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University of Freiburg, Freiburg, Germany.
To the Editors:
Several studies have proved that inhibitors of phosphodiesterase (PDE)5 are potent compounds for lowering pulmonary pressure in pulmonary arterial hypertension. With great interest we read the study conducted by Reichenberger et al. 1 about the effect of sildenafil on portopulmonary hypertension (PPHTN). This is a specific condition characterised by an elevated pulmonary arterial pressure (PAP), increased pulmonary vascular resistance and a normal wedge pressure in a setting of underlying portal hypertension. Effective medical therapy is of great importance, as a markedly increased pulmonary pressure has a very poor prognosis in cirrhotic patients and is a contraindication for liver transplantation. The results of the studies by Reichenberger et al. 1 and others 2, 3 show that in these patients, inhibitors of PDE5 also lower PAP. However, Reichenberger et al. 1 focused on the effect of sildenafil on PAP; the potential effect of this drug on portal pressure was not investigated.
In a recent study, we showed that the PDE5 inhibitor vardenafil lowers portal pressure and increases portal blood flow in healthy subjects as well as in patients with liver cirrhosis 4. We also found that sildenafil and tadalafil had similar effects (unpublished data). Recently, we investigated the acute effect of tadalafil on portal and pulmonary haemodynamics simultaneously in a patient with PPHTN.
In the 55-yr-old patient, alcoholic Child A cirrhosis had been diagnosed 7 yrs before. Alcohol consumption had stopped since cirrhosis was diagnosed. The reason for admission was increasing dyspnoea at physical exercise. The patient was taking no medication at the time of the study. The patient was obese (186 cm, 108 kg, body mass index 31.2), his blood pressure was 140/105 mmHg and his cardiac frequency was 79 bpm. ECG and Doppler echocardiogram showed right heart enlargement with systolic PAP 
75 mmHg. Spirometry show<1?show=[dh]?>ed a normal vital capacity (5.3 L, 103%) and forced expiratory volume in one second (3.3 L, 86%). Abdominal duplexsonography showed a slow (9 cm·s-1) and reduced portal flow, 0.15 L·min-1 with intrahepatic retrograde perfusion. The umbilical vein was reopened and a large splenorenal shunt was detected. Second-grade oesophageal varices were found on endoscopy.
After counselling the local ethics committee, we investigated the effect of tadalafil, a selective inhibitor of PDE5, on portal and pulmonary haemodynamics. Catheters were introduced into the pulmonary artery and one of the liver veins simultaneously. Haemodynamic parameters were recorded every 15 min for 75 min. After 10 mg tadalafil, mean PAP was reduced from 45 to 38 mmHg (fig. 1
). Cardiac index increased from 3.02 to 3.24 L·min-1·m-2 and pulmonary vascular resistance decreased from 459 to 351 dynes·s·cm-5, while arterial oxygen pressure increased from 70.5 to 78.2 mmHg. Hepatovenous pressure gradient decreased from 10 to 7 mmHg and systemic arterial pressure decreased from 167/89 to 152/87 mmHg. Our results show, that PDE5 inhibition reduces portal venous and PAP in this patient with PPHTN.
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In conclusion, by using inhibitors of phosphodiesterase 5 in portopulmonary hypertension, a double goal may be achieved: a reduction of elevated portal and pulmonary pressure simultaneously.
REFERENCES
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) and hepatovenous pressure gradient (HVPG; •) under inhibition of phosphodiesterase 5 in a patient with portopulmonary hypertension. 
: cardiac index (CI); 
: central venous pressure (CVP).