In this study, we report the incidence and outcomes of patients with PPMI after TAVI using both the VARC-2 and VARC-3 definitions over the last 12 years in a tertiary care setting. This cohort is among the largest to date with hs-cTnT level measurements taken before and after the procedure, applying both criteria. We present two major findings.

First, we observed that a majority of patients (82%) undergoing TAVI had elevated levels of hs-cTnT at baseline, consistent with prior reports [22,23,24]. Elevated hs-cTnT concentrations before the procedure highlight the older age of this patient cohort (median age 82.5 years) and the high prevalence of cardiovascular morbidities, such as coronary artery disease (60%), hypertension (83%), or impaired renal function (62% with eGFR ≤ 60 ml/min/1.73 m2). Baseline troponin elevation also correlated with adverse outcomes, including MACE and all-cause mortality at 1 year (HR: 2.2 (1.15–2.60), p = 0.0215 and HR: 2.6 (1.27–4.25), p = 0.026, respectively), corroborating previous studies [23, 25]. Ferrer-Sistach et al. reported that even a slight elevation in troponin concentration in asymptomatic patients with severe AS correlated with adverse outcomes, highlighting troponin as an independent predictor of adverse outcomes in patients with AS [23]. Our findings align, as nearly all patients had an elevated troponin post-procedure (> 99%), and 88% had at least a 20% relative increase in troponin. Interestingly, troponin levels after TAVI and the amount of increase before/after TAVI were not prognostic of adverse outcomes, aligning with some prior studies but contrasting others [23,24,25]. This suggest that the nature of troponin release during the procedure does not impact outcomes. Furthermore, we found that intrathoracic vascular access resulted in higher troponin concentrations and PPMI after TAVI compared to extrathoracic vascular access (54% vs 20%; p < 0.001). Despite this, the higher troponin levels did not result in higher rates of MACE or all-cause mortality at 1 year (13% vs 8%, p = 0.15; 20% vs 15%, p = 0.3). This finding is supported by existing literature [8], although some studies have reported better survival rates for transfemoral access [26, 27].

Second, VARC-2-defined PPMI was more common than VARC-3-defined PPMI (56% versus 4%). This finding is mainly based on the higher cutoff values for troponin [17]. VARC-3 criteria offered significantly better discrimination of short- and long-term outcomes. Both unadjusted 1-year mortality and MACE were significantly increased in patients with VARC-3-defined PPMI (p < 0.001 for both), whereas VARC-2-defined PPMI offered no distinction between groups (p = 0.76 and p = 0.11), corroborating the findings of Real et al.[17] The lack of a significant difference regarding death after 1 year between groups after adjustment for age and renal function (HR: 1.97 (0.94–4.13), p = 0.13) could have been influenced by the small number of events for VARC-3-defined PPMI. Nevertheless, even though VARC-3 appears to offer improved diagnostic clarity compared to VARC-2 and to better predict adverse outcomes, its specific impact on treatment strategies remains ambiguous. This raises the question of whether the differentiation provided by VARC-3 significantly alters clinical management or improves patient outcomes compared to the simpler approach of focusing on myocardial infarction as a primary diagnostic criterion. Especially type 1 myocardial infarction and some subtypes of type 2 myocardial infarction, such as coronary obstruction, embolism, or spasm, which should also be labeled as type 1 myocardial infarction, have shown to be reliable predictors of outcome. [28] Myocardial infarction either caused during the procedure or thereafter, by e.g., acute coronary occlusion, embolization, or acute plaque rupture/erosion, will result in immediate coronary interventions, rhythm monitoring, and dual antiplatelet therapy, whereas myocardial injury as defined by VARC-2 or VARC-3, highlighting a relevant increase in biomarkers irrespective of the reasons, results in no clear treatment strategy. Addressing these considerations is crucial for optimizing patient care and guiding future research in this field.

This study’s limitations primarily include the low number of events defined by the VARC-3 definition of PPMI, which hindered the ability to conduct a fully adjusted multivariable regression analysis. Additionally, the single-center design and retrospective nature of this analysis pose constraints. We acknowledge that external validation in a second, independent cohort would further strengthen the generalizability of our findings. However, due to the aforementioned limitations, this was not feasible in the present study. Our cohort, however, serves as a validation of previous research addressing the same hypothesis, reinforcing the consistency of the findings. Future studies should aim to replicate these results in additional cohorts to provide even stronger evidence. Despite these limitations, our cohort remains one of the largest to date using an hs-cTnT assay. Furthermore, the absence of significant differences in patient characteristics between those with and without troponin measurements mitigates this limitation to some extent, suggesting a balanced representation across the study population.

In conclusion, our 12-year study offers a comprehensive analysis of the incidence and outcomes of PPMI in TAVI patients, utilizing both VARC-2 and VARC-3 criteria. The high prevalence of elevated baseline hs-cTnT concentrations is indicative of the advanced age and pre-existing cardiovascular conditions in this patient cohort. The VARC-3 criteria have proven to be a more effective tool for outcome discrimination. However, its practical implications in clinical management, as compared to traditional myocardial infarction criteria, require further investigation. Elevated baseline hs-cTnT are strong predictors of mortality and MACE at 1 year, whereas post-TAVI hs-cTnT concentrations were not associated with adverse outcomes. Further research is necessary to validate our findings further and explore the clinical utility of elevated baseline hs-cTnT levels.

This study underscores the superiority of the VARC-3 criteria over VARC-2 in predicting post-TAVI, particularly highlighting the prognostic value of baseline hs-cTnT levels. It validates the relevance of VARC-3 for enhanced risk assessment, representing a significant advancement in patient care. Nonetheless, the integration of VARC-3 criteria into clinical practice and its impact on treatment strategies, especially in comparison to myocardial infarction diagnostics, warrants further research.