Relationship between hyperfibrinogenemia (HF), oxidative stress, and atherogenesis was established. Effect of atorvastatin (Ator) was assessed. Wistar male (6 months) rats were studied: Ctr, control, without HF induction; Ctr-Ator, without HF treated with atorvastatin; AI, atherogenesis induced, and AI-Ator, atherogenesis induced and treated with atorvastatin. Atherogenesis was induced by daily adrenaline injection (0.1？mL/day/rat) for 90 days; treatment started 15 days after induction. Fibrinogen (mg/dL) and nitric oxide (NO) were measured in plasma (mM) and superoxide dismutase (SOD) (U/mL) in red cell lysate by spectrophotometry. Slices of aorta were analyzed by electron microscopy (EM). ANOVA and chi-square test were used; was established. There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values. Comparing Ctr with AI an increase of fibrinogen is observed (), but it decreased after administration of atorvastatin in AI-Ator (). NO diminished in AI relative to Ctr and increased in AI-Ator (). SOD showed an increase in AI and AI-Ator compared to Ctr (). EM revealed expansion of intermembrane space and disorganization of crests in AI. In AI-Ator mitochondrial areas and diameters were similar to control. Atorvastatin normalizes HF, stabilizes NO, increases SOD, and produces a partial regression of mitochondrial lesions. 1. Introduction Cardiovascular diseases represent one of the main causes of morbimortality in developed and emerging countries. Atherogenesis has been established as the pathophysiological substrate of these pathologies, leading to abundant research on atherogenic triggers, progression, and possible treatments, as well as increased primary and secondary preventive measures. However, a high incidence of acute cardiovascular events has been reported in subjects classified as healthy according to the Framingham stratification criteria or to the guidelines elaborated by the National Cholesterol Education Program—Adult Treatment Panel III (ATP III) [1]. New risk factors and vascular disease markers, such as hyperfibrinogenemia (HF), participate in platelet aggregation, modulate endothelial function, promote the proliferation of smooth muscle, and express the inflammatory component in atherogenesis [2–4], mediated by TNF-α which reflects the endothelial activation level. Some years ago, several studies proved that fibrinogen values behave as risk indicators of an adverse cardiovascular event due to their participation in the stages of subclinical atherosclerosis [5, 6]. In previous studies, we have
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