Key result
A tricuspid coaptation gap ≥10 mm was independently associated with higher all-cause mortality (adjusted HR 1.47) compared to a gap <10 mm in patients with significant isolated functional tricuspid regurgitation.
Why the study?
Due to inherent limitations of EROA, the study evaluated whether tricuspid coaptation gap would be more suitable for defining very severe tricuspid regurgitation and predicting outcomes.
Does using a tricuspid coaptation gap ≥10 mm compared to an effective regurgitant orifice area ≥60 mm² better predict mortality in patients with isolated functional tricuspid regurgitation?
Cohort (n=606)
Yes
Does using a tricuspid coaptation gap ≥10 mm compared to an effective regurgitant orifice area ≥60 mm² better predict mortality in patients with isolated functional tricuspid regurgitation?
Answers are grounded in this paper and cite their sources.
In patients with isolated functional tricuspid regurgitation, a tricuspid coaptation gap ≥10 mm is a superior predictor of all-cause and cardiovascular mortality compared to an effective regurgitant orifice area ≥60 mm².
Introduction Various definitions of very severe (VS) tricuspid regurgitation (TR) have been proposed based on the effective regurgitant orifice area (EROA) or tricuspid coaptation gap (TCG). Because of the inherent limitations associated with the EROA, we hypothesized that the TCG would be more suitable for defining VSTR and predicting outcomes. Materials and methods In this French multicentre retrospective study, we included 606 patients with ≥moderate-to-severe isolated functional TR (without structural valve disease or an overt cardiac cause) according to the recommendations of the European Association of Cardiovascular Imaging. Patients were further stratified into VSTR according to the EROA (≥60 mm 2 ) and then according to the TCG (≥10 mm). The primary endpoint was all-cause mortality and the secondary endpoint was cardiovascular mortality. Results The relationship between the EROA and TCG was poor ( R 2 = 0.22), especially when the size of the defect was large. Four-year survival was comparable between patients with an EROA <60 mm 2 vs. ≥60 mm 2 (68 ± 3% vs. 64 ± 5%, p = 0.89). A TCG ≥10 mm was associated with lower four-year survival than a TCG <10 mm (53 ± 7% vs. 69 ± 3%, p < 0.001). After adjustment for covariates, including comorbidity, symptoms, dose of diuretics, and right ventricular dilatation and dysfunction, a TCG ≥10 mm remained independently associated with higher all-cause mortality (adjusted HR[95% CI] = 1.47[1.13–2.21], p = 0.019) and cardiovascular mortality (adjusted HR[95% CI] = 2.12[1.33–3.25], p = 0.001), whereas an EROA ≥60 mm 2 was not associated with all-cause or cardiovascular mortality (adjusted HR[95% CI]: 1.16[0.81–1.64], p = 0.416, and adjusted HR[95% CI]: 1.07[0.68–1.68], p = 0.784, respectively) Conclusion The correlation between the TCG and EROA is weak and decreases with increasing defect size. A TCG ≥10 mm is associated with increased all-cause and cardiovascular mortality and should be used to define VSTR in isolated significant functional TR.
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Bohbot et al. (2023) conducted a cohort in Isolated functional tricuspid regurgitation (n=606). Tricuspid coaptation gap ≥10 mm vs. Tricuspid coaptation gap <10 mm was evaluated on All-cause mortality (HR 1.47, 95% CI 1.13-2.21, p=0.019). A tricuspid coaptation gap ≥10 mm was independently associated with higher all-cause mortality (adjusted HR 1.47) compared to a gap <10 mm in patients with significant isolated functional tricuspid regurgitation.
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