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Sildenafil Alleviates Pulmonary Hypertension
Lancet
09/19/2002
By Harvey McConnell
Sildenafil has been found to cause preferential pulmonary vasodilation and to improve gas exchange in patients with severe lung fibrosis and secondary pulmonary hypertension.
Based on their findings, Dr Hans Ghofrani and colleagues at the Department of Internal Medicine, University Hospital, Giessen, Germany, think that "controlled randomized trials should be done to confirm our findings.
"However, the unique profile of sildenafil, not previously shown for a systemically administered agent, suggests that the drug is a promising candidate for long-term treatment of secondary pulmonary hypertension in lung fibrosis."
Among patients with primary pulmonary hypertension, intravenous epoprostenol acts as a potent pulmonary vasodilator, which improves exercise tolerance and survival after long-term infusion, the clinicians point out. However, in the presence of interstitial lung disease, systemic administration of vasodilators can increase blood flow to poorly-ventilated or non-ventilated areas of the lung by interfering with the physiological hypoxic vasoconstrictor mechanism, thereby worsening pre-existent ventilation/perfusion mismatch and shunt flow.
Dr Ghofrani and colleagues did a randomised controlled trial to compare the acute effects of oral sildenafil (Viagra) or intravenous epoprostenol after the inhalation of nitric oxide in 16 individuals with pulmonary hypertension secondary to lung fibrosis.
The clinicians found that pulmonary vascular resistance index was reduced by nitric oxide, epoprostenol, and sildenafil. However, ratio of pulmonary to systemic vascular resistance decreased only in individuals who received nitric oxide and sildenafil. No adverse effects were recorded.
"Our findings indicate that sildenafil causes pulmonary vasodilation in patients with lung fibrosis and pulmonary hypertension, with the overall potency corresponding to that of intravenous epoprostenol," the researchers said. "Furthermore, by contrast with infused epoprostenol, sildenafil showed selectivity for well ventilated areas of the lung, resulting in an improvement rather than a deterioration in gas exchange."
Enhancement of the effect of locally generated nitric oxide by sildenafil might cause an overall decrease in pulmonary vascular resistance while maintaining ventilation/perfusion matching, the clinicians conclude.
Lancet 2002; 360: 895-900
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