Abstract
Inflammation is crucially involved in the development of carotid plaques. We examined the relationship between plaque vulnerability and inflammatory biomarkers using intraoperative blood and tissue specimens. We examined 58 patients with carotid stenosis. Following carotid plaque magnetic resonance imaging, 41 patients underwent carotid artery stenting (CAS) and 17 underwent carotid endarterectomy (CEA). Blood samples were obtained from the femoral artery (systemic) and common carotid artery immediately before and after CAS (local). Seventeen resected CEA tissue samples were embedded in paraffin, and histopathological and immunohistochemical analyses for IL-6, IL-10, E-selectin, adiponectin, and pentraxin 3 (PTX3) were performed. Serum levels of IL-6, IL-1β, IL-10, TNFα, E-selectin, VCAM-1, adiponectin, hs-CRP, and PTX3 were measured by multiplex bead array system and ELISA. CAS-treated patients were classified as stable plaques (n = 21) and vulnerable plaques (n = 20). The vulnerable group showed upregulation of the proinflammatory cytokines (IL-6 and TNFα), endothelial activation markers (E-selectin and VCAM-1), and inflammation markers (hs-CRP and PTX3) and downregulation of the anti-inflammatory markers (adiponectin and IL-10). PTX3 levels in both systemic and intracarotid samples before and after CAS were higher in the vulnerable group than in the stable group. Immunohistochemical analysis demonstrated that IL-6 was localized to inflammatory cells in the vulnerable plaques, and PTX3 was observed in the endothelial and perivascular cells. Our findings reveal that carotid plaque vulnerability is modulated by the upregulation and downregulation of proinflammatory and anti-inflammatory factors, respectively. PTX3 may thus be a potential predictive marker of plaque vulnerability.
Highlights
Atherosclerosis is a systemic arterial disease involving the intima of large- and medium-sized systemic arteries, including the aorta, carotid, coronary, and peripheral arteries
Patients who met our criteria for carotid artery stenting (CAS) included those diagnosed with carotid lesions that were either symptomatic with .50% stenosis or were asymptomatic with .80% stenosis, as assessed by digital subtraction angiography performed as described by the North American Symptomatic Carotid Endarterectomy Trial [12]
Several significant differences were observed in the IL-6, IL-10, E-selectin, vascular cell adhesion molecule 1 (VCAM-1), and pentraxin 3 (PTX3) levels between local and systemic samples
Summary
Atherosclerosis is a systemic arterial disease involving the intima of large- and medium-sized systemic arteries, including the aorta, carotid, coronary, and peripheral arteries. Atherosclerosis is assumed to result from complex endothelial dysfunction induced by elevated and modified low-density lipoproteins, hypertension, smoking-induced toxins, free radicals, pathogenic microorganisms, shear stress, and/or a combination of these and other factors that lead to a compensatory inflammatory response [1]. Inflammation is currently recognized as an important factor involved in the development, progression, and rupture of atherosclerotic plaques, and subsequently, thrombosis [2,3,4,5,6]. Endothelial dysfunction is characterized by decreased nitric oxide synthesis and local oxidation of circulating lipoproteins and their entry into the vessel wall [7]. The levels of circulating inflammatory biomarkers, including high-sensitivity C-reactive protein (hs-CRP), and interleukin (IL), are important predictors of future vascular events [8,9]. Pentraxin 3 (PTX3) has been implicated in cardiovascular events [10]
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