Key result
Rapid pacing duration and subsequent blood pressure recovery time during TAVI correlated positively with myocardial injury (TnI AUC), whereas microembolisation did not.
Why the study?
Does hypoperfusion or microembolization contribute more to myocardial injury during transfemoral TAVI?
Observational (n=15)
Does hypoperfusion or microembolization contribute more to myocardial injury during transfemoral TAVI?
Myocardial injury after TAVI appears to be primarily driven by hypoperfusion-induced ischemia related to rapid pacing rather than periprocedural microembolization.
Answers are grounded in this paper and cite their sources.
Hypoperfusion from rapid pacing may predominate over microembolization in TAVI injury; hypothesis-generating pending prospective trials.
AIMS: Myocardial injury reflected by a post-procedural increase of serum troponin I (TnI) occurs frequently during transcatheter aortic valve implantation (TAVI). It is potentially caused by intraprocedural hypotension, periprocedural coronary microembolisation and post-procedural (para)valvular leakages (PVLs). We invasively assessed coronary flow dynamics including coronary flow velocity reserve (CFVR), embolic high-intensity transient signals (HITS) as well as rapid pacing induced hypotension and post-procedural PVLs to determine their contribution to post-procedural TnI increases. METHODS AND RESULTS: In 15 transfemoral TAVI patients, TnI was measured serially, and cardiac MRIs with late gadolinium enhancement (LGE) were performed pre- and post-interventionally. There were no significant correlations between coronary flow dynamics, CFVR and the area under the curve (AUC) of TnI over 72 hours. Despite the detection of HITS in all patients and during all procedural steps, there was also no correlation between the amount of HITS and the AUC of TnI. However, there were positive correlations between the duration of rapid pacing as well as the time of subsequent blood pressure recovery and the AUC of TnI. Both LGE and more than mild PVL were observed in a single case only. CONCLUSIONS: Myocardial injury after TAVI appears to be related more to hypoperfusion-induced ischaemia than to periprocedural microembolisation.
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Kahlert et al. (2016) conducted an observational in Transfemoral transcatheter aortic valve implantation (TAVI) (n=15). Transfemoral transcatheter aortic valve implantation (TAVI) was evaluated on Area under the curve (AUC) of serum troponin I (TnI) over 72 hours. Rapid pacing duration and subsequent blood pressure recovery time during TAVI correlated positively with myocardial injury (TnI AUC), whereas microembolisation did not.
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