Myocardial injury during TAVI with self-expanding prosthesis is not associated with patient-prosthesis features, hemodynamics or clinical outcome

Abstract Background Transcatheter aortic valve implantation (TAVI) has been associated with increases in markers of myocardial injury but underlying mechanisms as well as relevance for prosthesis hemodynamics, cardiac function and clinical outcome remain unclear. Purpose To study the trajectory of high-sensitivity troponin T (hs-TnT) during TAVI and elucidate putative associations with demographics, anatomical and procedural features, as well as clinical and echocardiographic outcome. Methods This prospective real-world registry study included all patients (n=275) undergoing transfemoral TAVI using a self-expanding or balloon-mounted system at a large tertiary university hospital over the most recent three-year period. Plasma levels of hs-TnT (reference level 0–14 ng/l) at 24 hours (h) before TAVI and at 9h, 18h, 30h, 42h and 72h after TAVI were analyzed. Patients with ongoing myocardial ischemia and acute coronary syndrome were excluded. We studied the association between hs-TnT values and patient characteristics, echocardiographic and CT findings at baseline as well as procedural features including the use of pre- and postdilatation. Moreover, we studied the association between hs-TnT and and echocardiography and clinical outcome at 1 year after TAVI. Results In this real-world TAVI cohort (median age 83.2±0.2 years; 48.7% women; 5.2±0.2 comorbidities; eGFR 58.0±6.0 ml/min/1.73m2; mean±standard error), 100% of patients exhibited significant elevations of hs-TnT at approximately 9-fold (207.0±11.0) compared to baseline (23±0.2 ng/L, median±SE). Peak hs-TnT values were reached at 9 h post-TAVI (207±11 ng/L) with subsequent gradual decline (figure). Myocardial injury was confirmed by elevated creatin kinase (CK) and CKMB isozyme. No significant association was found between peak hs-TnT, delta hs-TnT (peak minus baseline values) or area under the curve (AUC) of hs-TnT on the one hand, and patient demographics including renal dysfunction, comorbidity, age and gender on the other side. Moreover, no significant association between hs-TnT and anatomical features, prosthesis sizing, or use of pre- and postdilatation was found. No association between hs-TnT during TAVI and NYHA functional class, transvalvular pressure gradient, cardiac function or survival at 1 year was found. In subjects with at least one year of follow-up after TAVI (n=138), NYHA functional class (1.7 vs 2.7) and NT-proBNP plasma levels (1126±316 vs 1581±563 ng/L) were significantly lower compared to pre-TAVI. Conclusions Modest transient elevations of hs-TnT occur in all patients undergoing TAVI and are consistent with subtle myocardial injury. The lack of significant association between the extent of myocardial injury during TAVI and clinical and hemodynamic outcome as well as all-cause mortality is reassuring for current real-world practice.