ABSTRACT
Pulmonary artery hypertension (PAH) is a progressive disorder which leads to heart failure and death. Development of dilated right ventricle (RV), progressive RV dysfunction and increased right atrial (RA) pressure make the RV transition from a compensated to a decompensated phase and eventually leads to heart failure. However, the relationship between elevated RA pressure and left ventricular contractility and ventricular arterial coupling (VAC) has not been well studied. 36 patients were recruited and underwent both right heart catheterization (RHC) and cardiac magnetic resonance (CMR). Left ventricular (LV) pressure-volume loops were reconstructed from RHC and CMR. LV contractility was assessed by end-systolic elastance (Ees) using single-beat method and arterial elastance (Ea) was estimated as the ratio of end-systolic pressure and stroke volume (SV). The VAC was calculated as the ratio of Ees and Ea (i.e. Ees/Ea). The results demonstrated a nonlinear relationship between RA pressure and Ees, RA pressure and VAC. Ees increased when RA pressure increased to 7 mmHg and then decreased when RA pressure exceeded 7 mmHg. Ees were 2.79 ± 1.61 mmHg/ml, 4.27 ±1 33 mmHg/ml, 2.69 ± 0.89 mmHg/ml and 2.36± 1.10 mmHg/ml at ascending quartiles of RA pressure, respectively (quartile 1: RAP≤5 mmHg; quartile 2: 5<; RAP≤7 mmHg; quartile 3: 7<; RAP 10 mmHg and quartile 4: RAP>10 mmHg). Similarly, VAC were 1.36 ± 0.61, 1.93±0.86, 1.16 ± 0.55 and 0.95± 0.27 the four quartiles (both ANOVA P <; 0.05). We found that there was a nonlinear relationship between RA pressure and LV contractility, and between RA pressure and ventricular-arterial coupling. A cut-off value of 7 mmHg of RAP may indicate a decompensated LV hemodynamics.
