Relationship between lipoproteins, thrombosis, and atrial fibrillation

The prothrombotic state in atrial fibrillation (AF) occurs as a result of multifaceted interactions, known as Virchow’s triad of hypercoagulability, structural abnormalities, and blood stasis. More recently, there is emerging evidence that lipoproteins are implicated in this process, beyond their traditional role in atherosclerosis. In this review, we provide an overview of the various lipoproteins and explore the association between lipoproteins and AF, the effects of lipoproteins on haemostasis, and the potential contribution of lipoproteins to thrombogenesis in AF. There are several types of lipoproteins based on size, lipid composition, and apolipoprotein category, namely: chylomicrons, very low-density lipoprotein, low-density lipoprotein (LDL), intermediate-density lipoprotein, and high-density lipoprotein. Each of these lipoproteins may contain numerous lipid species and proteins with a variety of different functions. Furthermore, the lipoprotein particles may be oxidized causing an alteration in their structure and content. Of note, there is a paradoxical inverse relationship between total cholesterol and LDL cholesterol (LDL-C) levels, and incident AF. The mechanism by which this occurs may be related to the stabilizing effect of cholesterol on myocardial membranes, along with its role in inflammation. Overall, specific lipoproteins may interact with haemostatic pathways to promote excess platelet activation and thrombin generation, as well as inhibiting fibrinolysis. In this regard, LDL-C has been shown to be an independent risk factor for thromboembolic events in AF. The complex relationship between lipoproteins, thrombosis and AF warrants further research with an aim to improve our knowledge base and contribute to our overall understanding of lipoprotein-mediated thrombosis.

CARDIOPROTECTIVE EFFECT OF VITAMIN E AGAINST MYOCARDIAL INFARCTION INDUCED BY ISOPRENALINE IN ALBINO RATS

Objective: Vitamin E is an antioxidant which can help in the prevention of cardiovascular disease. The objective of this study was to estimate the effects of Vitamin E on cardiac marker enzymes in isoprenaline (ISO)-induced myocardial infracted rats.Methods: Adult male albino rats were divided into three groups. The first group was the control negative group. The second group was the control positive group that was subcutaneously injected with ISO (100 mg/kg). The third group was pretreated with Vitamin E (100 mg/kg) once daily for 30 days, then subcutaneously injected with ISO at an interval of 24 h for 2 days. Aspartate aminotransferase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), cardiac troponin-I (CTn-I), glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and histopathological examinations were measured. Comparison between groups was achieved by one-way analysis of variance (ANOVA) test through SPSS software.Results: The levels of AST, ALT, LDH, creatine kinase (CK), and CTn-I significantly decreased in pretreated group with Vitamin E compared to its increasing in the control positive group. The level of GSH and SOD markedly increased in pretreated group with Vitamin E compared to its decreasing in the control positive group, while the level of MDA significantly decreased in pretreated group with Vitamin E compared to its increasing in the control positive group. ISO + Vitamin E rats group reflected a cardioprotective role of Vitamin E in myocardial infarcted rats.Conclusion: Pretreatment with Vitamin E can protect the myocardial membranes against ISO-induced oxidative stress in rats and can be used for routine clinical and epidemiological purposes.