Systemic and intraplaque mediators of inflammation are increased in patients symptomatic for ischemic stroke

Fabrizio Montecucco, Sébastien Lenglet, Angèle Gayet-Ageron, Maria Bertolotto, Graziano Pelli, Domenico Palombo, Bianca Pane, Giovanni Spinella, Sabine Steffens, Lizzia Raffaghello, Vito Pistoia, Luciano Ottonello, Aldo Pende, Franco Dallegri, François MacH

Research output: Contribution to journalArticle

Abstract

Background and purpose: The concept of "vulnerable plaque" has been extended to the more recent definition of the "cardiovascular vulnerable patient," in which "intraplaque" and "systemic" factors contribute to the cumulative risk of acute cardiovascular events. Thus, we investigated the possible role of systemic and intraplaque inflammation in patients asymptomatic versus symptomatic for ischemic stroke. Methods: Regions upstream and downstream the blood flow were isolated from internal carotid plaques of patients asymptomatic (n=63) or symptomatic (n=18) for ischemic stroke. Specimens were analyzed for lipid, collagen, macrophage, lymphocyte, neutrophil, mast cell and smooth muscle cell content, and chemokine and cytokine mRNA expression. Chemokine receptors and adhesion molecules were assessed on circulating leukocytes by flow cytometry. Systemic inflammatory markers and biochemical parameters were measured on total blood, plasma, and serum. Results: Tumor necrosis factor-α and CCL5 serum levels as well as intercellular adhesion molecule-1 expression on circulating neutrophils were increased in symptomatic as compared with asymptomatic patients. Collagen content and smooth muscle cell infiltration were decreased in symptomatic plaques. In upstream regions of symptomatic plaques, lipid content and lymphocyte infiltration were increased. In downstream regions of symptomatic plaques, macrophage, neutrophil, and mast cell infiltration were increased. Intraplaque collagen content was positively correlated with smooth muscle cell infiltration and inversely correlated with macrophages, neutrophils, or serum tumor necrosis factor-α. Collagen reduction in downstream regions and serum tumor necrosis factor-α were independently associated with the likelihood of being symptomatic. Conclusions: Inflammatory mediators are increased in ischemic stroke. Despite statistically significant, the correlation between tumor necrosis factor-α serum level and intraplaque vulnerability was weak and probably of limited biological importance.

Original languageEnglish
Pages (from-to)1394-1404
Number of pages11
JournalStroke
Volume41
Issue number7
DOIs
Publication statusPublished - Jul 2010

Keywords

  • carotid artery
  • carotid endarterectomy
  • inflammation
  • leukocytes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialised Nursing
  • Medicine(all)

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    Montecucco, F., Lenglet, S., Gayet-Ageron, A., Bertolotto, M., Pelli, G., Palombo, D., Pane, B., Spinella, G., Steffens, S., Raffaghello, L., Pistoia, V., Ottonello, L., Pende, A., Dallegri, F., & MacH, F. (2010). Systemic and intraplaque mediators of inflammation are increased in patients symptomatic for ischemic stroke. Stroke, 41(7), 1394-1404. https://doi.org/10.1161/STROKEAHA.110.578369