Inflammatory burden index and mortality following transcatheter aortic valve replacement

Backgrounds Inflammation significantly influences transcatheter aortic valve replacement (TAVR) outcomes, affecting both procedural success and long-term valve durability. The inflammatory burden index (IBI) is a new composite index that reflects systemic inflammation and immune balance; however, the association between IBI and TAVR outcomes remains unknown. Purpose This study aimed to assess the impact of IBI on mortality following TAVR. Methods A total of 972 patients with available IBI data before the procedure were included from our prospective registry. IBI before TAVR and at their peak were assessed as high-sensitivity C-reactive protein (hs-CRP) × neutrophils / lymphocytes. The primary endpoint was 2-year all-cause mortality following TAVR. ROC curve analysis was used to determine the cut-off values of IBI for predicting 2-year mortality. The adjusted factors for multivariate analysis to predict 2-year all-cause mortality included age, sex, BMI, diabetes, CKD, atrial fibrillation, LVEF <40%, and active cancer. Results Pre- and peak IBI values were calculated as 18.1 [11.4–40.9] and 468 [214–1146], respectively (p<0.0001). In our population, 248 patients (26%) experienced all-cause death at 2 years following TAVR. Pre-IBI showed a higher ROC-AUC for predicting 2-year all-cause death compared to each preprocedural inflammatory variable (Fig. 1A-1C). The optimal threshold for pre-IBI to predict 2-year all-cause death was 25.2. Patients with pre-IBI >25.2 (n=436, 45%) were older and had a higher prevalence of diabetes, CKD, anemia, peripheral artery disease, atrial fibrillation, low LVEF, and active cancer compared to those without (n=436, 55%). Patients with pre-IBI >25.2 had a higher incidence of 2-year all-cause death (38.4% vs. 18.1%, log-rank p<0.0001; aHR, 2.16 [1.67–2.80]) (Fig. 2A). The optimal threshold for peak IBI to predict 2-year all-cause death was 893. Peak IBI also demonstrated a higher ROC-AUC for predicting 2-year all-cause death compared to peak hs-CRP (Figure 1D-1F). Patients with peak IBI >893 (n=280, 30%) had a higher prevalence of severe aortic atheroma, low LVEF, and a non-femoral approach compared to those without (n=640, 70%). Patients with peak IBI >893 also had a higher incidence of 2-year all-cause death (36.4% vs. 19.8%, log-rank p<0.0001; aHR, 2.05 [1.58–2.67]) (Fig. 2B). Although there was no significant difference in ROC-AUC for predicting 2-year all-cause death between pre- and peak IBI (Fig. 1G), even among patients with lower pre-IBI, those with peak IBI >893 had a higher incidence of 2-year all-cause death (28.1% vs. 14.7%, log-rank p=0.0002; aHR, 2.11 [1.39–3.20]) (Fig. 2C). Conclusions IBI was more strongly associated with mortality following TAVR than any individual inflammatory marker. Both patient-specific and TAVR-induced inflammation may significantly influence outcomes. Therapeutic strategies targeting the reduction of inflammatory burden warrant further investigation to improve TAVR outcomes.