interestingly, in our study, we found that a caIMR value of 25.95 U was the cutoff for predicting CI-AKI in STEMI patients after PCI. To our knowledge, this is the first study to establish a cutoff for caIMR in relation to CI-AKI, potentially providing additional insights for IMR-based prognosis assessment in STEMI patients. Differently, in another previous study on STEMI patients, the cutoff value of the angiography-derived IMR was higher than that in our study. This may be attributed to the differences in the measurement software for IMR and the end-point events (34). Our study also demonstrates that caIMR can effectively enhance risk models for CI-AKI. Given its simplicity and safety, caIMR represents a valuable tool for optimizing risk stratification for CI-AKI after PCI in STEMI patients. These findings suggest that patients with elevated caIMR may require more clinical attention and intervention to reduce the risk of CI-AKI.

There are several limitations to this study. First, given its retrospective and observational design, the current study remains inherently descriptive, hypothesis-generating, and speculative in nature. While our study provides a compelling association between CMD and CI-AKI, the capacity for causal inference remains limited. The observed elevation in caIMR in these patients may not solely reflect isolated microvascular dysfunction but rather a broader picture of myocardial damage, impaired reperfusion, and a generally more adverse in-hospital clinical course. Consequently, caIMR might function as a surrogate marker of overall disease severity rather than a direct mechanistic contributor to CI-AKI. Second, the sample size is relatively small, and some conclusions may need to be validated in larger cohorts. Third, this study specifically involves STEMI patients who underwent successful primary PCI, meaning the findings may not be applicable to other patient populations. Fourth, in our study, caIMR was evaluated after the completion of PCI, which made strategies to reduce the use of contrast agents no longer feasible. This limits the clinical utility of caIMR as a tool for early risk stratification or surgical planning. For STEMI patients undergoing primary PCI, the practical measurement of caIMR at an earlier stage may still be a significant challenge. In addition, the implementation of postoperative renal protection strategies mainly based on saline hydration may precisely be restricted in the subgroup of patients identified as high-risk, who have poorer cardiac function. These factors highlight the importance of considering caIMR in a way that can effectively provide a basis for personalized treatment decisions. Fifth, given that the application of functional coronary angiography remains limited in clinical practice, it may still be too early to incorporate caIMR into the prediction model for CI-AKI. Finally, CI-AKI is a surrogate marker for adverse outcomes, but whether the elevated caIMR is associated with persistent renal dysfunction or mortality may require more follow-up in the future to determine.

Elevated caIMR is an independent risk factor for the development of CI-AKI after PCI in STEMI patients. Integrating caIMR significantly improves the risk model for CI-AKI.