Objective: Infective endocarditis (IE) is a rare disease with a high mortality. Therefore, prognostic markers can play an important role in the follow-up. In this study, we investigated the relationship between the D-dimer (DD) level and in-hospital mortality and complications in patients with IE, because DD indicates both the fibrin turnover in vegetation and the autoimmune inflammatory response in patients with IE.
Methods: Seventy-nine patients with IE were included in the study. In-hospital death for any reason was considered to be the primary endpoint. Secondary endpoints were embolism and in-hospital death or embolism.
Results: In-hospital mortality occurred in 31 (39%) patients. The DD level was significantly higher in the group with in-hospital mortality [median (interquartile range) values 3048.0 (4911.0) vs. 556.0 (1100.2) ng/mL, p<0.001]. When the DD level was 795 ng/mL or higher, the sensitivity was 83.5%, specificity was 66.7%, the positive predictive value was 66.4%, and the negative predictive value was 94.1%, to determine in-hospital mortality. Categorically, the DD level of 795 ng/mL or higher was found to increase the risk of in-hospital mortality by 29 times (odds ratio=29; 95% confidence interval=6.13–137.11; p<0.001). In a multiple logistic regression analysis, the DD level was found to be the best independent predictor of in-hospital mortality (the AUC value only for DD was 0.86, and for the multiple logistic regression model, it was 0.89, p=0.48). A significant correlation was found between the DD level and in-hospital death or embolization [1863.0 (4914, 0) vs. 376 (607, 0) ng/mL, p<0.001]. In the multiple logistic regression analysis, DD was found to be the best independent parameter showing in-hospital mortality or embolization (the AUC value was 0.83 for DD, and 0.84 for the multiple logistic regression analysis, p=0.69).
Conclusion: These findings support that a high DD is a strong parameter predicting in-hospital mortality, and in-hospital mortality or embolic events in patients with IE.