From the authors

I am grateful for the comments by A.H. Morice and coworkers, although their case report leaves several questions unanswered. More information than just the systolic pulmonary artery pressure is needed to appraise the haemodynamic response to tadalafil. One wonders whether this patient ever underwent pulmonary vasoreactivity testing. With such a dramatic fall in pulmonary artery pressure, the patient might fulfil the responder criteria (fall in mean pulmonary artery pressure by >10 mmHg to <40 mmHg in the presence of a cardiac output), and may, therefore, be a candidate for treatment with calcium channel blockers 1.

I agree with A.H. Morice and coworkers that the relatively short half-life of sildenafil (3–4 h) may be a drawback of this drug. Patients' compliance may rarely be an issue. However, the fluctuations in sildenafil plasma concentrations are poorly tolerated by some patients. A drug with a much longer half-life, such as tadalafil (∼18 h), might be advantageous, but caution is necessary. Ghofrani et al. 2 have demonstrated substantial variability in the haemodynamic effects of several phosphodiesterase-5 inhibitors. For the time being, there is a strong body of evidence for the safety and efficacy of sildenafil in pulmonary arterial hypertension, but there is a lack of comparable data for other phosphodiesterase-5 inhibitors, such as tadalafil.