Coronary Angioplasty Results in Leukocyte and Platelet Activation With Adhesion Molecule Expression

Abstract

Coronary angioplasty increases neutrophil, monocyte and platelet adhesion molecule expression and induces a significant decrease in ex vivo-stimulated neutrophil superoxide generation and aggregation. These findings suggest that coronary angioplasty triggers cellular activation with an inflammatory response that could contribute to restenosis.

Marcadores inflamatórios intracoronarianos após intervenções coronarianas percutâneas

“…The time spent for coronary sinus catheterization is very variable, with some cases in which patients were excluded from the protocol due to technical impossibility. Possibly, due to the cost and difficulties mentioned, the number of patients, which is really small, is similar, though, to that of studies with similar technology published in international literature [12][13][14] . We used rigid catheters for collections in the coronary sinus, often deeply inserted, especially in cases of anterior interventricular…”

“…Serrano et al 12 , using sophisticated techniques, such as flow cytometry that allows for adhesion molecule quantification incorporated to cell membranes of white blood cells, investigated the neutrophil inflammatory activation during coronary angioplasty. The comparative analysis between samples obtained at aorta root and coronary sinus evinced an increase of the expression of adhesion molecules on neutrophiles, which demonstrated induction of post-PCI inflammatory response.…”

Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting

“…23,24 In addition, a dysfunctional interaction between the endothelium, platelets, and leukocytes results in a proinflammatory state with free radical production and microvascular plugging. 25,26 Attenuation of Ach-mediated increases in CBF with preserved responses to adenosine would imply a defect at the level of the endothelium. However, this does not clarify whether the diminished Ach response is attributable to abnormalities in stimulated NO production, decreased endothelium-derived hyperpolarizing factor or prostacyclin production, enhanced vasoconstrictors such as serotonin, 22 thromboxane, 27 and endothelin-1, 28 or a combination of these mechanisms.…”

A Central Role of PTP1B in Hyperinsulinemia-Enhanced IL-6 Signaling in Dedifferentiated Vascular Smooth Muscle Cells

“…It is well established that vascular inflammation in response to angioplasty-induced injury is the initiator of increased neointima formation. Several experimental and clinical observations indicate that up regulation of pro-inflammatory cytokines in activated SMCs contributes to angioplasty-induced restenosis through promoting vascular smooth muscle cell migration and proliferation, a manifestation of an inflammatory wound healing process occurring in injured vessels [15][16][17]. Of the many cytokines involved in injury-induced inflammation, IL-6 is the major pro-inflammatory cytokine that contributes to vascular injuryinduced neointima thickening [18].…”