Pulmonary arterial hypertension (PAH) is a severe and progressive disease. The genetic basis of idiopathic PAH is well recognized but rarely utilized in a diagnostic setting. Hundreds of mutations in seven genes have been reported to associate with idiopathic and familial forms of PAH. Next-generation sequencing for comprehensive genetic testing improves diagnostics, prognostics and treatment optimization of the index patient and allows an effective screening of asymptomatic family members. We utilized novel next-generation sequencing and bioinformatics approaches for genetic diagnostics of PAH. We applied Oligonucleotide-Selective Sequencing (OS-Seq) and custom data analysis and interpretation pipelines to identify pathogenic base substitutions, insertions and deletions in seven genes associated with PAH (BMPR2, BMPR1B, ACVRL1, ENG, SMAD9, CAV1 and exon 2 of KCNK3). Targeted sequencing covered all coding exons, exon-intron boundaries and known intronic mutations (12,638 bases). In OS-Seq, oligonucleotide-functionalized Illumina flow cells are used for both capture and sequencing of DNA. We automated target DNA capture and sequencing using the MiSeq Sequencing system. We analyzed 21 Finnish PAH patients. Sequencing depth was evaluated in each target base to demonstrate the efficiency of targeted sequencing. Average sequencing depth was 791 and 99.88% of target regions were covered >15x. We identified six idiopathic PAH patients with likely pathogenic variants in the BMPR2 gene. The identified mutations caused stop, frameshift and missense changes and had minor allele frequency of <0.001 reported in the 1000 genomes database. Mutations or potential variants were not identified from 6 other analyzed genes. Our results show that a comprehensive next-generation sequencing panel is an effective tool for genetic diagnostics of PAH and 29% of the Finnish PAH patients carried mutations in BMPR2.