Journal of cardiovascular pharmacology
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J. Cardiovasc. Pharmacol. · Nov 2020
Comparative Study Observational StudyIn-Hospital Management and Outcomes of Acute Myocardial Infarction Before and During the Coronavirus Disease 2019 Pandemic.
The outbreak of coronavirus disease 2019 (COVID-19) has rapidly spread worldwide. This study sought to share our experiences with in-hospital management and outcomes of acute myocardial infarction (AMI) during the COVID-19 pandemic. We retrospectively analyzed consecutive AMI patients, including those with ST-elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI), from February 1, 2020, to April 15, 2020 (during the COVID-19 pandemic), and from January 1, 2019, to December 31, 2019 (before the COVID-19 pandemic), respectively. ⋯ AMI combined with COVID-19 infection was associated with higher rates of mortality than AMI alone. This study demonstrates that the COVID-19 pandemic results in significant reperfusion delays in STEMI patients and has a marked impact on the treatment options selection in AMI patients. The mortality rate of STEMI patients exhibits an increasing trend during the pandemic of COVID-19.
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J. Cardiovasc. Pharmacol. · Nov 2020
Myocardial Infarction-associated Transcript Knockdown Inhibits Cell Proliferation, Migration, and Invasion Through miR-490-3p/Intercellular Adhesion Molecule 1 Axis in Oxidized Low-density Lipoprotein-induced Vascular Smooth Muscle Cells.
Emerging evidence has demonstrated that long noncoding RNAs are related to the pathogenesis of atherosclerosis. We aimed to investigate the roles and molecular mechanisms of myocardial infarction-associated transcript (MIAT) in the proliferation, migration, and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p), and intercellular adhesion molecule 1 (ICAM1). ⋯ ICAM1 was a direct target of miR-490-3p, and ICAM1 silencing repressed the proliferation, migration, and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration, and invasion. MIAT knockdown could depress cell proliferation, migration, and invasion through miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.