PubMed Health⌕ Search

PubMed · 15174908

Residual stenosis poststenting and subsequent decrease in the proximal reference diameter are correlated: excessive axial wall stress is a plausible explanation.

Abstract

PURPOSE: To test the hypothesis that edge restenosis in stented lesions might be due to an increase in axial wall stress in the adjacent proximal vessel segment by examining whether the proximal reference diameters of conventionally stented lesions are reduced at follow-up and whether this reduction depends on the degree of residual stenosis poststenting. METHODS: The literature published in the past 5 years dealing with restenosis following implantation of standard stents was screened for the availability of (1) reference vessel diameters poststenting, (2) mean residual stenosis poststenting, and (3) mean reference vessel diameters at follow-up in the same patients or groups of patients. Data collected from 11 publications were pooled and used to compute the change in reference segment diameter over time. These differences were compared to the residual stenosis poststenting by nonlinear regression. RESULTS: The reduction in the mean reference diameters over time and the mean residual stenosis poststenting appear to be strongly correlated (r2 = 0.838), which supports the idea that the evolution of a stenosis adjacent to a stent margin depends on the severity of the residual stenosis. CONCLUSIONS: This finding indicates that edge restenosis might be due to excessive axial wall stress. It may also explain, at least partly, why edge restenosis is observed with catheter-based brachytherapy and radioactive or drug-eluting stents.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Pierre-André Doriot, Pierre-André Dorsaz. 2004. Residual stenosis poststenting and subsequent decrease in the proximal reference diameter are correlated: excessive axial wall stress is a plausible explanation.. https://doi.org/10.1583/03-1109.1

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

VEGF inhibits PDGF-stimulated calcium signaling independent of phospholipase C and protein kinase C.

INTRODUCTION: Despite advances in both open and endovascular techniques for treatment of arterial occlusive disease, restenosis because of neointimal hyperplasia continues to be a major cause of graft failure and restenosis. This phenomenon has been attributed to vascular smooth muscle cell (VSMC) activation by several potent mitogens including platelet derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) released at the site of injury. PDGF is known to stimulate calcium influx in VSMC that has been shown to be critical for VSMC migration and proliferation. We have previously shown that VEGF inhibits PDGF-stimulated VSMC proliferation. The objective of this set of experiments was to investigate whether VEGF modulated PDGF-stimulated Ca2+ influx in VSMC. MATERIALS AND METHODS: Primary cultured human aortic SMC were grown to subconfluency and assigned to the following groups: no stimulation, stimulation with PDGF-BB (20 ng/ml), stimulation with VEGF165 (40 ng/ml), or a combination of PDGF-BB + VEGF165. Ca2+ influx was measured using a Fura-2 fluorescence assay. The intracellular Ca2+ fraction was assayed with the Fura-2 assay by using Ca2+-free media. Phospholipase Cgamma1 (PLCgamma1), protein kinase C (PKC), and Akt phosphorylation was assessed with standard immunoblotting techniques at 1, 5, and 10 min time points. Ca2+-calmodulin kinase II (CaMKII) activity was extrapolated from the phosphorylation of Phospholamban B (PLB), a well-known protein substrate, at 1, 5, and 10 min time points. RESULTS: PDGF stimulation resulted in a 328 +/- 9 nm total calcium influx in VSMC. The combination of VEGF + PDGF resulted in a 273 +/- 21 nm total calcium influx, an amount significantly less than with PDGF alone (P < 0.04). PDGF stimulation resulted in a 72 +/- 35 nm intracellular calcium release. The addition of VEGF to PDGF resulted in an intracellular calcium release of only 15 +/- 11 nm, a significant decrease compared to PDGF alone (P < 0.01). The phosphorylation of PLCgamma1, PKC, and Akt was equivalent at 1, 5, and 10 min between the PDGF and the PDGF + VEGF treatment groups. There was an increase in CaMKII activity at 1 and 5 min time points in both the PDGF and PDGF + VEGF treatment groups suggesting that extracellular calcium influx is sufficient for CaMKII activation. CONCLUSION: VEGF inhibits PDGF-stimulated total calcium influx and, in particular, PDGF-stimulated intracellular calcium release in VSMC. The equivalent phosphorylation of PLCgamma1, PKC, and Akt suggests that the inhibitory mechanism by VEGF on calcium influx occurs downstream of these proximal mediators. The inhibition of intracellular calcium release did not inhibit CaMKII activity. VEGF may play an important role in modulating PDGF induced VSMC proliferation by specifically inhibiting intracellular calcium release in response to PDGF.

Arterial Occlusive Diseases↗

Cilioretinal artery occlusions following embolization of an artery to an intracranial meningioma.

PURPOSE: To report a case in which a prophylactic embolization of a feeder artery to an intarcranial meningioma led to an occlusion of a cilioretinal artery. DESIGN: A case report. METHODS: A 48-year-old man with an intracranial meningioma presented with ocular pain and visual loss in his right eye following embolization of a feeder artery to the meningioma with polyvinyl alcohol. RESULTS: Ophthalmoscopy 1 month later showed a cilioretinal artery occlusion which was confirmed by fluorescein angiography. His visual acuity was 0.01 in the right eye. The patient was not treated for his ocular symptoms, and his visual acuity 9 month postoperatively improved slightly to 0.1. CONCLUSIONS: Our case demonstrated that an occlusion of a retinal artery can be a complication of preoperative embolization of an artery to an intracranial tumor and can lead to severe visual loss.

Arterial Occlusive Diseases↗