Drug-coated balloons for the treatment of ostial left anterior descending or ostial left circumflex artery lesions: a patient-level propensity score-matched analysis.

Background: Controversy exists as to the optimal treatment approach for ostial left anterior descending (LAD) or ostial left circumflex artery (LCx) lesions. Drug-coated balloons (DCB) may overcome some of the limitations of drug-eluting stents (DES). Therefore, we investigated the security and feasibility of the DCB policy in patients with ostial LAD or ostial LCx lesions, and compared it with the conventional DES-only strategy.

Stentless at ostium: a novel approach for treating ostial left anterior descending or left circumflex coronary artery lesions with drug-coated balloons.

Background: Currently, there is no optimal treatment strategy for ostial left anterior descending (LAD) or ostial left circumflex artery (LCx) lesions. This study explored effectiveness and safety of drug-coated balloons (DCB) in individuals presenting with ostial LAD or LCx lesions.

Methods: A total of 137 patients with ostial LAD or LCx lesions scheduled for DCB treatment were prospectively recruited into the study.

Notch1 signaling activation alleviates coronary microvascular dysfunction through histone modification of Nrg-1 via the interaction between NICD and GCN5.

The Notch signaling pathway is related to endothelial dysfunction in coronary atherosclerosis. Our objective was to explore the role of Notch signaling in coronary microvascular dysfunction (CMD). CMD models were constructed by sodium laurate injection in vivo and homocysteine (Hcy) stimulation in vitro.

E3 ubiquitin ligase mind bomb 1 overexpression reduces apoptosis and inflammation of cardiac microvascular endothelial cells in coronary microvascular dysfunction.

Background: The apoptosis and inflammation in cardiac microvascular endothelial cells (CMECs) promote the development of coronary microvascular dysfunction (CMD). The present study aimed to explore the role of E3 ubiquitin ligase mind bomb 1 (MIB1) in the apoptosis and inflammation in CMECs during CMD.

Methods: In vivo, CMD in rats was induced by sodium laurate injection.

Bailcalin Protects against Diabetic Cardiomyopathy through Keap1/Nrf2/AMPK-Mediated Antioxidative and Lipid-Lowering Effects.

Previous studies demonstrated that Bailcalin (BAI) prevented cardiac injuries under different disease models. Whether BAI protected against type 2 diabetes mellitus- (T2DM-) associated cardiomyopathy was investigated in this study. T2DM was established by the combination of streptozotocin injection and high-fat diet in mice.

Activin A inhibition attenuates sympathetic neural remodeling following myocardial infarction in rats.

Inflammation serves a critical role in driving sympathetic neural remodeling following myocardial infarction (MI), and activin A has been implicated as an important mediator of the inflammatory response post‑MI. However, whether activin A impacts sympathetic neural remodeling post‑MI remains unclear. In the present study, the authors assessed the effects of activin A on sympathetic neural remodeling in a rat model of MI.

Comparison of Intracoronary and Intravenous Ultrasound-targeted Microbubble Destruction-mediated Ang1 Gene Transfection on Left Ventricular Remodeling in Canines With Acute Myocardial Infarction.

Intravenous ultrasound-targeted microbubble destruction (IV-UTMD) has made distinct but limited progress in gene therapy. Intracoronary (IC) injection may lead to more gene transfection than IV injection. This study compared the therapeutic effects of IC-UTMD-mediated and conventional IV-UTMD-mediated gene transfection in acute myocardial infarction (MI).