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Effects of Nintedanib on Pulmonary Hypertension in IPF Patients
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A1651 - Effects of Nintedanib on Pulmonary Hypertension in IPF Patients
Author Block: M. Tahara, K. Oda, T. Kido, K. Yatera; Respiratory Medicine, University of Occupational and Environmental Health, Fukuoka, Japan.
Background: Nintedanib, a tyrosine kinase (TKI) targeting the PDGF, FGF, and VEGF receptor, slows a reduction of the rate of decline in forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). It has been shown that VEGF, FGF and PDGF receptor inhibition by BIBF1000 does not adversely affect the morphology or RV function in rats. However, a clinical study to confirm effect of nintedanib treatment of pulmonary hypertension in human IPF is warranted.Methods: In the present study, we have investigated the effect of nintedanib to the pulmonary hypertension in IPF patients by a prospective cohort study. The diagnosis of IPF was based on the criteria in the ATS/European Respriratory Society guidelines. During 24 weeks follow-up, systolic pulmonary artery pressure (sPAP) by transthoracic echocardiography, serum B type natriuretic peptide (BNP) and the ratio of pulmonary artery diameter to ascending aorta (rPA) diameter on chest CT were assessed at four periods (baseline, 4weeks, 12weeks, and 24weeks after starting nintedanib treatment). Result: A total of consecutive 21 IPF patients were enrolled. Median patient age was 73 years (age range: 57-80 years, 81% male). Median FVC% pred was 60% and GAP score was 5 at baseline. Median sPAP (mmHg) were 35.0, 41.4, 41.1 and 37.2, at beseline, 4weeks, 12weeks, and 24weeks after starting nintedanib treatment, respectively (P=0.108). Similarly, there are no significant changes during the follow-up in BNP (37.0, 33.6, 45.3, 37.0 pg/mL, P=0.627) and rPA (0.85, 0.82, 0.83, 0.83, P=0.692). Conclusion: Our findings suggest that treatment with nintedanib does not adversely affect pulmonary hypertension in IPF patients.
Author Block: M. Tahara, K. Oda, T. Kido, K. Yatera; Respiratory Medicine, University of Occupational and Environmental Health, Fukuoka, Japan.
Background: Nintedanib, a tyrosine kinase (TKI) targeting the PDGF, FGF, and VEGF receptor, slows a reduction of the rate of decline in forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). It has been shown that VEGF, FGF and PDGF receptor inhibition by BIBF1000 does not adversely affect the morphology or RV function in rats. However, a clinical study to confirm effect of nintedanib treatment of pulmonary hypertension in human IPF is warranted.Methods: In the present study, we have investigated the effect of nintedanib to the pulmonary hypertension in IPF patients by a prospective cohort study. The diagnosis of IPF was based on the criteria in the ATS/European Respriratory Society guidelines. During 24 weeks follow-up, systolic pulmonary artery pressure (sPAP) by transthoracic echocardiography, serum B type natriuretic peptide (BNP) and the ratio of pulmonary artery diameter to ascending aorta (rPA) diameter on chest CT were assessed at four periods (baseline, 4weeks, 12weeks, and 24weeks after starting nintedanib treatment). Result: A total of consecutive 21 IPF patients were enrolled. Median patient age was 73 years (age range: 57-80 years, 81% male). Median FVC% pred was 60% and GAP score was 5 at baseline. Median sPAP (mmHg) were 35.0, 41.4, 41.1 and 37.2, at beseline, 4weeks, 12weeks, and 24weeks after starting nintedanib treatment, respectively (P=0.108). Similarly, there are no significant changes during the follow-up in BNP (37.0, 33.6, 45.3, 37.0 pg/mL, P=0.627) and rPA (0.85, 0.82, 0.83, 0.83, P=0.692). Conclusion: Our findings suggest that treatment with nintedanib does not adversely affect pulmonary hypertension in IPF patients.
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