RIGHT VENTRICULAR - PULMONARY VASCULAR COUPLING DURING EXERCISE IN PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION OR PULMONARY HYPERTENSION DUE TO LEFT HEART DISEASE

Pulmonary hypertension (PH) is a state of high afterload to the right ventricle (RV), which is described as afterload sensitive. The purpose of this study was to examine the effect of exercise on the relationship between RV systolic performance [measured as end-systolic elastance (Ees)], and RV afterload [measured as pulmonary arterial (PA) elastance (Ea)] between 2 groups of patients with pulmonary arterial hypertension (PAH) or PH due to left heart disease (PH-LHD).

Patients with suspected PH underwent right heart catheterization with cycle-ergometry and classified by their exercise hemodynamic responses: 1) Normal 2) PAH and 3) PH-LHD. RV, right atrium (RA), and PA pressures were recorded continuously and analyzed offline. As our lab previously reported, RV Ees and PA Ea were calculated using the single-beat method, and Ees:Ea ratio expresses RV-PA coupling. Ees:Ea is defined as uncoupled if < 0.8. Results were analyzed at semi-upright rest and exercise. Data is presented as Mean ± SD or Median [25th – 75th Percentiles]. We included 40 patients (35%Female; 58±15 years); exercise hemodynamic classification comprised 18 Normal, 11 PAH, and 11 PH-LHD. At rest Ea and Ees were significantly elevated in PAH (0.45[0.38-0.98], p=0.002 and 0.85[0.65-1.20], p=0.003) and PH-LHD (0.51[0.32-0.67], p=0.001 and 0.74[0.39-1.20], p=0.017) vs. Normal (0.22[0.17-0.27] and 0.41[0.29-0.54]). Ea increased significantly with exercise in PAH (0.60[0.51-1.36], p=0.003) and PH-LHD (0.59[0.37-0.91], p=0.002) compared to Normal (0.29[0.21-0.36]). Exercise was associated with a significant decline in Ees:Ea ratio in PH-LHD (∆-0.23±0.72, p=0.022). Ees:Ea ratio was uncoupled at rest/exercise in 6% of the Normal group, 55% of the PAH group and 36% of the PH-LHD group. Figure 1 illustrates the trend to Ees:Ea uncoupling if Ea increased by more than 0.2mmHg/mL. Compared to patients with preserved Ees:Ea coupling, patients with PH and Ees:Ea uncoupling with exercise demonstrated significantly higher increases in RA pressures (∆9±5mmHg vs ∆4±3mmHg, p=0.012) and more impaired stroke volume indexed to body surface area (∆3±9mL/m2 vs ∆12±8mL/m2 p=0.032).

During exercise, RV afterload increases in patients with PAH and PH-LHD. In both PH groups, the proportion of patients with Ees:Ea uncoupling was high, and the decline in Ees:Ea ratio reached statistical significance in PH-LHD. Uncoupling of the Ees:Ea ratio occurred with larger increases in Ea and was associated with evidence of impaired RV systolic and diastolic function with exercise. Limiting the increase in Ea with exercise and/or preservation of Ees:Ea coupling may optimize RV function in PH patients.