Elevated Right Atrial Pressure Associated with Alteration of Left Ventricular Contractility and Ventricular-Arterial Coupling in Pulmonary Artery Hypertension

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 (E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> ) using single-beat method and arterial elastance (E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">a</inf> ) was estimated as the ratio of end-systolic pressure and stroke volume (SV). The VAC was calculated as the ratio of E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> and E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">a</inf> (i.e. E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> /E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">a</inf> ). The results demonstrated a nonlinear relationship between RA pressure and E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> , RA pressure and VAC. E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> increased when RA pressure increased to 7 mmHg and then decreased when RA pressure exceeded 7 mmHg. E <inf xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">es</inf> 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.