Abstract

Vitamin D plays a pivotal role in bone homeostasis and calcium metabolism. However, recent research has indicated additional beneficial effects of vitamin D on the cardiovascular system. This review aims to elucidate if vitamin D can be used as an add-on treatment in coronary artery disease (CAD). Large-scale epidemiological studies have found a significant inverse association between serum 25(OH)-vitamin D levels and the prevalence of essential hypertension. Likewise, epidemiological data have suggested plasma levels of vitamin D to be inversely correlated to cardiac injury after acute myocardial infarction (MI). Remarkably, in vitro trials have showed that vitamin D can actively suppress the intracellular NF-κB pathway to decrease CAD progression. This is suggested as a mechanistic link to explain how vitamin D may decrease vascular inflammation and atherosclerosis. A review of randomized controlled trials with vitamin D supplementation showed ambiguous results. This may partly be explained by heterogeneous study groups. It is suggested that subgroups of diabetic patients may benefit more from vitamin D supplementation. Moreover, some studies have indicated that calcitriol rather than cholecalciferol exerts more potent beneficial effects on atherosclerosis and CAD. Therefore, further studies are required to clarify these assumptions.

Highlights

  • Cardiovascular disease (CVD) is a major concern of global health

  • 17.9 million people died from CVD in 2015, with 7.3 million of these deaths due to coronary artery disease (CAD) [1]

  • A possible mechanistic link was provided by Chen et al [58], who explained how vitamin D alters the inflammatory response of CAD through suppression of the NF-κB

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Summary

Introduction

Cardiovascular disease (CVD) is a major concern of global health. Health Organization (WHO), CVD is the most common cause of mortality worldwide. 17.9 million people died from CVD in 2015, with 7.3 million of these deaths due to coronary artery disease (CAD) [1]. CAD is formerly considered a disease mediated by lipid accumulation, its pathophysiology is complex, and the exact underlying mechanisms are still unknown. More recent investigations have suggested an additional excessive inflammatory response in the subintimal arterial space followed by thrombus formation [2,3]. Several studies have found that blood microparticle levels are elevated in individuals with CAD [4,5]. Different molecules on the surface of the microparticles mediate procoagulant properties that may lead to an acute coronary event [6]

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