Search

Peripheral artery disease (PAD) is a common manifestation of atherosclerosis. Inflammation is important for initiation and progression of the disease. Dendritic cells (DCs) as antigen-presenting cells play an important role in the immune system. Therefore, we hypothesize that, in patients with PAD, DCPs might be reduced in blood due to their recruitment into the vascular wall and induce a proinflammatory response. The numbers of myeloid DCPs, plasmacytoid DCPs, and total DCPs were analyzed by flow cytometry in blood of patients with PAD (n=52) compared to controls (n=60). Femoralis plaques (n=12) of patients who underwent surgery were immunostained for CD209 and CD83 (mDCs) as well as CD304, CD123 (pDCs), and HLA-DR. In patients with PAD, a significant decrease in mDCPs, pDCPs, and tDCPs was observed. In immunostaining, markers indicative for mDCs (CD209: 16 versus 8 cells/0.1 mm2, P=0.02; CD83: 19 versus 5 cells/0.1 mm2, P=0.03) were significantly elevated in femoralis plaques compared to control vessels. We show for the first time that mDCPs, pDCPs, and tDCPs are significantly reduced in patients with PAD. Immunohistochemical analysis unraveled that the decrease in DCPs might be due to their recruitment into atherosclerotic plaques. [ABSTRACT FROM AUTHOR]

Objectives: The recanalization of chronic total occlusions (CTOs) is a complex procedure with high rates of target vessel failure (TVF), i.e., restenosis or reocclusion. Little is known about the localization of lesion recurrence, and whether extensive stenting should be performed. In this prospective analysis, the area at high risk for restenoses after recanalization of CTO was localized. Methods: Angiograms of 97 consecutive patients and control angiograms after a mean period of 5 ± 1.3 months were analyzed for location and length of the CTO and the sites of recurrences. Results: In total, 158 stents were implanted (1.6 ± 0.9 per lesion). Restenoses occurred in 39% and reocclusions in 17% of the patients. Patients with a TVF had a longer CTO than patients without TVF (17.9 ± 10.2 vs 13.9 ± 8.6 mm; P = 0.023). The TVF rate increased with the number of implanted stents. The stent diameter was smaller in lesions with subsequent reocclusions than in restenotic and nonrestenotic lesions (2.8 ± 0.5 vs 3.0 ± 0.4 and 3.2 ± 0.4 mm resp.; P = 0.007). Analyzing the localization of the 38 restenoses, we only found 45% restricted to the area of the former CTO, while 82% were located in the area of the former CTO plus 10 mm in proximal and distal direction. Conclusions: Stents should not only cover the site of the CTO, but should enclose the high-risk area of recurrence within 10 mm proximal and distal of the former CTO. This may guide the rational use of drug-eluting stents. [ABSTRACT FROM AUTHOR]