The hemodynamic basis of exercise intolerance in tricuspid regurgitation.

Abstract

Patients with severe tricuspid regurgitation (TR) frequently present with exertional fatigue and dyspnea, but the hemodynamic basis for exercise limitation in people with TR remains unclear. Twelve subjects with normal left ventricular (LV) ejection fraction and grade ≥3 TR underwent high-fidelity invasive hemodynamic exercise testing with simultaneous expired gas analysis and were compared with 13 age- and sex-matched controls. At rest, TR subjects had lower pulmonary blood flow (3.6±0.4 versus 5.1±1.9 L/min; P=0.01), increased right atrial pressure (12±5 versus 4±1 mm Hg; P=0.0002), and higher pulmonary capillary wedge pressure (17±5 versus 9±3 mm Hg; P=0.0001). However, LV transmural pressure (pulmonary capillary wedge pressure-right atrial pressure), which reflects LV preload independent of right heart congestion and pericardial restraint, was similar in TR and controls (6±3 versus 4±2 mm Hg; P=0.3). With exercise, TR subjects displayed lower peak VO2 (10.3±2.8 versus 13.8±4.2 mL/min per kg; P=0.02), lower pulmonary blood flow (6.4±1.3 versus 10.3±3.3 L/min; P=0.001), and less increase in pulmonary blood flow relative to VO2 (+4.6±1.1vs +6.2±0.7; P=0.001). TR subjects displayed higher pulmonary capillary wedge pressure with exercise, but this was solely because of RA hypertension (27±9 versus 8±3 mm Hg; P<0.0001), because LV transmural pressure dropped with exercise in subjects with TR (-5±6 versus +3±3 mm Hg; P=0.0007), suggesting inadequate LV diastolic filling, despite high pulmonary capillary wedge pressure. Impaired exercise capacity in people with severe TR is related to low cardiac output reserve relative to metabolic needs, coupled with elevated systemic and pulmonary venous pressures. Left heart pressures are elevated with exercise in subjects with TR, despite low LV preload, secondary to enhanced ventricular interaction.