Impaired left atrial reservoir strain and its increase following transcatheter tricuspid valve repair is associated with reduced 1-year survival

AIMS: Left atrial reservoir strain (LARS) is a key echocardiographic marker for assessing left ventricular (LV) diastolic function. Besides the presence of atrial fibrillation (Afib+), significant tricuspid regurgitation (TR) has been shown to further impair left atrial (LA) function. This study aimed to (i) evaluate the effects of tricuspid edge-to-edge repair (T-TEER) on LA function in patients with heart failure with preserved ejection fraction (HFpEF) (NCT04782908) and (ii) determine if LARS and its changes after T-TEER are predictive of 1-year survival in a large-scaled T-TEER cohort.

METHODS: For the first aim HFpEF patients with relevant TR (HFpEF TR) undergoing T-TEER were included (Figure 1). All participants underwent cardiac magnetic resonance (CMR) imaging at baseline and 1-month post-T-TEER. Periprocedural invasive pressure-volume loop (PVL) analysis assessed immediate changes in LV diastolic function, quantified by the LV end-diastolic pressure (EDP) to end-diastolic volume (EDV) ratio (LVEDP/EDV). LARS was measured using biplane analysis with cardiovascular imaging software 42. For the second aim, LARS was evaluated in patients undergoing T-TEER from 2016 to 2021, with echocardiographic assessment via speckle tracking at baseline and 1-month follow-up. Associations of baseline LARS and its acute changes at 1-month with 1-year survival were analyzed using Kaplan-Meier estimates.

RESULTS: A total of 15 HFpEF TR patients were included, with follow-up CMR data collected at a median of 43 days (IQR 32 to 62). PVL analysis revealed a significant improvement in LV diastolic function post-T-TEER (LVEDP/LVEDV ratio: 0.13 mmHg/ml [IQR 0.10 to 0.17] vs. 0.10 mmHg/ml [IQR 0.08 to 0.13], p<0.01), primarily driven by an increase in LVEDV (p<0.01), while LVEDP remained stable (p=0.18). CMR follow-up showed a significant increase in LV stroke volume (LVSV, p<0.01), indicating enhanced ventricular filling. In HFpEF TR patients, LARS improved significantly (6.3% [IQR 5.1 to 8.4], p<0.01), with ΔLARS inversely correlating with ΔLVSV (r=0.56, p=0.03). No significant correlation was found between ΔLARS and ΔLVEDP/EDV, suggesting LARS changes relate more to LV filling than diastolic function.

In the larger T-TEER cohort of 200 patients, baseline LARS below the median of 8.4% (IQR 5.9 to 11.7) was associated with reduced 1-year survival (Figure 2A). Interestingly, improvement in LARS during 1-month follow-up, which occurred in 40% of patients, also correlated with impaired 1-year survival (Figure 2B).

CONCLUSION: T-TEER improves LV filling while maintaining LV filling pressures. LARS, reflecting passive LA stretching in response to LA pressures, increased following T-TEER, potentially due to LA overfilling in response to increased right ventricular forward flow following T-TEER despite improved LV filling. This either indicates a severe deterioration of LA function in patients with increased LARS during follow-up, contrasting with those exhibiting lower LARS and less LA overfilling. In line with this observation, an inverse relationship between increasing LARS post-T-TEER and 1-year survival was identified in this large-scaled cohort.