Annual Meeting of the Belgian Society of Cardiology edition:29th location:Brussels, Belgium date:28-01-2010
Background. The normal pulmonary vasculature can easily accomodate the increment in right ventricular output as seen in the setting of exercise. However, persistent increased pulmonary blood flow causes progressive lesions of the pulmonary vasculature. In order to detect early vascular disease, it has been suggested to measure right ventricular systolic pressure during incremental exercise. However, RVSP measurements during exercise should be used with caution in patients with left-to-right shunt. A prospective, single centre study was initiated to evaluate pulmonary hemodynamics in ASD patients and aimed to identify ASD patients with mild pulmonary vascular disease using stress echocardiography.
Methods. Tricuspid regurgitation velocity (TRV), left ventricular (LV) and right ventricular (RV) velocity time integral (VTI) were measured by Doppler echocardiography during supine bicycle exercise in 10 patients with an open ASD, 21 patients with a closed ASD and 15 healthy controls. The protocol started at 25 Watts with an increment of 25 Watts at every 2-minute stage. 2D, Doppler and Tissue Doppler images were digitized at each stage for off-line analysis. Right ventricular systolic pressure (RVSP) was calculated using the simplified Bernouillie equation; total pulmonary vascular resistance index (TPVR-I) at each stage was estimated as the ratio of RVSP and RV cardiac index. The slope and intercept of each individual multipoint RVSP – RV cardiac output (CO) plot was calculated using linear regression analysis.
Results. RVSP at rest was not statistically different between patient groups (P = 0.625). However, patients with open ASD had significantly higher RVSP at maximal exercise than patients with closed ASD (59.3 versus 42.4; mmHg; P = 0.003) and controls (59.3 versus 46.9 mmHg; mmHg; P = 0.019). The increase in pulmonary artery pressures was higher in patients with open ASD compared to patients with a repaired ASD (40.0 versus 19.3; mmHg; P < 0.001) and controls (40.0 versus 25.3; mmHg; P = 0.016). RV cardiac output at rest was higher in patients with an open ASD than in patients with a repaired ASD or in healthy controls (6.0 versus 4.3 and 3.7; L/min; P < 0.001 and P = 0.001 respectively). RV cardiac output at maximal effort was higher in patients with an open ASD than in patients with a repaired ASD (13.8 versus 9.8; L/min; P = 0.004). The increase in RV cardiac output was not statistically different between patient groups (P = 0.094). TPVR-I at rest was lower in patients with an open ASD than in patients with a closed ASD or controls (3.54 versus 5.72 and 6.08; mmHg/L/min/kg; P = 0.020 and P 0.001 respectively).
The slope of the multipoint RVSP – RV cardiac output plots tended to be steeper in patients with open ASD than in patients with an repaired ASD or healthy controls (5.2 versus 3.55 and 3.43; mmHg/L/min; P = 0.091 and P = 0.063 respectively).
Conclusions. The increase of pulmonary artery pressures during exercise is higher in patients with an open ASD than in patients with a closed ASD and controls. This response is likely due to a combination of left-to-right shunting and a decreased capacity of the pulmonary vasculature to lower PVR at high RV cardiac output in patients with an open ASD. Multipoint RVSP - RV CO plot analysis may be useful to detect early pulmonary vascular disease in these patients.