Cor et vasa
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Ten patients with severe pulmonary hypertension due to Toxic Oil Syndrome underwent cardiac catheterization to analyse the acute effect of intrapulmonary injection of 1.25 mg of enalaprilat. Haemodynamic parameters were obtained at basal state, 15, 30, 45 and 60 minutes after administration of the drug. Enalaprillat did not produce any statistically significant changes in pulmonary pressures and resistances or cardiac output. This lack of response is unknown but may be related to the presence of endothelial damage and fixed pulmonary vascular lesions observed at autopsy in three patients.
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The authors studied the pulmonary haemodynamic response to exercise in eleven patients with toxic oil syndrome (TOS) (mean age 38.3 +/- 15.7 years; 10 women, 1 man) and abnormal pulmonary diffusing capacity (39.1 +/- 10.3% of predicted value) without clinical evidence of pulmonary hypertension. Eight patients had normal pulmonary pressure at rest (mean PAP less than 25 mmHg) and three showed mild pulmonary hypertension. ⋯ Pulmonary artery oxygen saturation decreased from 72.9 +/- 1.9% at rest to 52.3 +/- 10.1% during exercise (p less than 0.01). In conclusion, in this subset of TOS patients, an early diagnosis of their subclinical pulmonary hypertension can be made on the basis of the presence of dyspnoea and abnormal pulmonary diffusing capacity for carbon monoxide and can be then confirmed with the exercise haemodynamic test.
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Ten patients with severe pulmonary hypertension due to Toxic Oil Syndrome (TOS) (3 men, 7 women; mean age 27.9 +/- 11.23 yrs.) are presented. The pulmonary vessels were examined with a micromorphometric technique. All patients had intimal fibrosis of the arteries and veins. ⋯ Plexiform lexions were found in eight cases. It is concluded that TOS can produce severe pulmonary hypertension histologically undistinguishable from the primary form. TOS can be added to the list of diseases causing plexogenic arteriopathy.