Acute basilar artery occlusion (ABAO) accounts for about 5% of all intracranial large vessel occlusions (LVO) [18], which has longer prodrome that different from hemispheric ischemia [19]. Early neurological deficits are atypical, such as dizziness, vertigo, maliciousness, and ataxia [20–21]. It is essential to realize vascular recanalization in the early stage. However, many recanalizations are futile due to complications such as postoperative hemorrhagic transformation, malignant cerebral edema, and pulmonary infection. Moreover, the rates of futile recanalization (mRS score ≥ 3 points at 90 days after the operation) in endovascular treatment groups of BASILAR, BAOCHE, ATTENTION, BEST, and BASICS were 72.6%,61%,67%,66.7%, and 64.9%, respectively. Similarly, their mortality was 46.2%,31%,37%,33.3%, and 38.3%, respectively [4–6, 22–23]. The rates of futile recanalization and mortality were similar to our study.
This paper studied the prediction of futile recanalization from two aspects: collateral circulation status evaluation and Inflammatory response level. Previously reported that the mechanism of futile recanalization may be related to reperfusion injury and the "No-reflow" phenomenon [9]. In addition, the patency of collateral circulation can effectively identify reperfusion and determine the infarct size and even the clinical outcome of AIS [24]. Several collateral scores for the posterior circulation have emerged in recent years, such as PC-CS [25], pc-CTA [26], BATMAN [27], and pc-ASPECTS [28]. With the development of neuro-interventional technology, the number of patients receiving EVT treatment is gradually increasing, and the evaluation of collateral circulation is not limited to CT/CTA. DSA can dynamically observe blood perfusion and play an irreplaceable role in evaluating collateral circulation. The angiographic collateral grading system for basilar artery occlusion (ACGS-BAO) is based on DSA, which visualizes the degree of posterior circulation and pial branches along with basilar artery tip and can evaluate the collateral compensation of basilar artery with reasonable accuracy [17].
Inflammation is an essential factor affecting acute ischemic stroke's severity and prognosis (AIS) [29]. After vascular occlusion, neuronal necrosis, and inflammatory cascade are activated immediately [30]. Leukocytes and platelets aggregate under the action of the fibrin, and adhesion molecule p-selectin, forming blood plate-leukocyte clusters, causing microvascular embolism and aggravating ischemic injury [31–32]. Neutrophils damage the blood-brain barrier by releasing matrix metalloproteinases, producing many free radicals, releasing inflammatory mediators, and further aggravating and promoting brain injury [33–34]. In animal experiments, T cells decreased continuously for several weeks after occlusion of the MCA in mice, which may be related to systemic immunosuppression. In addition, the decrease of lymphocytes will also weaken the protective effect on neurons [35–36]. Previous studies have shown that higher neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) levels are closely associated with AIS prognosis [37]. However, the SII used in this study included three indicators of neutrophils, platelets, and lymphocytes, reflecting the overactive coagulation and inflammatory pathways simultaneously. Compared with NLR and PLR, SII can more comprehensively reflect the inflammatory state of patients and the relationship between stroke and inflammation. Therefore, SII can be considered a more sensitive predictor of inflammation.
The efficacy of SII to reflect levels of inflammation and immune balance has been validated in various cancers and cardiovascular diseases [38–40]. Hou et al. reported that SII was an independent predictor of stroke severity (OR 1.351, 95% CI 1.084–1.684, P = 0.007) in AIS [41]. Furthermore, SII in AIS patients who received intravenous thrombolysis was an independent risk factor for poor prognosis at 3 months (OR = 3.953, 95% CI = 1.702–9.179, p = 0.001) [42]. Ho Jun Yi et al. showed that the SII threshold < 853 was an independent predictor of good prognosis in the EVT of large artery occlusion [43]. The preprocedural use of SII as an auxiliary method for predicting prognosis has proven effective and an excellent clinical application prospect.
This study still has some limitations: This study is a single-center retrospective study with a small sample size (n = 73), which may have selection bias. SII was analyzed only in this study and other inflammatory markers such as hs-CRP, IL-1, IL-6, and TNF were not included. We only analyzed SII at admission and without dynamic monitoring, which may affect the correlation between SII and ineffective recanalization. The efficacy of ACGS-BAO has only been confirmed in some single-center studies and multi-center prospective studies are needed to verify it. Multiple neuro-interventional specialists performed all procedures in this study, and the operators' experience and operation methods may impact the vessels' recanalization.
In conclusion, ACGS-BAO and preprocedural SII are standard and readily available in clinical practice, which respectively will evaluate the status of basilar collateral circulation and the level of inflammatory response and are closely related to futile recanalization after surgery. Our study confirmed that collateral circulation status is negatively correlated with prognosis, while inflammation level is positively correlated. The combined use of these two biomarkers is more predictive of postoperative futile recanalization than the use of either marker alone, which is of great significance for developing individualized treatment plans and reducing additional injuries.