Objectives .– Pulmonary hypertension (PH) and right ventricular (RV) systolic dysfunction are two prognostic factors in advanced heart failure (AdHF). RV and pulmonary artery coupling is one of the main determinants of global RV systolic function. Assessment of PH reversibility is routinely performed and uses different pharmacological protocols. Conversely, RV contractile reserve response during such pharmacological challenges has not been described. Our study compared RV contractile reserve during isolated inhaled nitric oxyde (iNO) challenge or comprehensive pharmacological test with diuretics, nitrates and positive inotropes in AdHF patients (pts) addressed for PH reversibility testing.

Methods .– All AdHF pts addressed in our institution for PH reversibility testing from November, 2009 till July, 2010 were screened. We included after informed consent every pts with a mean pulmonary arterial pressure (PAP) ≥ 25 mmHg. iNO testing was performed after basal measurements, followed by a comprehensive pharmacological test after 15 minutes of wash-out. RV systolic function was assessed at each step from transthoracic echocardiography with TAPSE and the maximal velocity of the systolic wave of tricuspid annulus in tissue doppler (Sa). Contractile reserve was defined as the difference between post-test TAPSE or Sa and basal or post-wash out TAPSE or Sa (ΔTAPSE, ΔSa).

Results .– Nineteen pts were included. Mean left ventricular ejection fraction was 22 ± 3%. Mean PAP was 40 ± 6 mmHg; pulmonary vascular resistances (PVR) were 4 ± 2 Wood Units. TAPSE was 14 ± 5 mm, Sa was 10 ± 3 cm/s. iNO had no significant effect on both PAP and PVR, and RV systolic function. Comprehensive pharmacological testing showed a significant decrease in mean PAP (−38.1%, P < 0.001), PVR (−39.6%, P = 0.03), and a significant RV contractile reserve (TAPSE: +22%, P = 0.004; Sa: +12%, P = 0.03). In a subgroup of 11 pts with basal Sa ≤ 10 cm/s, PAP and PVR at baseline were not different from the whole population of the study, and iNO did not reverse PH but led to a significant RV contractile reserve (ΔTAPSE: +2.5 ± 2 mm; ΔSa: +1 ± 0.05 cm/s). ΔSa with iNO was correlated with Δsystolic PAP ( r = −0.619, P = 0.04) and Δ transpulmonary pressure gradient ( r = −0.533, P < 0.05).

Conclusion .– As previously described by our team, isolated iNO challenge fails to prove PH reversibility in AdHF pts. However, iNO induces a significant RV contractile reserve in pts with the more altered RV, which is correlated to PAP and PVR decrease. These findings underline the importance of targeting ventriculo-arterial interaction in RV failure in AdHF, particularly in the more severe pts.