Myocardial Injury Post Transcatheter Aortic Valve Implantation Comparing Mechanically Expanded Versus Self-Expandable Versus Balloon-Expandable Valves

Abstract

Background: Myocardial injury (MI) is common with transcatheter aortic valve implantation (TAVI) and may predict poor outcome. We aim: 1) to evaluate the difference in change of high-sensitivity-Troponin-T (hsTnT) within 24h after transfemoral-TAVI between mechanically-expanded (MEV), self-expanding (SEV) and balloon-expandable-valves (BEV); 2) to determine predictors for MI post-TAVI; and 3) to assess whether MI is associated with 30-day mortality.Methods: This multicenter retrospective observational study included 1208 consecutively treated transfemoral-TAVI patients from three European centers. All patients treated with a MEV, SEV or BEV with available hsTnT measurements at baseline and within 24 h post-TAVI were included. Significant MI was defined as an elevation of hsTnT ≥ 15x the upper-reference-limit.Results: Overall, the median hsTnT rise was 741 ng/L and was lower with MEV (MEV 335 vs. SEV 901 vs. BEV 649 ng/L, p < 0.001). MI occurred in 925 patients (77%) and was less frequent with MEV (MEV 67%, SEV 79% and BEV 76%, p = 0.007). Occurrence of MI was similar after implantation of first vs. second-generation SEV (79 vs. 80%, p = 0.72) and BEV (77 vs. 76%, p = 0.90). There was no association between frequency of annulus manipulation and MI. On multivariable analysis (OR (95% CI) non-MEV (1.63 (1.06-2.49)), mean aortic gradient (1.02 (1.01-1.03)), left ventricular ejection fraction (1.03 (1.01-1.04)), and previous myocardial infarction (1.62 (1.04-2.56)) were positively associated with MI. There was no association between MI and 30-day mortality.Conclusion: Transcatheter valve design determines peri-procedural MI and is less frequent with MEV. MI is not associated with 30day mortality.

Impact of bioprosthetic valve type on peri-procedural myocardial injury and mortality after transcatheter aortic valve replacement

“…In agreement with previous data, we demonstrate an association between PPMI and higher LVEF, probably because viable myocardial tissue results in higher enzymes release, and also with worse baseline kidney function [8,[22][23][24], whereas we could not observe an independent association between PPMI and pre-TAVR valvuloplasty, mean procedural duration, and previous MI or CAD as reported in other cohorts [8,9,17,[22][23][24], probably due to heterogenous sampling and selection biases. PPMI has a mainly procedural origin, related to mechanical trauma to the myocardium due to contact with valve struts, potential multiple episodes of hypotension during valve release, and myocardial ischemia due to balloon valvuloplasty and/or valve implantation itself [15,17].…”

“…PPMI has a mainly procedural origin, related to mechanical trauma to the myocardium due to contact with valve struts, potential multiple episodes of hypotension during valve release, and myocardial ischemia due to balloon valvuloplasty and/or valve implantation itself [15,17]. Of note, we found that SEV implantation might be associated to a higher risk of PPMI has already been reported, but mainly as a collateral result, and without adjustment for other procedural and clinical variables [8,17,[22][23][24]. We employed a rigorous analytic approach that included multivariable and non-parsimonious propensity-weighted analysis: the important implication of our study, thus, is that, when the choice of implanting a SEV is made, a two-to threefold higher risk of PPMI should be accounted.…”

“…Myocardial infarction (MI) is a rare and potentially life-threatening complication of TAVR, usually caused by mechanical interference of prosthesis with coronary ostia, nonetheless a PPMI which is based on bio-humoral markers of myocardial injury is commonly reported and generally clinically silent [7-9, 14-16, 19, 21]. In our cohort, we observed a PPMI rate of 79.0% which is one the highest reported in the literature so far [6,15,[22][23][24]. This result is probably explained by several factors: first and foremost, we adopted the new VARC-2 definition of myocardial injury and used the troponin I as the biomarker of choice: TnI seems to be less stable and more related to peri-procedural complications and non-cardiac cause of PPMI (e.g., ischemia related to anemia or dehydration, acute kidney injury, or severe hypoxia due to acute respiratory failure) than CK-MB [19], which was used in some previous studies [7][8][9].…”

“…We could not identify a significant relationship between PPMI and 30-day and 1-year all-cause mortality post-TAVR: the literature data are highly controversial on this topic, since several publications [7,8,17,22,26] found that PPMI is clearly linked to higher mortality, whereas other reports have been unable to find any significant association [5,23,24]. Nevertheless, a possible reason for this discrepancy is that we evaluated all-cause mortality, whereas PPMI was shown to be mainly associated with cardiovascular mortality [7,8,22,26].…”

“…The reasons for the increased PPMI risk and SEV technology are multiple: whereas in SEV implantation, the need for rapid pacing and the consequent extreme periods of hypotension are less than in BEV, SEV usually leads to peri-valvular myocardial compression (often for greater valve oversizing leading to deeper positioning of the metal frame), the release time can be longer, and there is more arrhythmic potential due to more frequent need for inotropic support [9,10,15,23,25]. All these mechanisms may lead to hypoperfusion-induced ischemia and hemodynamic instability occurring more frequently than in BEV.…”