Inflammation after TAVI: an emerging therapeutic target?

Cardiac conduction disturbances (CCD) and the need for permanent pacemaker implantation (PPI) remain common after transcatheter aortic valve intervention (TAVI), with a median incidence of about 15%, and have been associated with an increased risk of heart failure and mortality.1 Mechanical injury to the His bundle due to radial expansion of the prosthesis is generally considered the primary mechanism. However, several clinical observations raise questions as to whether this has a purely mechanical explanation. Postprocedural atrioventricular block is often transient, and many patients who require a pacemaker early after TAVI are not pacemaker-dependent at follow-up.12 These patterns suggest a reversible process rather than permanent structural damage.

Inflammation has thus been proposed as a complementary mechanism of CCD (Figure 1). At the systemic level, TAVI triggers an inflammatory response syndrome in 22-63% of transfemoral procedures. The proposed mechanisms include endothelial injury and microparticle release, ischaemia-reperfusion injury from rapid pacing and hypoperfusion, and immune responses against xenogenic bioprosthetic antigens.3 This results in early cytokine activation followed by a C-reactive protein (CRP) peak at 48-72 hours after TAVI...