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Background: Soluble suppression of tumorigenicity (sST2) has been proposed to be a marker for biomechanical strain and a possible predictor of mortality in patients with chronic heart failure. The use of sST2 in pulmonary arterial hypertension (PAH) has not been well defined. Hypothesis: Plasma sST2 levels may correlate with the disease severity and predict clinical worsening in PAH. Methods: We performed a cohort study of 40 idiopathic PAH patients with data on demographics, exercise capacity, echocardiographic parameters, laboratory tests, hemodynamics, and medications. Plasma sST2 was assessed with the high-sensitivity ST2 ELISA kit at diagnostic catheterization. All patients were followed up from the date of blood sampling. The endpoint was clinical worsening. Results: sST2 was significantly elevated in patients with idiopathic PAH compared with control subjects (28.9 ± 13.9 vs 20.7 ± 7.5 ng/mL, P = 0.003). Pearson correlation analysis revealed that sST2 levels correlated with cardiac index (r = −0.534, P = 0.000) and pulmonary vascular resistance (r = 0.350, P = 0.027), and could reflect disease severity of PAH. After a mean follow-up of 14 ± 5 months, 12 patients showed clinical worsening. Receiver operating characteristic analysis suggested that sST2 levels >31.4 ng/mL discriminated clinical worsening with a sensitivity and specificity of 83.3% and 78.6%, respectively. Kaplan-Meier analysis showed that higher sST2 levels (>31.4 ng/mL) were associated with poor clinical outcomes (P = 0.008). Multivariate Cox regression analysis showed that sST2 was an independent predictor of clinical worsening (hazard ratio: 6.067, 95% confidence interval: 1.317-27.948, P = 0.021). Conclusions: sST2 correlates with disease severity and is a significant predictor of clinical worsening in patients with PAH.

In women with pulmonary hypertension, mean QTc and QTcd are positively correlated to mean pulmonary arterial pressure and are significantly increased in patients with severe pulmonary hypertension.

Background: Percutaneous transluminal angioplasty and stent implantation for stenotic lesions of renal arteries and other branches of the aorta in Takayasu's arteritis have been reported to show good outcomes. However, this form of therapy has been reported in few cases with pulmonary artery involvement. Hypothesis: The aim of this study was to evaluate the role of this interventional treatment for pulmonary stenosis due to Takayasu's arteritis. Methods: A total of 4 patients (3 female and 1 male, ages 30-40 yrs) with Takayasu's pulmonary arteritis underwent percutaneous transluminal balloon angioplasty and stent implantation and were followed up for 1 to 4 years. Results: One patient underwent balloon angioplasty alone, 3 patients underwent balloon angioplasty and stent implantation. The stenoses were relieved acutely, oxygen saturation improved immediately due to improvement in lung perfusion and relief of dyspnea. The pressure gradient fell from 58.3 ± 8.7 mm Hg to 14 ± 3.2 mm Hg and mean pulmonary arterial pressure decreased from 48.5 ± 12.0 mm Hg to 37.3 ± 6.0 mm Hg. At a follow-up period of 34.5 ± 15.8 months, the patient with balloon angioplasty alone developed a recurrence of symptoms 18 months after the procedure. The other 3 patients continued to be asymptomatic and the stent remained patent without restenosis after the procedure. Conclusion: Percutaneous transluminal angioplasty and stent implantation is a safe and effective treatment in patients with pulmonary stenosis caused by Takayasu's arteritis.