Pulmonary Vascular Disease |

Switch to Macitentan From Bosentan in Patients With Pulmonary Arterial Hypertension FREE TO VIEW

Aishwarya Thakur; Zeenat Safdar, MD
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Baylor College of Medicine, Houston, TX

Chest. 2014;146(4_MeetingAbstracts):842A. doi:10.1378/chest.1991732
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SESSION TITLE: DVT/PE/Pulmonary Hypertension Posters III

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PM

PURPOSE: Pulmonary arterial hypertension (PAH) is a progressive disease for which several therapies have become available. Macitentan was recently FDA approved for PAH treatment. Macitentan is an endothelin receptor antagonist (ETRA), which prevents the binding of endothelin-1 to both endothelin A and B receptors, similar to bosentan. We present our experience in switching to macitentan from bosentan in PAH patients to decrease the need for monthly liver function testing.

METHODS: At Baylor Pulmonary Hypertension Program, 11 PAH patients were switched from bosentan 125 mg orally twice a day to macitentan 10 mg orally daily (between October 2013 and January 2014) when macitentan became commercially available. We collected baseline data for these patients and post-switch data assessments by way of 6 minute walk distance (6MWD), BNP, ALT and AST levels, WHO functional class, Borg dyspnea score and presence of peripheral edema. Date presented as mean±SD. All analyses are two sided and significance judged as p value < 0.05.

RESULTS: Mean age was 61±11 (mean±SD) years, 10 were females; 5 were Caucasians, 1 was Asian, 2 were African-American and 3 were Hispanics. At baseline, six-minute walk was 338±76 meters, BNP was 128±235 pg/ml, AST was 12±21 U/L and ALT was 12±16 U/L. At baseline, WHO FC II status and edema was noted in 50% of the patients. After macitentan switch, follow-up data was available for 9 patients (2±1 months). As compared to baseline, follow-up BNP was 219±364 pg/ml (p=0.568), AST was 38±54 U/L (p=0.247), ALT was 22±14 U/L (p=0.130) and 6MWD was 356±153 meters (data available for 4 patients) (p=0.767). Edema was noted in same patients who had edema present at baseline. One patient with portopulmonary hypertension had macitentan stopped due to increase in AST and ALT (>5x ULN).

CONCLUSIONS: Transition to macitentan was well tolerated with no change in edema and liver function status except for one patient with portopulmonary hypertension. Switching between ETRA appears to be safe with maintained exercise capacity.

CLINICAL IMPLICATIONS: Patients on bosentan can be switched to macitentan to decrease the need for monthly liver function testing and to improve patient compliance.

DISCLOSURE: The following authors have nothing to disclose: Aishwarya Thakur, Zeenat Safdar

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