Conduction disturbances and the need for permanent pacemaker implantation remain common complications following TAVI, with an incidence approaching 15%. Although they have traditionally been attributed to mechanical injury of the cardiac conduction system, the transient nature of many atrioventricular blocks suggests the involvement of reversible mechanisms. This editorial reviews the role of post-TAVI inflammation as a potential pathophysiological mechanism and therapeutic target.
The main evidence analyzed comes from the GLUCO-TAVI study, a randomized pilot trial that enrolled 100 patients with symptomatic severe aortic stenosis undergoing TAVI, who were assigned in a 1:1 ratio to receive perioperative glucocorticoids or conventional treatment. The intervention group received intravenous methylprednisolone one hour before the procedure, followed by oral prednisone for five days. The primary endpoint was the need for permanent pacemaker implantation at 30 days, while secondary endpoints included conduction disturbances, QRS duration, inflammatory response, and safety.
The incidence of permanent pacemaker implantation was 8% in the glucocorticoid group compared with 16% in the control group, without reaching statistical significance (p=0.23). However, treatment significantly reduced the inflammatory response, as evidenced by a smaller increase in C-reactive protein levels (p<0.001), and was associated with a shorter QRS duration at one month. No differences were observed in bleeding, vascular complications, or mortality.
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The authors compare these findings with the results of the Co-STAR trial, which randomized 120 patients to colchicine (0.5 mg every 12 hours from 48 hours before TAVI until 14 days after the procedure) or placebo. The composite endpoint of new-onset atrial fibrillation or conduction disturbances requiring pacemaker implantation was reduced from 25% to 10%, representing an absolute reduction of 15%. Likewise, the isolated need for permanent pacemaker implantation was numerically lower in the colchicine group (8.3% vs. 18.3%), although the difference did not reach statistical significance (p=0.107).
Conclusion: Inflammation Emerges as a Potential Therapeutic Target After TAVI
Overall, both studies provide preliminary evidence supporting inflammation as a mechanism involved in post-TAVI conduction disturbances. Although anti-inflammatory therapies were shown to attenuate the inflammatory response and numerically reduce the need for permanent pacemaker implantation, the available evidence remains insufficient to support their routine use in clinical practice.
Original Title: Inflammation after TAVI: an emerging therapeutic target?
Reference: Thomas Pilgrim1, MD, MSc;Ottavia Cozzi1,2, MD.
