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Objective: To investigate the in vivo gene expression of adenovirus-mediated human tissue factor pathway inhibitor (hTFPI) and its inhibition effects on intimal proliferation in rabbit carotid arteries after balloon injury., Methods: Rabbits underwent carotid artery balloon injuries were treated with Ad-TFPI (n = 25), Ad-LacZ (n = 25) or PBS (n = 10), respectively. Sham operated rabbits (n = 10) serve as normal controls. The expressions of human TFPI at mRNA and protein levels were detected by RT-PCR and ELISA respectively on the 3rd, 7th, 10th, 14th, 28th day after operation. Intimal proliferation was detected by angiograms and morphometric analysis., Results: TFPI mRNA and protein expressions were detected at 3 days and peaked at the 10th and 14th day after TFPI gene transfer. The expressions were still detectable on the 28th day. There was no TFPI expression in Ad-LacZ group. The carotid angiogram results indicated that the minimal lumen diameter in TFPI group was significantly larger and the lumina stenosis percentage was significantly lower in TFPI group compared those in Ad-LacZ and PBS groups (all P < 0.05). The morphometric analysis showed that the intimal area, the ratio of the intimal/media area, the lumina stenosis percentage in TFPI group were all significantly reduced compared with those in Ad-LacZ and PBS groups (all P < 0.01)., Conclusions: The TFPI gene could be effectively transferred by adenovirus vector to injured carotid arteries and transferred Ad-TFPI could significantly attenuate intimal proliferation in balloon injured carotid arteries in rabbits.

Objective: To evaluate the value of combined optical coherence tomography (OCT) and intravascular ultrasound (IVUS) examinations in detecting coronary artery plaque during percutaneous transluminal coronary intervention (PCI)., Methods: OCT and IVUS examinations were performed on 30 diseased coronary vessels from 27 patients underwent PCI from Feb. 2008 to July. 2008., Results: Seventeen vulnerable plaques (4 intima tearing which were not detected by IVUS), 5 plaque rupture (1 out of 5 was detected by IVUS), 5 thrombus lesions (1 out of 5 was found by IVUS), 12 thin-cap lipid-rich lesions (2 detected by IVUS) were detected by OCT in 22 lesions (without 8 lesions post DES stents). Analysis result of plaque burden by IVUS was superior to that obtained by OCT. In 8 DES stents (implanted for 6 months to 4 years), OCT detected 2 had severe restenosis, 6 stents struts were completely covered with neointima without restenosis, 1 stent had aneurysm-like dilatation. IVUS results were similar except for limitations on exactly detecting neointima post stenting. In 19 newly implanted stents, the incidence of stent under-expansion detected by OCT was 26.0% (same as that by IVUS), stent malposition was 63.2% (10.5% by IVUS, P < 0.01), near stent tearing was 10.5% (not detected by IVUS), tissue prolapse between coronary stent struts was 52.6% (10.5% in IVUS, P < 0.05)., Conclusions: OCT imaging is superior to IVUS on detecting vulnerable plaques and change of structure around stents while IVUS is superior to OCT on estimating plaque burden in patients underwent PCI.