Clinical outcomes of transcatheter mitral edge-to-edge repair in cancer survivors according to MR etiology
L Barreiro Mesa, C Barreiro Mesa, R Gonzalez Manzanares, S Ojeda Pineda, M Pan Alvarez-Ossorio, F Carrasco Chinchilla, T Benito-Gonzalez, I Pascual, L Nombela Franco, A M Serrador Frutos, R Estevez Loureiro, M Xavier Freixa, D Mesa RubioAbstract
Background/Introduction
In cancer survivors, severe mitral regurgitation (MR) can be a direct consequence of therapy-related cardiotoxicity (such as functional MR due to anthracycline-induced dysfunction or degenerative MR following left-sided chest radiotherapy) or an incidental overlap. The prognostic implications of the MR etiology in this high-risk population undergoing percutaneous treatment remain underexplored.
Purpose
To evaluate whether the cardiotoxic etiology of MR impacts the clinical outcomes of patients with a prior cancer diagnosis undergoing mitral transcatheter edge-to-edge repair (M-TEER).
Methods
We conducted a multicenter observational sub-study from the Spanish M-TEER registry, including 155 cancer survivors treated with M-TEER. Patients were stratified into two groups based on MR etiology: MR attributable to cardiotoxicity (MR-CTOX) and MR not attributable to cardiotoxicity (MR-NCTOX). The primary endpoint was a composite of all-cause mortality or unplanned heart failure (HF) hospitalization at mid-term follow-up.
Results
Among the 155 patients, 60 (38.7%) had MR-CTOX and 95 (61.3%) had MR-NCTOX. Baseline characteristics differed significantly: MR-CTOX patients were younger (71.8 vs. 75.5 years, p=0.035), more frequently female (56.7% vs. 26.3%, p<0.001), had a higher prevalence of hematological malignancies (35.0% vs. 10.5%, p<0.001), and presented a lower EuroSCORE II (4.6 vs. 6.5, p=0.012). They also had lower rates of comorbidities such as diabetes, hypertension, and anemia (all p<0.05). During follow-up, the primary composite endpoint occurred at similar rates between groups: 29 (48.3%) in MR-CTOX and 47 (49.5%) in MR-NCTOX (HR 1.05, 95% CI 0.66-1.67, p=0.824). There were no significant differences in all-cause mortality (36.7% vs. 32.6%, p=0.498) or HF hospitalization (33.3% vs. 33.7%, p=0.840) (Figure 1). In multivariable Cox regression analysis, a cardiotoxic etiology of MR was not an independent predictor of the primary endpoint (HR 1.41, 95% CI 0.83-2.39, p=0.203). Independent predictors of adverse outcomes were diabetes, anemia, EuroSCORE II, and hematological malignancies (Figure 2).
Conclusion(s)
MR attributable to cancer-therapy cardiotoxicity is common among cancer survivors undergoing M-TEER. Despite differences in baseline clinical profiles, the origin of MR (cardiotoxic vs overlap) does not significantly impact mid-term mortality or HF hospitalizations, suggesting that M-TEER is a safe and equally effective therapeutic option regardless of MR etiology in this population.