Lower Expression of Neutrophil Adhesion Molecule Indicates Less Vessel Wall Injury and Might Explain Lower Restenosis Rate After Cutting Balloon Angioplasty

Abstract

Background-The Cutting Balloon is a novel dilatation catheter for coronary angioplasty (InterVentional Technologies Inc). It produces longitudinal, microsurgical incisions in the vessel wall before the actual dilatation. It is assumed that these controlled surgical incisions relieve hoop stress and reduce vessel wall injury and eventually restenosis. However, no clinical indicator to support the theory of reduced injury has been described. Certain clusters of differentiation (eg, CD11, CD18 on the leukocytes) are implicated in leukocyte adhesion, increased permeability, and opsonization. Therefore, they might serve as clinical indicators of the injury level of the vessels after angioplasty. Methods and Results-We randomly selected 64 patients with isolated left anterior descending coronary artery disease for either Cutting Balloon angioplasty or conventional balloon angioplasty. The expression of CD18 and CD11b on the surface of neutrophils was determined by flow cytometric analysis. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) were also measured. The expression of both the CD18 and CD11b in the coronary sinus blood gradually increased and reached its maximum at 48 hours after angioplasty. The sICAM-1 levels in the coronary sinus serum also increased after angioplasty. Percentage increases of CD18 and CD11b expression and the increase of the sICAM-1 levels at 48 hours after angioplasty (as ratios to baseline values before angioplasty) were less in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group (CD18, 1.10Ϯ0.05 versus 1.31Ϯ0.05, PϽ0.05; CD11b, 1.23Ϯ0.06 versus 1.72Ϯ0.10, PϽ0.001; sICAM-1, 1.12Ϯ0.05 versus 1.25Ϯ0.02, PϽ0.05). In all patients, the late lumen loss at follow-up angiogram positively correlated with the increased levels of CD11b (Rϭ0.59, PϽ0.001) and sICAM-1 (Rϭ0.38, PϽ0.05) at 48 hours after angioplasty. Conclusions-Balloon angioplasty upregulated Mac-1 (CD11b/CD18) on the surface of the neutrophils and increased sICAM-1 levels in association with late loss increase. These changes were significantly smaller in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group. This suggests that Cutting Balloon angioplasty may produce less vessel wall injury and, consequently, less neutrophil activation, which may account for the lower rate of restenosis.

8-Iso-PGF 2α Induces β 2 -Integrin–Mediated Rapid Adhesion of Human Polymorphonuclear Neutrophils

“…Neutrophils are major players in the pathogenesis of ischemia-reperfusion injury, and their adherence to vascular endothelium is one of the earliest steps in this pathogenetic process leading to reperfusion damage 23 and in the development of restenosis after angioplasty. 24 In the present report, we investigated the potential relationship between isoprostanes and leukocyte proadhesive activities. From our results, the following conclusions can be drawn: (1) 8-iso-PGF 2␣ triggers a PTx-sensitive signaling pathway in human neutrophils leading to rapid integrin activation; (2) 8-iso-PGF 2␣ is likely to exert its effects on neutrophils via the TP; (3) integrin activation is restricted to the ␤ 2 -integrins CD11b/CD18 (CR3) and CD11c/CD18 (gp150/95) and supports binding to fibrinogen but not to ICAM-1; (4) 8-iso-PGF 2␣ does not trigger integrin activation in monocytes and lymphocytes; and (5) the signaling capabilities of 8-iso-PGF 2␣ appear to be restricted and selective, because it does not induce LFA-1 activation, chemotaxis, or NADPH-oxidase activity.…”

The influence of composition and location on the toughness of human atherosclerotic femoral plaque tissue

“…The potential of CBA is based on a decrease in inflammatory response [36], a decrease in proliferative response [37], and an increase in plaque reduction with accompanying decrease in vessel stretch following CBA compared with PTA [13].…”

CD40 Ligand Promotes Mac-1 Expression, Leukocyte Recruitment, and Neointima Formation after Vascular Injury

“…24 Clinical studies demonstrate that activation of circulating neutrophils (as determined by enhanced Mac-1 expression) is associated with late lumen loss and restenosis. [25][26][27][28][29] However, the mechanism underlying neutrophil activation and recruitment in the response to vascular injury is largely unknown. The present study investigated the role of elevated sCD40L in leukocyte recruitment and neointimal formation in response to vascular injury in an atherogenic animal model, and explored the molecular mechanisms involved.…”