Cancer has a high incidence worldwide, with rates continuing to rise due to environmental, lifestyle, and genetic factors (1). The increasing incidence of cancer directly correlates with an elevated risk of thromboembolism (TE), which affects around 15% of cancer patients (2). This is particularly concerning given that TE in cancer patients is associated with a significantly higher mortality rate−2–6 times greater than in non-TE patients (3, 4). The elevated incidence of TE further exacerbates the risks of metastasis and adversely affects patient prognosis (5). However, traditional coagulation tests, which provide limited insight into the dynamic nature of blood coagulation, are inadequate for comprehensive risk assessment (6). Therefore, there is a pressing need for more advanced diagnostic methods to evaluate coagulation function in cancer patients. Thromboelastography (TEG) represents a promising tool that allows for a dynamic and comprehensive evaluation of coagulation status, offering a more accurate risk assessment for TE in cancer patients (7).

Coagulation factor testing is a commonly used clinical method, but it can only evaluate partial stages of coagulation, and thus does not provide a complete picture of coagulation status (8). Thromboelastography (TEG) is increasingly recognized as a more comprehensive method for evaluating coagulation function, as it can dynamically measure the stability, strength, and formation rate of blood clots (9). TEG allows for the evaluation of fibrinolytic function, platelet activity, and coagulation factor performance. Various TEG parameters, such as Angle, K, and MA, have been shown to correlate with coagulation abnormalities and thrombotic risk in different clinical settings, such as post-surgical and trauma patients (10). However, its application in cancer patients, especially in the context of malignancy-related thromboembolism, remains underexplored (11). Studies in other clinical areas, such as trauma and surgery, have demonstrated the potential of TEG to provide real-time, dynamic insights into blood coagulation, but its role in cancer patients' thromboembolism risk assessment is a research gap that our study aims to address (12).

Therefore, this study aims to investigate whether the integration of thromboelastography (TEG) and traditional coagulation indices—such as D-dimer and fibrinogen—can enhance the prediction of thromboembolism risk in cancer patients. Addressing this clinical question may help establish a more dynamic and comprehensive approach to hypercoagulability assessment in oncology.

A total of 160 patients were included in this study. Among them, 87 males and 73 females; there were 45 cases in the thromboembolic group and 115 cases in the non-TE group. There was no significant difference in baseline data between the two groups of patients (P > 0.05; Table 1).

Among all analyzed parameters, thromboelastography (TEG) indicators showed the most significant differences between groups. Specifically, Angle (66.76 ± 5.68 vs. 64.3 ± 4.47 °, P = 0.011), MA (67.16 ± 7.4 vs. 57.97 ± 4.74 mm, P < 0.001), K (1.41 ± 0.37 vs. 1.96 ± 0.66 min, P < 0.001), and R (4.76 ± 1.13 vs. 6.57 ± 1.47 min, P < 0.001) differed significantly between the TE and non-TE groups (Table 2). These results indicate a hypercoagulable profile among patients with thromboembolism.

In addition to the TEG indicators, several conventional coagulation parameters also showed statistically significant differences between the TE and non-TE groups. As shown in Table 3, the TE group exhibited higher levels of D-dimer (294.49 ± 40.77 vs. 231.12 ± 46.23 mg/L, P < 0.001) and fibrinogen (4.22 ± 0.99 vs. 3.78 ± 0.74 g/L, P = 0.008), and lower values of APTT (27.44 ± 3.73 vs. 31.63 ± 4.06 s, P < 0.001) and PT (9.47 ± 2.25 vs. 11.71 ± 1.81 s, P < 0.001). In contrast, the platelet count was significantly lower in the TE group compared to the non-TE group (145.82 ± 25.03 vs. 164.35 ± 32.42 × 10⁹/L, P < 0.001). These findings further support a hypercoagulable state in cancer patients with thromboembolism.

Perform binary logistic regression analysis with Angle, MA, K, R, D-D, FIB, APTT, PT, PLT as independent variables and TE in cancer patients as dependent variables showed that Angle, MA, K, R, D-D, APTT, PT, and PLT were all important influencing factors for the occurrence of TE in cancer patients (P < 0.05; Table 4).

The ROC curve analysis results showed that Angle, MA, K, R, D-D, APTT, PT, and PLT all have high predictive value for TE, with the predictive value of D-D being the highest (AUC = 0.854; Figure 1, Table 5).

The results of this study showed that Angle, MA, D-D, and FIB in the thromboembolic group were higher than those in the non-TE group, while K, R, APTT, PT, and PLT were lower than those in the non-TE group. Our study identified optimal cut-off values through ROC analysis, such as D-D >253 mg/L and MA >63.5 mm, which slightly differ from those reported in previous studies (13, 14). These variations may be attributed to differences in tumor types, study populations, and the specific TEG instruments used. Thus, we suggest that future research should validate these thresholds in different oncological cohorts to ensure broader applicability. Moreover, our multiple linear regression analysis confirmed that Angle, MA, K, R, D-D, APTT, PT, and PLT were significant predictors of thromboembolism in cancer patients. These findings are consistent with previous clinical studies demonstrating the predictive value of TEG-derived parameters and coagulation indices—particularly Angle, MA, and D-Dimer—in identifying hypercoagulability and TE risk in malignancy (15, 16). This supports the integration of TEG with conventional coagulation testing for improved TE risk stratification. In clinical practice, coagulation function and TEG testing can be performed on cancer patients to assess the risk of TE, and targeted interventions can be administered in a timely manner to reduce the risk of TE and ensure the effectiveness of disease prognosis (17, 18).

Our findings demonstrate that TEG parameters, particularly MA and Angle, along with conventional indicators such as D-Dimer and PT, exhibit significant differences between patients with and without thromboembolism. The combination of TEG and traditional coagulation tests improved the risk assessment of TE in cancer patients. Notably, MA and D-Dimer were independently associated with TE risk, supporting their potential utility as biomarkers for hypercoagulability. This integrated testing approach may facilitate early identification of high-risk individuals and enable timely anticoagulant interventions, thereby improving clinical outcomes. This observation aligns with the known pathophysiology of malignancy-associated thrombosis, where tumor cells can activate coagulation cascades through procoagulant factors, inflammatory cytokines, and endothelial damage (18, 19). TEG, by capturing dynamic clot formation and strength, complements traditional coagulation tests, offering a more holistic view of the prothrombotic tendency in these patients (20).

Several studies have demonstrated the value of coagulation markers and TEG in assessing thromboembolic risk in cancer patients. Gezelius et al. (21) confirmed the predictive value of coagulation indices for venous thromboembolism (VTE) and prognosis in small cell lung cancer. Lobastov et al. (22) reported high sensitivity and specificity of coagulation parameters for predicting postoperative thrombosis in colorectal cancer. However, Lundbech et al. (23) observed perioperative fluctuations in fibrinogen levels without consistent association with TE events, highlighting the need for further validation.

TEG has also been applied in various malignancies as a dynamic tool for coagulation assessment. Feinchtein et al. (24) found that although prostate cancer itself may not be highly thrombotic, TEG abnormalities were observed in ~69% of patients, implicating its role in hypercoagulability evaluation. Similarly, Qin et al. (13) and Lawson et al. (25) confirmed the predictive role of TEG parameters such as R, K, and MA in lung cancer patients, which aligns with the present study's findings.

TEG offers dynamic and holistic insights into the coagulation cascade, complementing traditional tests. Wang et al. (26) showed that TEG outperformed conventional assays in detecting both hypo- and hypercoagulable states, suggesting higher sensitivity and specificity. While routine coagulation testing reflects plasma factor activity at a static point in time, TEG simulates physiological conditions and captures the full process of clot formation and fibrinolysis (25–28).

Furthermore, Gong et al. (14) and subsequent studies have emphasized that TEG's MA parameter—mainly influenced by platelets and fibrinogen—correlates strongly with thrombotic risk. A higher MA indicates enhanced platelet aggregation and stronger clot strength, which is consistent with our findings. This mechanistic evidence supports the utility of TEG in individualized thrombosis risk stratification (14, 29).

To our knowledge, few studies have explored the combined predictive value of thromboelastography and traditional coagulation markers for thromboembolism in patients with malignancies (29, 30). Our findings suggest that this integrated approach may enhance the understanding of coagulation dynamics and provide a promising tool for individualized risk stratification and early intervention in oncology care. Future studies should aim to conduct prospective, multicenter investigations incorporating dynamic monitoring of TEG and coagulation parameters. Additionally, the clinical value of TEG-guided anticoagulation strategies in high-risk cancer patients should be explored. Investigating longitudinal changes in coagulation markers over time and their correlation with the occurrence of thromboembolic events will further elucidate the temporal relationship between coagulation abnormalities and thrombosis risk in malignancy.

TEG and coagulation index level detection have a high application value in the risk assessment of TE in cancer patients. In clinical practice, two comprehensive detection methods can be used to evaluate the risk of TE in patients, thereby guiding the implementation of targeted prevention and treatment in clinical practice.