Effects of two lipid lowering therapies on immune responses in hyperlipidemic subjects

Effects of four antiplatelet/statin combined strategies on immune and inflammatory responses in patients with acute myocardial infarction undergoing pharmacoinvasive strategy: Design and rationale of the B and T Types of Lymphocytes Evaluation in Acute Myocardial Infarction (BATTLE-AMI) study: study protocol for a randomized controlled trial

“…Other possible players such as highly inflammatory T cells, lymphocyte-derived microparticles, extracellular vesicles, and exosomes may also reach the damaged myocardium, affecting the clotting process [ 8 ], oxidative stress [ 13 ], and microcirculation [ 14 ], thus influencing the recovery of the ischemic tissue [ 14 ]. We previously reported that hyperlipidemic individuals treated with rosuvastatin presented better immune responses (higher titers of anti-oxLDL) than those receiving simvastatin/ezetimibe, thus suggesting that the choice of lipid lowering therapy may have possible beneficial role in the acute phase of myocardial infarction [ 15 ]. Figure 1 summarizes the study hypothesis regarding B and T lymphocytes.…”

Rosuvastatin may stabilize atherosclerotic aortic plaque: Transesophageal echocardiographic study in the EPISTEME trial

“…Thus, it is suggested that rosuvastatin resulted in a relative decrease of lowechoic AAPs. Rosuvastatin decreased high-sensitivity-CRP and ox40L, a tumor necrosis factor receptor family member, and also modulated the adaptive immune system for atherosclerosis [27], [30], [31]. In experimental studies, rosuvastatin decreased macrophage content in aortic plaques in vivo and increased peroxisome proliferator-activated receptors gamma in human umbilical vein endothelial cells [31], [32].…”

Novel therapies for alopecia areata: The era of rational drug development

“…Simvastatin/ezetimibe therapy has been associated with reductions in oxidized lipoproteins when compared with statin monotherapy. 31 This is believed to contribute to its superiority in suppressing atherosclerosis, which can have a significant T H 17 component. Initial reports on the efficacy of this treatment in patients with AA were negative 32 ; however, the results of a more robust and controlled clinical trial are awaited (Clinical Trial no.…”