Abstract
Cardiovascular diseases (CVD) cause about 1/3 of global deaths. Therefore, new strategies for the prevention and treatment of cardiovascular events are highly sought-after. Vitamin E is known for significant antioxidative and anti-inflammatory properties, and has been studied in the prevention of CVD, supported by findings that vitamin E deficiency is associated with increased risk of cardiovascular events. However, randomized controlled trials in humans reveal conflicting and ultimately disappointing results regarding the reduction of cardiovascular events with vitamin E supplementation. As we discuss in detail, this outcome is strongly affected by study design, cohort selection, co-morbidities, genetic variations, age, and gender. For effective chronic primary and secondary prevention by vitamin E, oxidative and inflammatory status might not have been sufficiently antagonized. In contrast, acute administration of vitamin E may be more translatable into positive clinical outcomes. In patients with myocardial infarction (MI), which is associated with severe oxidative and inflammatory reactions, decreased plasma levels of vitamin E have been found. The offsetting of this acute vitamin E deficiency via short-term treatment in MI has shown promising results, and, thus, acute medication, rather than chronic supplementation, with vitamin E might revitalize vitamin E therapy and even provide positive clinical outcomes.
Highlights
Cardiovascular diseases (CVD) such as atherosclerosis are a major cause of mortality and morbidity worldwide
The aim of the present review is to critically summarize the data available on vitamin E supplementation in diseases in general and systematically investigate potential reasons for the observed conflicting results, and we provide a perspective on what we have learned from the past trials for future trials
This study suggested that combined treatment with antioxidant vitamins A, E, C, and β-carotene in patients with recent acute myocardial infarction (MI) improved clinical outcomes and may have been protective against cardiac necrosis and oxidative stress
Summary
Cardiovascular diseases (CVD) such as atherosclerosis are a major cause of mortality and morbidity worldwide. Multiple factors are involved in the complex etiology of atherosclerosis. One of the most important factors that drives atherosclerosis and its complications, such as myocardial infarction (MI) and stroke, is inflammation. Inflammation plays a pivotal role in both the initial, as well as the advanced, phases of atherosclerosis, including plaque destabilization and ultimate rupture. The advanced phase of atherosclerosis is characterized by a high degree of inflammation that includes high-level production of reactive oxygen species (ROS), due to excessive oxidative stress [1,2]. One of the major initial inducers of oxidative stress in atherosclerosis is pathological shear stress levels and flow patterns [3]. An imbalance between oxidants and antioxidants enhances oxidative stress and promotes
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