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Background: Amplatzer occluder and Cardio-O-fix occluder are currently used in percutaneous closure of patent foramen ovale. However, there is still a lack of relevant reports comparison the differences between them. The aim of this study was to evaluate the short-term and mid-term safety and efficacy of the Cardi-O-fix occluder in preventing recurrent cerebrovascular events in patients with a patent foramen ovale (PFO)., Methods: We enrolled 246 patients (105 men) with a PFO from May 30, 2013 to March 30, 2015 in this single-center prospective study. All patients were treated by PFO interventional closure, with the Cardi-O-fix PFO occluder being used in 180 patients and the Amplatzer PFO occluder being utilized in the remaining 66 patients. After the procedure, we verified the safety and efficacy of different devices using contrast transthoracic echocardiography., Results: Neither recurrent stroke nor death was encountered during the follow-up of 12 months. Transient ischemic attack (TIA) was noted in 2 patients (1.1%) in the Cardi-O-fix PFO occluder group, and 1 patient suffered from TIA (1.5%) in the Amplatzer PFO occluder group. Among them, only 1 patient exhibited a small right to left shunt (RLS). There was no statistical difference in recurrent cerebral ischemic events. Three cases of paroxysmal atrial fibrillation were observed in the Cardi-O-fix PFO occluder group. One reverted spontaneously to sinus rhythm and the other 2 cases had pharmacologic conversion to sinus rhythm. One case of paroxysmal atrial fibrillation occurred in the Amplatzer group, which underwent pharmacologic conversion to sinus rhythm. There was no significant difference between the 2 groups regarding incidence of arrhythmia. No occluder translocation, erosion, pericardial effusion, and puncture site bleeding were observed in the 2 groups within 12 months of follow-up. The complete closure rates of the Cardi-O-fix and Amplatzer PFO occluder devices at the 12 months after the procedure were 73.9% and 63.6%, respectively, and the effective closure rates were 90.6% and 86.4%, respectively. There was no statistically significant difference in the complete closure rate and effective occlusion rate (P > 0.05) between the devices., Conclusions: There was no significant difference in the short- and mid-term efficacy and safety between the Cardi-O-fix PFO occluder and Amplatzer PFO occluder. The efficacy and safety of the Cardi-O-fix occluder were comparable to those of the Amplatzer PFO occluder.

Endothelial dysfunction and inflammation are believed to be 2 primary instigators of pulmonary arterial hypertension (PH). C1q/TNF-related protein 9 (CTRP9) plays important roles in anti-inflammation and improvement of epithelial function. However, the role of CTRP9 in the progression of PH remains still unclear. In this study, the role and mechanism of CTRP9 in the PH progression were explored. First, serum CTRP9 contents and CTRP9 mRNA expression in the pulmonary artery epithelial cells from patients with PH were detected. Our data on enzyme-linked immunosorbent assay and real-time quantitative Polymerase Chain Reaction showed that CTRP9 mRNA and protein content were markedly downregulated in the patients with PH. Then the pcDNA-CTRP9 expression vector or CTRP9 siRNA was transfected into the primary pulmonary artery epithelial cells from the patients with PH in vitro. CTRP9 overexpression significantly improved endothelial NOS protein expression and reduced the secretion of endothelin-1 (ET-1) and matrix metalloproteinase-2 (MMP-2), whereas knockdown of CTRP9 sharply reduced eNOS protein expression and promoted the secretion of ET-1 and MMP-2 in the cultured human epithelial cells. Moreover, the levels of phosphatidylinositol 3-kinase (PI3K) and pAkt were reduced in the epithelial cells and CTRP9 overexpression activated the PI3K/Akt pathway. CTRP9 could inhibit cell apoptosis and eNOS expression reduction in the cells pretreated with the PI3K/Akt inhibitor LY294002 and resist LY294002-induced ET-1 and MMP-2 secretion. Finally, to verify the role of CTRP9 in the progression of PH in vivo, the pcDNA-CTRP9 expression vector or CTRP9 siRNA was intravenously injected into rats with PH. Pulmonary arterial pressures of the rats were notably reduced by the pcDNA-CTRP9 injection and elevated by the CTRP9 siRNA injection. In conclusion, CTRP9 ameliorated PH by attenuating inflammation and improving endothelial cell survival and function.