COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still a pandemic with high mortality and morbidity rates. Clinical manifestation is widely variable, including asymptomatic or mild respiratory tract illness to severe pneumonia and death. Myocardial injury is a significant pathogenic feature of COVID-19 and it is associated with worse in-hospital outcomes, mainly due to a higher number of hospital readmissions, with over 50% mortality. These findings suggest that myocardial injury would identify COVID-19 patients with higher risk during active infection and mid-term follow-up. Potential contributors responsible for myocardial damage are myocarditis, vasculitis, acute inflammation, type 1 and type 2 myocardial infarction. However, there are few data about cardiac sequelae and its long-term consequences. Thus, the optimal screening tool for residual cardiac sequelae, clinical follow-up, and the benefits of a specific cardiovascular therapy during the convalescent phase remains unknown. This mini-review explores the different mechanisms of myocardial injury related to COVID-19 and its short and long-term implications.
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http://dx.doi.org/10.3389/fcvm.2022.901245 | DOI Listing |
Biochem Biophys Res Commun
January 2025
Center for Molecular Medicine, Maine Health Institute for Research, 81 Research Drive, Scarborough, ME, USA.
Hepatic stores of Vitamin A (retinol) are mobilized and metabolized in the heart following myocardial infarction. The physiological consequences of this mobilization are poorly understood. Here we used dietary depletion in a lecithin retinol acyltransferase mutant mouse line to induce Vitamin A deficiency and investigate the effects on cardiac function and recovery from myocardial infarction.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Department of Cardiology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 1 Minde Road, Nanchang, Jiangxi Province 330006, China. Electronic address:
Aims: Nanoplastics (NPs) are emerging organic pollutants generated by plastic degradation and are ubiquitous in the environment. They can be accumulated through the food webs and enter the human body through dietary intake, posing health risks. The main target organs of NP accumulation are the lungs, liver, heart, and kidneys.
View Article and Find Full Text PDFExpert Opin Ther Targets
January 2025
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands.
Introduction: Cardiovascular disease (CVD) is the leading cause of death worldwide. Platelet-derived extracellular vesicles (PEV) have attracted extensive attention in cardiovascular disease research in recent years because their cargo is involved in a variety of pathophysiological processes, such as thrombosis, immune response, promotion or inhibition of inflammatory response, promotion of angiogenesis as well as cell proliferation and migration.
Areas Covered: This review explores the role of PEV in various cardiovascular diseases (such as atherosclerosis, myocardial infarction, ischemia-reperfusion injury, and heart failure), with relation to its molecular cargo (nucleic acids, bioactive lipids, proteins) and aims to provide new insights in the pathophysiologic role of PEV, and methods for preventing and treating cardiovascular diseases based on PEV.
J Clin Invest
January 2025
Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, with inflammation playing a pivotal role in its pathogenesis. T lymphocytes are crucial components of the adaptive immune system that have emerged as key mediators in both cardiac health and the development and progression of CVD. This Review explores the diverse roles of T cell subsets, including Th1, Th17, γδ T cells, and Tregs, in myocardial inflammatory processes such as autoimmune myocarditis and myocardial infarction.
View Article and Find Full Text PDFAnn Transl Med
December 2024
[This corrects the article DOI: 10.21037/atm-22-222.].
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