OBJECTIVE:The aim of the present study was to assess the effects of rosuvastatin on renal injury and inflammation in a model of nitric oxide deficiency.METHODS:Male Wistar rats were randomly divided into four groups (n = 10/group) and treated for 28 days with saline (CTRL); 30 mg/kg/day L-NAME (L-name); L-NAME and 20 mg/kg/day rosuvastatin (L-name+ROS-20); or L-NAME and 2 mg/kg/day rosuvastatin (L-name+ROS-2). Systolic blood pressure was measured by plethysmography in the central artery of the tail. The serum total cholesterol, triglycerides, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, creatinine, nitric oxide, interleukin-6, and tumor necrosis factor alpha levels were analyzed. Urine samples were taken to measure the albumin∶urinary creatinine ratio. Kidneys were sectioned and stained with hematoxylin/eosin and Masson's trichrome. Immunohistochemical analysis of the renal tissue was performed to detect macrophage infiltration of the glomeruli.RESULTS:The systolic blood pressure was elevated in the L-name but not the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups. The L-name group had a significantly reduced nitric oxide level and an increased interleukin-6 and tumor necrosis factor alpha level, albumin∶urinary creatinine ratio and number of macrophages in the renal glomeruli. Rosuvastatin increased the nitric oxide level in the L-name+rosuvastatin-2 group and reduced the interleukin-6 and tumor necrosis factor alpha levels, glomerular macrophage number and albumin∶urinary creatinine ratio in the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups.CONCLUSION:Rosuvastatin treatment reduced glomerular damage due to improvement in the inflammatory pattern independent of the systolic blood pressure and serum lipid level. These effects may lead to improvements in the treatment of kidney disease.

introduction: Atherosclerotic cardiovascular disease is a leading cause of death and disability worlwide. The LDL-C causes atherosclerosis and therefore lowering the levels of these lipoproteins reduces the risk of acute myocardial infarction and other cardiovascular events. Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase and are the most cost-effective medicines for lowering LDL-C. Up to 80% of patients treated with statins do not achieve optimal LDL-C levels, explained by high baseline LDL-C levels, aggressive LDL-C treatment goals, lack of sufficient statin efficacy or drug intolerance. Objective: This review discusses the characteristics of statin intolerance and the mechanism of action, efficacy, and safety of Bempedoic Acid as a lipid-lowering agent. Methods: We searched PubMed, ScienceDirect, the Virtual Health Library and Latin American and Caribbean Health Sciences Literature for articles published in the last five years using the following health descriptors: “bempedoic” OR “ATP-citrate lyase” AND hypercholesterolemia AND “coronary artery disease”. Results: Bempedoic acid is a prodrug that is converted to its active form (bempedoyl-CoA) by the acyl-CoA synthetase-1 enzyme. Acts two steps upstream from HMG-CoA reductase, the target of statins, in the same metabolic pathway, representing an additional lipid-lowering therapy. Conclusions:Bempedoic Acid’s active metabolite is an effective treatment option, alone or in combination with statin or ezetimibe, to lower LDL-C and reduce hsCRP, which is a marker of systemic inflammation associated with future risk of cardiovascular events, suggesting an anti-inflammatory response. Outcomes and cost-effectiveness are currently being investigated in the CLEAR Outcomes study, with results expected in 2023.

The aim of this review was to summarize current data that support the efficacy and safety of colchicine therapy in atherosclerotic cardiovascular disease. Vascular inflammation plays a central role in coronary atherosclerosis, and the antiinflammatory action of colchicine in low doses (0.5 mg per day) has a recognized effect on reducing ischemic events. We conducted a bibliographic review that included free access publications from the PubMed platform, using the descriptors "colchicine" and "coronary disease". There were included metaanalysis studies, randomized controlled trials, reviews and systematic reviews between 2018 and 2022. Colchicine has important actions in the interruption of cellular inflammatory activities, as it binds to free tubulin dimers, preventing elongation of the microtubule, and interferes with intracellular protein trafficking, secretion, and ionic organization of homeostasis. It also impairs neutrophils recruitment, inhibits nuclear factor-kappa B (NF-κ B) signaling and affects inflammatory receptor protein 3 (NLPR3) activation, leading to the suppression of interleukins 1 β , 18 and 6 release. Gastrointestinal intolerance limits its use in 10% of patients approximately. Attention is needed for drug interactions with CYP3A4 and p-glycoprotein inhibitors/competitors. Its use in acute and chronic coronary syndromes and in coronary angioplasty procedures have been studied in several trials, showing promising results. However, an increase in cases of non-cardiovascular death in patients treated with colchicine was observed in a metaanalysis study, in comparison with placebo or standard therapy. Thus, it is imperative to identify those who will adapt or be harmed by colchicine treatment. In conclusion, coronary arteriopathy is the leading cause of mortality in the world, it justifies the research of lowcost agents that can minimize the impact of this pathology.