INTRODUCTION AND OBJECTIVES: Endothelial function can be modulated by growth factors produced by activated smooth muscle cells, inflammatory cells and plasma products that infiltrate the lesion. The aim of this study was to quantify neovessels in human coronary arteries with atherosclerotic lesions of different severity and analyze their relationship with inflammatory cell and plasma product infiltrates. PATIENTS AND METHOD: We studied 60 coronary arteries from patients who underwent heart transplant. Cellular markers (smooth muscle cell, monocyte/macrophage), the presence thrombin/prothrombin and expression of vascular endothelial growth factor (VEGF) were analyzed and quantified by conventional histology, immunohistochemistry and image analysis techniques. RESULTS: Neovessels were detected in advanced lesions, and a positive correlation was observed with the degree of vessel remodeling, monocyte/macrophage infiltration and lipid deposition. Smooth muscle cells were the main producers of VEGF in both the intima and media layers of advanced lesions. In these lesions thrombin/prothrombin-positive areas colocalized with activated smooth muscle cells. CONCLUSIONS: The presence of neovessels in coronary arteries correlated with inflammatory cell infiltration, lipid deposition and thrombin/prothrombin content. VEGF expression was mainly associated with smooth muscle cells, indicating a key role of these cells in the modulation of endothelial cell function.
INTRODUCTION AND OBJECTIVES: Endothelial function can be modulated by growth factors produced by activated smooth muscle cells, inflammatory cells and plasma products that infiltrate the lesion. The aim of this study was to quantify neovessels in human coronary arteries with atherosclerotic lesions of different severity and analyze their relationship with inflammatory cell and plasma product infiltrates. PATIENTS AND METHOD: We studied 60 coronary arteries from patients who underwent heart transplant. Cellular markers (smooth muscle cell, monocyte/macrophage), the presence thrombin/prothrombin and expression of vascular endothelial growth factor (VEGF) were analyzed and quantified by conventional histology, immunohistochemistry and image analysis techniques. RESULTS: Neovessels were detected in advanced lesions, and a positive correlation was observed with the degree of vessel remodeling, monocyte/macrophage infiltration and lipid deposition. Smooth muscle cells were the main producers of VEGF in both the intima and media layers of advanced lesions. In these lesions thrombin/prothrombin-positive areas colocalized with activated smooth muscle cells. CONCLUSIONS: The presence of neovessels in coronary arteries correlated with inflammatory cell infiltration, lipid deposition and thrombin/prothrombin content. VEGF expression was mainly associated with smooth muscle cells, indicating a key role of these cells in the modulation of endothelial cell function.