Abstract
Dyslipidemia is one of the primary causes of cardiovascular disease. Therefore, attention has been focused on the development of drugs that normalize lipid levels and exert an effect on markers of atherothrombosis, insulin resistance (IR), and inflammation. Atorvastatin is a drug with not only lipid-lowering potential, but it has multiple non-lipid effects. This study aimed to evaluate atorvastatin effects on lipid, adipokine, IR, and inflammatory statuses in patients with myocardial infarction (MI) in an in-hospital setting. This study included 66 patients with confirmed ST-segment elevation MI, who were treated with atorvastatin 20 mg/day starting on day 1 of MI, without any dose changes. The comparison group consisted of 60 patients receiving standard anti-anginal and anti-thrombotic therapy. During the hospital stay, both groups showed a reduction in total cholesterol level and free fatty acids and increased concentrations of apolipoprotein A, especially those patients receiving atorvastatin. On day 1 of MI, patients in both groups had elevated levels of leptin by 2.9- to 3.3-fold, but the leptin levels decreased by 40.3% and were significantly lower than in patients not taking statins. The treatment with atorvastatin was associated with a decrease in C-reactive protein and interleukin-6 by 23.1 and 49.2%, respectively, compared with baseline values. In the group of patients on standard therapy, there was a decrease of interleukin-6 by 31.7%. Atorvastatin administered early on during hospitalization to patients with MI contributed to the improvement of lipid, adipokine and pro-inflammatory statuses and decreased IR.
Highlights
Despite recent advances in treatment options aimed at reducing the rate of ischemic events in the first days following disease onset, patients with myocardial infarction (MI) remain at high risk of cardiovascular events
The aim of this study was to study the effects of atorvastatin on lipid parameters, leptin, adiponectin, insulin resistance (IR) markers, plasminogen activator inhibitor type 1 (PAI-1), and inflammatory parameters in patients with MI in an in-hospital setting
Our results showed that levels of inflammatory markers, C-reactive protein (CRP) and IL-6, were significantly higher in both groups of patients in the acute phase of MI, and in the early hospitalization period compared with the control group
Summary
Despite recent advances in treatment options aimed at reducing the rate of ischemic events in the first days following disease onset, patients with myocardial infarction (MI) remain at high risk of cardiovascular events. 38% of women and 25% of men will die within 1 year of a first recognized heart attack (Rosamond et al, 2008) These data suggest the need to develop clinically effective strategies to target pathophysiological mechanisms responsible for the development and course of MI. Its development is associated with a diverse set of interrelated pathological mechanisms, namely atherothrombosis. These mechanisms involve the activation of local and progressive inflammatory processes in the atherosclerotic plaque concurrent with endothelial dysfunction, which subsequently contribute to the development of MI (Cefalu, 2001).
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