Key result
Patients with pulmonary arterial hypertension carrying pathogenic mutations in BMPR2, ACVRL1, or KCNA5 genes had significantly higher mean pulmonary artery pressure (57 vs 45 mmHg) compared to non-carriers.
Observational (n=91)
Yes
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Pathogenic mutations in BMPR2, ACVRL1, and KCNA5 genes are frequent in PAH patients and are associated with more severe hemodynamic impairment.
BACKGROUND: Pulmonary arterial hypertension (PAH) is a rare and progressive vascular disorder characterized by increased pulmonary vascular resistance and right heart failure. The aim of this study was to analyze the Bone Morphogenetic Protein Receptor 2 (BMPR2), Activin A type II receptor like kinase 1 (ALK1/ACVRL1) and potassium voltage-gated channel, shakerrelated subfamily, member 5 (KCNA5) genes in patients with idiopathic and associated PAH. Correlation among pathogenic mutations and clinical and functional parameters was further analyzed. METHODS AND RESULTS: Forty one patients and fifty controls were included in this study. Analysis of BMPR2, ACVRL1 and KCNA5 genes was performed by polymerase chain reaction (PCR) and direct sequencing. Fifty one nucleotide changes were detected in these genes in 40 of the 41 patients; only 22 of these changes, which were classified as pathogenic, have been detected in 21 patients (51.2%). Ten patients (62.5%) with idiopathic PAH and 10 (40%) with associated PAH showed pathogenic mutations in some of the three genes. Several clinical and hemodynamics parameters showed significant differences between carriers and non-carriers of mutations, being more severe in carriers: mean pulmonary artery pressure (p = 0.043), pulmonary vascular resistence (p = 0.043), cardiac index (p = 0.04) and 6 minute walking test (p = 0.02). This differences remained unchanged after adjusting for PAH type (idiopathic vs non idiopathic). CONCLUSIONS: Pathogenic mutations in BMPR2 gene are frequent in patients with idiopathic and associated PAH group I. Mutations in ACVRL1 and KCNA5 are less frequent. The presence of these mutations seems to increase the severity of the disease.
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Pousada et al. (2014) conducted an observational in Pulmonary Arterial Hypertension (n=91). Pathogenic mutations in BMPR2, ACVRL1 and KCNA5 genes vs. Non-carriers of mutations was evaluated on Mean pulmonary artery pressure (mPaP) (p=0.043). Patients with pulmonary arterial hypertension carrying pathogenic mutations in BMPR2, ACVRL1, or KCNA5 genes had significantly higher mean pulmonary artery pressure (57 vs 45 mmHg) compared to non-carriers.
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