Effects of atorvastatin and ezetimibe on CD147, HIF-1, MMP-2 and VEGF in carotid atherosclerotic plaque under the guidance of IVUS.

Atherosclerosis (AS), as the main pathophysiological basis of coronary heart disease, can develop into carotid atherosclerotic plaque (CAP) through intimal inflammation, necrosis, fibrosis and calcification. However, there are few reports on the clinical drug selection of CAP. The aim of this study was to explore the effects of atorvastatin and ezetimibe on CD147, HIF-1, MMP-2 and VEGF in CAP under the guidance of IVUS, so as to provide basis for CAP of the best drug.

A novel rabbit model of atherosclerotic vulnerable plaque established by cryofluid-induced endothelial injury.

Acute thrombosis secondary to atherosclerotic plaque rupture is the main cause of acute cardiac and cerebral ischemia. An animal model of unstable atherosclerotic plaques is highly important for investigating the mechanism of plaque rupture and thrombosis. However, current animal models involve complex operations, are costly, and have plaque morphologies that are different from those of humans.

Effect of Statins on Clinical Outcomes in Patients With Coronary Artery Spasm: A Meta-Analysis.

Purpose: The purpose of this meta-analysis was to assess the effect of statins on major adverse cardiovascular events (MACE) related to coronary artery spasm (CAS) and to evaluate the effectiveness of statins in patients with CAS.

Methods: A systematic search of electronic databases, including Google Scholar, the Cochrane Central Register of Controlled Trials, and PubMed, was conducted. These studies were all published in English, and the databases were searched from inception to July 2021.

[Mobilization of Bone Marrow Mesenchymal Stem Cells Inhibits TGF-β Non-classical Pathway Against Myocardial Fibrosis in Rats].

Objective: To observe the relationship between the mechanism of bone marrow stem cell mobilization mediated the myocardial fibrosis inhibition in rats and the non-classical pathway mediated by transforming growth factor-β (TGF-β).

Methods: Twenty two Wistar rats were subcutaneously injected with isoproterenol (Iso) to establish the model of myocardial fibrosis, and then were randomly divided into control group and granulocyte colony-stimulating factor (G-CSF)-treat group (GT group). The rats in GT group were subcutaneously injected with recombinant human granulocyte stimulating factor for 5 days, and the control group was injected with normal saline.