Abstract 220: Contrasting Mechanisms of Functional TR With and Without Pulmonary Hypertension
Background: Mechanism of functional (no intrinsic valve disease) tricuspid regurgitation (TR) remains unclear and the role of valve deformation (tenting) vs. annular enlargement is uncertain.
Methods: To verify the hypothesis that pulmonary hypertension affects mechanisms of functional TR, we performed a triple quantitative (tricuspid valve deformation, regurgitation, right ventricular and atrial quantitation) study. We enrolled 141 patients with functional TR (no valve disease,, left heart disease, pacemaker, or congenital disease) without pulmonary hypertension (PHT−) and 141 patients with functional TR and systolic pulmonary pressure>50mmHg (PHT+) matched for age (71.4±1.2 vs.70.3±1.2 years, p=0.56) sex(32.3% vs. 31.2% male p=0.64 ), and regurgitant orifice (ERO, 0.47±0.02 vs. 0.44±0.02 mm2 p=0.33).
Results: Patients with PHT− vs. PHT+ had smaller right atrial area (23.5±8.2 vs 26.2±0.7 cm2, p=0.01), and right ventricular (RV) area (27.8±9.4 vs. 31.1±1.0 cm2, p=0.02). The pattern of RV remodeling was different between groups. PHT− vs. PHT+ displayed increased RV basal diameter (4.5±0.1 vs. 3.8±0.1cm p<0.0001), but lower RV length (7.5±0.1 vs. 8.7±0.1cm p<0.0001), and RV wall thickness (5.9±0.2 vs. 9.4±0.2mm p<0.0001). Valve deformation was also significantly different between groups. PHT− vs. PHT+ displayed increased annular width (3.5±0.05 vs. 3.2±0.05 cm p=0.0008), but lower tenting area (0.8±0.05 vs.1.3±0.05cm2 p<0.0001), and tenting height (0.41±0.02 vs. 0.8±0.02cm, p<0.0001).
Conclusions: Mechanistic aspects of functional tricuspid are profoundly different depending on causal pulmonary hypertension. Despite similar TR severity, RV remodeling differs, with increased RV width rather than height in PHT− while in PHT+, the RV is larger and remodeling affects both width and length. This more extensive RV remodeling with PHT+ is associated with apical displacement of the valve apparatus and larger valve tenting contributing to the TR. Conversely, in PHT−, RV widening is associated with annular dilatation, which is the major mechanism of TR. These mechanistic data provide important clues on approaches to surgical correction of functional TR, usefulness of annuloplasty and the potential for TR recurrence post-repair.