alexa Inflammation, Metalloproteinases, Chronic Venous Disease and Sulodexide
ISSN: 2329-9517

Journal of Cardiovascular Diseases & Diagnosis
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Review Article

Inflammation, Metalloproteinases, Chronic Venous Disease and Sulodexide

Alberto C. Frati Munari1* and Luis Fernando Flota Cervera2
1Department of Internal Medicine, Médica Sur Hospital, Puente de Piedra 150-1-929, Toriello Guerra, Tlalpan, México D.F. 14050, México
2Director CEDIME Instituto Vascular, Calle 33 – 138, Mérida Yuc. 97129, México
Corresponding Author : Alberto C. Frati Munari
Department of Internal Medicine
Médica Sur Hospital, Puente de Piedra 150-1-929, Toriello Guerra
Tlalpan, México D.F. 14050, México
Tel: (52)5556665847
E-mail: [email protected]
Received: April 30, 2015; Accepted: May 29, 2015; Published: June 01, 2015
Citation: Munari ACF, Cervera LFF (2015) Inflammation, Metalloproteinases, Chronic Venous Disease and Sulodexide. J Cardiovasc Dis Diagn 3: 203. doi:10.4172/2329-9517.1000203
Copyright: © 2015 Munari ACF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Abstract Inflammation and extracellular Matrix Metallo Proteinases (MMPs) have been recently considered as an important step in the pathogenesis of Chronic Venous Disease (CVD). To understand how inflammation and MMP may affect venous tissue, a review on these items and on the pathogenesis of CVD was performed. Prolonged or repeated venous hypertension due to well-known predisposing factors causes abnormal shear stress leading to shredding of endothelial glycocalyx and activation of endothelial cells. The latter expose adhesion molecules and release pro-inflammatory cytokines. Diapedesis follows, leading to leukocytes infiltration of Extra Cellular Matrix (ECM) in the sub endothelial space of vein walls and valves. Activated leukocytes, mainly monocytes-macrophages, release chemotactic cytokines that amplify the inflammatory response, they also produce Nitric Oxide molecules (NO) and proteases, including MMPs. High concentration of MMPs, especially MMP-9, is found in venous wall with CVD and in venous ulcers. The role of MMP-9 in CVD is also supported by experimental data. MMP-9 can degrade components of ECM as collagen, elastin, fibronectin and laminin. MMP-9 and other proteolytic enzymes may disrupt ECM structure, damaging and debilitating venous wall that lead to varicose veins and venous ulcers. Sulodexide, a glycosaminoglycan, counteracts several of these inflammatory changes. In subjects with CVD administration of sulodexide improves venous hemodynamic changes and CVD symptoms and accelerates venous leg ulcers healing.

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