The clinical manifestations of APE range from asymptomatic to hemodynamic disturbances and even death. Studies have shown that the 7-day all-cause mortality rate for APE was 1.9–2.9% and that the 30-day all-cause mortality rate for APE was 4.9–23.8% [11, 12]. The present study showed a 30-day mortality rate of 9.54% (31/325), which was generally consistent with previous studies. In addition, this study showed that NPS is an independent prognostic marker of 30-day all-cause mortality in patients with APE and that patients in NPS Groups 1 and 2 had a worse prognosis compared with NPS Group 0.

NPS not only includes serum Alb and total cholesterol levels, which reflect the nutritional status of the body, but also immunoinflammatory markers such as NLR and LMR, allowing for a more comprehensive and effective assessment of the patient’s body condition at the time of admission. Alb is closely associated with the development and progression of thrombosis [13]. Patients with lung cancer are susceptible to hypoproteinemia. When the body is in a hypoalbuminemic state, it stimulates the liver to synthesize Alb. The synthesis of coagulation factors will concurrently increase, resulting in a hypercoagulable state [13]. However, when hypoproteinemia is present, water accumulates in the interstitial spaces, resulting in increased blood viscosity and a higher risk of thrombosis [15]. In the present study, a significant intergroup difference (P < 0.001) was observed, and patients with lower Alb levels had a poorer prognosis. In addition, lipids, especially HDL cholesterol, play a key role in the metabolism of normal lung tissue [14], and some studies have shown that cholesterol is crucial in the inflammatory response after acute lung injury [15]. The pathogenesis of APE is often accompanied by an inflammatory response, which can affect the synthesis of cholesterol and the absorption and transport of hepatic lipids [16]. A study by Karatas et al. showed that total serum cholesterol levels were strongly associated with short-term prognosis and recurrence rates in patients with APE [17]. In the ROC analysis, total cholesterol levels were compared with triglyceride, LDL cholesterol, and HDL cholesterol levels, a parameter with better discriminatory power for mortality. This negative correlation of lipid levels with mortality rates is known as the lipid paradox [18]. The results of the present study were consistent with those of previous studies in that the TC in the nonsurvivor group was significantly lower than that in the survival group (P = 0.073), and the negative correlation between TC and mortality may be attributable to the depletion of lipids in the acute inflammatory response.

Previous studies have shown that NLR, which is considered a novel inflammatory marker, better reflects systemic inflammation in patients and is closely related to the prognosis of pulmonary embolism [19, 20]. The NLR values of patients in the nonsurvivor group in the present study were significantly higher than those in the survivor group, supporting the results of previous studies. In addition, inflammation and endothelial damage play important roles in the progression of APE due to oxidative stress, reperfusion injury, and elevated reactive oxygen species in the lungs of patients with APE, and LMR has been proposed as a surrogate marker of endothelial dysfunction and inflammation in different populations as it has prognostic and predictive values [21]. To the best of our knowledge, only one study has shown LMR as a novel marker of inflammation. That study found that LMR was significantly lower in nonsurvivors after APE (P < 0.001), and LMR appears to be an independent predictor of short-term mortality in patients with APE [22]. The results of our study were similar in the three NPS groups and showed that APE patients with lower LMR values had a poorer prognosis (P = 0.031).

The components of NPS (TC, Alb, NLR, and LMR) are common clinical biomarkers in daily clinical practice that provide a comprehensive picture of a patient’s inflammatory and nutritional status. The prognostic effects of NPS on patients with APE are currently unknown. In view of this, this study analyzed the effect of NPS on 30-day all-cause mortality in 325 patients with APE at admission, and the results of the comparison revealed that patients with older age, faster heart rate, lower systolic blood pressure, low Alb and total cholesterol levels, high NLP, low LMR, right heart dilatation, heart failure, malignancy, and lower extremity venous thrombosis have higher 30-day all-cause mortality, and these differences were statistically significant (P < 0.05). In addition, the results revealed that the AUC for NPS to predict all-cause death within 30 days in patients with APE was 0.780 (95% CI = 0.678–0.855), with sensitivity being 80.6% (95% CI = 0.667–0.946) and specificity being 72.1% (95% CI = 0.670–0.772). This indicated that NPS at admission has good guidance for the short-term prognosis of patients with APE. In addition, Cox multivariate analysis showed that NPS was an independent risk factor for 30-day all-cause mortality in patients with APE (P = 0.0004), and stratified analysis suggested that lower scores had a better prognosis in both uncorrected and corrected covariates models. This suggested that timely nutritional support and appropriate improvement of the inflammation and immune status during the treatment of APE patients with high NPS would improve the long-term prognosis of these patients.

The accuracy and generalisability of the PESI are now supported by derivation and validation of data from multiple countries [23, 24]. The PESI reliably and accurately identifies patients at low risk of death when assessed between 7 and 90 days of follow-up. However, the PESI uses 11 clinical variables with different assigned weights, and its scores depend on calculations that may be difficult to apply clinically. The NPS prediction rules reduce this complexity. In addition, some components of the PESI, such as a patient’s disease history and clinical presentation, may be influenced by a physician’s subjective judgement. This may lead to slightly different PESI scores for the same patient by different physicians. All components of the NPS are derived from objective laboratory tests, and the results are not affected by patient recall bias and subjective judgement of clinicians. We believe that the simplified NPS is useful because we were surprised to find that the area under the ROC curve for the predictive value of the NPS was not lower than that of the PESI [2]. Thus, the NPS, a simplified scoring system, may be more applicable to busy hospital emergency departments.

The present study has some limitations. First, potential selection bias is inevitable as this was a retrospective cohort study. Second, this study is a single-center study that lacked external validation, and the moderate sample size may be the reason for the decreased power. Therefore, a multicenter, large-scale, prospective validation study is needed. Third, we did not stratify the study patients by risk, and further studies are needed to simultaneously risk-stratify patients to validate the predictive value of this prediction tool for the prognosis of patients in different strata, with a focus on short-term all-cause mortality risk. Fourth, postdischarge NPS has not been used as a follow-up marker for patients with APE, and there is a need to prospectively validate the dynamic prognostic role of NPS in order to apply a simple and easily accessible NPS in the future to enhance risk stratification and condition assessment of patients with pulmonary embolism and to guide the clinical management of APE. Fifth, due to limitations in research design and available resources, we were unable to collect hemodynamic data in this study. Hemodynamic data could provide valuable insights into the severity and prognosis of acute pulmonary embolism. Future research endeavors should aim to incorporate these data to enhance the comprehensive assessment of patients with APE.