GLUCO-TAVI trial: treatment with glucocorticoids in patients undergoing TAVI to reduce the incidence of atrioventricular block and pacemaker implantation

Abstract Background Despite growing demand for transcatheter aortic valve implantation (TAVI), an effective treatment for its most common complication remains elusive. Cardiac conduction defects (CCD) often necessitate pacemaker implantation (PPI), leading to higher morbidity, and healthcare costs (1). While mechanical injury is the main mechanism behind post-TAVI CCD, evidence suggests that a transient, inflammation-driven mechanism may play a role (2, 3). Previous studies targeting inflammation showed inconsistent results (4, 5). Purpose This study aimed to evaluate the safety and efficacy of glucocorticoids in preventing PPI in patients undergoing TAVI. Methods In this randomized, controlled, open-label trial, we included 100 patients who met the latest guideline criteria for TAVI (6). These patients were randomized in a 1:1 ratio to receive usual care or methylprednisone 7 mg/kg an hour before the procedure, followed by prednisone 15 mg / 12 hours for 5 days (Figure 1 depicts the study protocol). Inflammatory biomarkers and electrocardiograms were assessed pre- and post-intervention, at discharge, and one month. The primary efficacy endpoint was the incidence of PPI at one month. Secondary outcomes included new-onset LBBB, mortality, and procedural complications. Results A total of 100 patients met the inclusion criteria; 60% were women with a mean age of 81.4 (SD 5.2) years. Baseline characteristics, including established risk factors for post-TAVI CCD such as prosthetic valve type (balloon-expandable vs. self-expandable), clinical frailty, and membranous septum length, were balanced between groups (7). No patients were lost to follow-up. Glucocorticoid therapy resulted in a lower increase of inflammatory markers post-TAVI (ΔCRP OR 0.01 (- 0.16 – 0.24); p value 0.001). The primary efficacy outcome was observed in 16% of the control group (CG), similar to previous studies (8), and 8% of the intervention group (IG) (OR 0.50; 95% CI 0.16–1.55; p = 0.23), suggesting a potential reduction of 50% PPI risk, though not statistically significant. The statistical power for this outcome was low (23.1%). LBBB was more frequent in the IG compared to controls (OR 1.12; 95% CI 0.66 – 1.89; p value = 0.66), but a higher one-month resolution rate was noted (63.15% vs. 47.05%; OR 0.78; 95% CI 0.31-1.93; p value 0.587). No significant differences were observed between groups in vascular complications (10% in the IG vs. 2% in the CG; p = 0.20) or mortality (2% vs. 4%; p = 0.60). Three adverse events related to glucocorticoid use were detected, one hyperglycemia and two heart failure decompensations. Tables 1 and 2 summarise clinical outcomes and adverse events between groups. Conclusion Glucocorticoid therapy in TAVI showed a non-significant trend toward reducing PPI, without increasing adverse events. The study was limited by low statistical power which may have prevented the detection of a true effect. Larger studies are needed to confirm these findings.