[Differences in hemodynamics of thromboembolic and primary pulmonary hypertension]

It is not clear whether right ventricle to pulmonary artery coupling is modified by the site of vascular obstruction in patients with chronic severe pulmonary hypertension. We compared invasively (Swan Ganz) and non-invasively (echo/ /Doppler) assessed hemodynamics between two groups of patients with severe chronic thromboembolic pulmonary hypertension (CTEPH)--(n = 6; 52 +/- 24 yrs) and pulmonary arterial hypertension (PAH) (n = 5; 42 +/- 9 yrs) who had similar invasively measured right ventricular systolic pressure (CTEPH: 78 +/- 14 mm Hg; PAH: 83 +/- 17 mm Hg; p = NS), mean pulmonary arterial pressure (CTEPH: 51 +/- 10; PAH 56 +/- 11 mm Hg, p = NS) and pulmonary vascular resistance (CTEPH: 15.6 +/- 4.4 l/min; PAH: 19.2 +/- 6.1; p = ns). Patients with CTEPH have significantly shorter acceleration time corrected to ejection time (RVET): (AcT/RVET % = 24 +/- 5% vs 32 +/- 6% in PAH; p = 0.04) as well as AcT corrected by RR distance was highly significantly shorter (8 +/- 2% vs 12 +/- 2%; p = 0.006). AcT in the CTEPH group was shorter than in the PAH (60 +/- 5 vs 75 +/- 15; p = 0.047). The mid-systolic deceleration was significantly more frequent in the CTEPH group than in the PAH group (88% vs 30%; p = 0.005). If the mid-systolic deceleration was present in patients with PAH, the time to mid-systolic deceleration (t-N) had tendency to be longer in CTEPH group (118 +/- 22 ms vs 150 +/- 28 ms in PAH; p = 0.09). Significant differences appeared after correction t-N to RVET (t-N/RVET % = 46 +/- 9% vs 61 +/- 4%; p = 0.027) and to RR interval (t-N/RVET % = 16 +/- 2% vs 24 +/- 1%; p = 0.002). Doppler derived RV index proposed by Tei was slightly higher in CTEPH (0.81 +/- 0.18 vs 0.65 +/- 0.32 in PAH) but not significantly. Taken together our observations indicate that dynamical coupling between RV and pulmonary arteries is more disturbed in CTEPH than in PPH despite similar levels of chronically increased PAP.