Nanopartículas calcificantes como factor etiológico del desarrollo de hiperplasia y calcificación vascular

Abstract

ObjectiveCalcifying nanoparticles (NP) have been detected recently in calcified human arterial specimens, and are involved in the process of calcification. This study was designed to test the hypothesis that human-derived NP could worsen the response to arterial endothelial injury and induce vascular calcification. MethodsThe right carotid artery of 24 New Zealand rabbits was injured with an angioplasty balloon. Animals were perfused intravenously with saline (100mL) during the experiment and divided into 3 groups: group A, control; group B, exposed to NP (2mL) obtained from calcified aortic valves; and group C, exposed to NP (2mL) and treated post-operatively with atorvastatin (2.5mg/kg/24h). At 30 days, both carotid arteries were removed and examined histologically. Blood measurements were monitored during the study. ResultsThe intimal hyperplasia area was significantly larger in the injured right carotid artery compared with the left un-operated carotid artery in all groups. There was no significant variation in medial area between groups. Morphometrically, the intima/media ratio (IMR) was significantly higher in damaged carotids compared with controls. A significant increase in the IMR was found in group B (1.81±0.41) compared with group A (0.38±0.59; P=.004) or group C (0.89±0.79; P=.035). Differences between groups C and A were not significant (P=.064). Calcifications were observed in 6 animals, all of which had been exposed to NP (4 in group B, and 2 in group C, P=.027). Plasma levels of cholesterol and triglycerides remained stable. ConclusionsThis study confirms the ability of systemic inoculation of human-derived NP to accelerate hyperplasia and stimulate calcification in localised areas of arteries previously submitted to endothelial damage, while it was harmless in healthy arteries. Atorvastatin was demonstrated to slow down this process.