This was a single-center prospective study in 106 CHD patients. Serum HMGB1 levels were measured by enzymelinked immunosorbent assay. HMGB1 levels were significantly increased in patients with PAH compared to patients without PAH (P < 0.01) and healthy controls (P < 0.001). HMGB1 levels significantly correlated with pulmonary arterial pressure (P < 0.001) and pulmonary vascular resistance (PVR) (P < 0.001). In patients with severe PAH, HMGB1 levels were significantly higher in patients with Eisenmenger syndrome (ES) than in patients exhibiting low PVR (P < 0.001). Severe PAH and ES was identified by serum HMGB1 with a cutoff value of 13.62 ng/mL (P < 0.001) with a specificity of 82.8% and a sensitivity of 90%, and a cutoff value of 21.62 ng/mL (P = 0.001) with a specificity of 85.2% and a sensitivity of 64.3%, respectively. HMGB1 levels were significantly decreased after sildenafil therapy for 6 months (P < 0.01).
Our study suggests that serum HMGB1 level may be used as a biomarker to identify PAH in CHD patients, assess pulmonary vascular remodeling, and evaluate the treatment response to sildenafil.