OBJECTIVES: To gain more knowledge of changes in main pulmonary artery flow and right ventricular mass and volumes in patients with pulmonary hypertension during epoprostenol therapy. METHODS: Eleven patients (9 women) were evaluated before the start of therapy and every 4 months thereafter. Right and left ventricular volumes and masses were measured by cine MRI. Flow was measured with MRI velocity quantification. At the same times, 6-min walking tests were performed. Right-heart catheterizations were performed at baseline and after 1 year. RESULTS: Right ventricular mass in the patient group was significantly higher from that in a control group of healthy volunteers (95 +/- 26 g vs 42 +/- 10 g, p < 0.05 [mean +/- SD]), whereas the stroke volume was lower (34 +/- 11 mL vs 81 +/- 11 mL, p < 0.05). The greatest improvement in right ventricular stroke volume (to 41 +/- 11 mL, p < 0.05) took place in the first 4 months. During the 1-year follow-up, right ventricular end-diastolic volume and mass did not change, and mean pulmonary artery pressure remained nearly stable at 55 mm Hg at baseline and 53 mm Hg after 1 year. Pulmonary vascular resistance decreased by 12.5% (p = 0.06). CONCLUSIONS: From these data we conclude that epoprostenol lowers pulmonary vascular resistance, leading to an increase in pulmonary artery flow. This increase in pulmonary artery flow corresponds well with the increase in 6-min walking distance and can be noninvasively monitored by MRI (flow quantification). Right ventricular dilatation and hypertrophy are not reversed by epoprostenol therapy, but do not progress either.
OBJECTIVES: To gain more knowledge of changes in main pulmonary artery flow and right ventricular mass and volumes in patients with pulmonary hypertension during epoprostenol therapy. METHODS: Eleven patients (9 women) were evaluated before the start of therapy and every 4 months thereafter. Right and left ventricular volumes and masses were measured by cine MRI. Flow was measured with MRI velocity quantification. At the same times, 6-min walking tests were performed. Right-heart catheterizations were performed at baseline and after 1 year. RESULTS: Right ventricular mass in the patient group was significantly higher from that in a control group of healthy volunteers (95 +/- 26 g vs 42 +/- 10 g, p < 0.05 [mean +/- SD]), whereas the stroke volume was lower (34 +/- 11 mL vs 81 +/- 11 mL, p < 0.05). The greatest improvement in right ventricular stroke volume (to 41 +/- 11 mL, p < 0.05) took place in the first 4 months. During the 1-year follow-up, right ventricular end-diastolic volume and mass did not change, and mean pulmonary artery pressure remained nearly stable at 55 mm Hg at baseline and 53 mm Hg after 1 year. Pulmonary vascular resistance decreased by 12.5% (p = 0.06). CONCLUSIONS: From these data we conclude that epoprostenol lowers pulmonary vascular resistance, leading to an increase in pulmonary artery flow. This increase in pulmonary artery flow corresponds well with the increase in 6-min walking distance and can be noninvasively monitored by MRI (flow quantification). Right ventricular dilatation and hypertrophy are not reversed by epoprostenol therapy, but do not progress either.
Authors: S A van Wolferen; A Boonstra; J T Marcus; K M J Marques; J G F Bronzwaer; P E Postmus; A Vonk-Noordegraaf Journal: Heart Date: 2006-12 Impact factor: 5.994
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