Effects of vitamin D supplementation on markers of vascular function after myocardial infarction--a randomised

Miles D Witham1, Fiona J Dove, Faisel Khan

  • 1Ageing and Health, University of Dundee, Ninewells Hospital, Dundee DD1 9SY, United Kingdom. m.witham@dundee.ac.uk

Insights

Vitamin D supplementation did not improve vascular function in heart attack survivors. While vitamin D levels rose, key markers like endothelial function and blood pressure remained unchanged, with only C-reactive protein showing a slight decrease.

Area of Science:

  • Cardiology
  • Endocrinology
  • Nutritional Science

Background:

  • Low vitamin D is prevalent and linked to increased vascular events.
  • Endothelial dysfunction is a key factor in cardiovascular disease progression.

Purpose of the Study:

  • To investigate if vitamin D supplementation improves endothelial function in myocardial infarction patients.
  • To assess the impact of vitamin D on other vascular health markers post-myocardial infarction.

Main Methods:

  • A double-blind, placebo-controlled trial randomized patients with myocardial infarction history to vitamin D3 or placebo.
  • Primary outcome was reactive hyperaemia index; secondary outcomes included blood pressure, lipids, and inflammatory markers.
  • Intervention involved 100,000 units of oral vitamin D3 at baseline, 2, and 4 months, with measurements at 2 and 6 months.

Main Results:

  • Vitamin D supplementation significantly increased 25-hydroxyvitamin D levels compared to placebo.
  • No significant difference was observed in the primary outcome (reactive hyperaemia index) between groups.
  • A significant reduction in C-reactive protein was noted in the vitamin D group, but blood pressure and cholesterol levels were unaffected.

Conclusions:

  • Vitamin D supplementation does not enhance vascular function markers in patients with a history of myocardial infarction.
  • The observed reduction in C-reactive protein warrants further investigation but does not outweigh the lack of improvement in primary vascular endpoints.
Abstract

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