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Diabetic heart disease
Diabetes, incretin hormones and cardioprotection
  1. A Myat1,
  2. S R Redwood1,
  3. B J Gersh2,
  4. D M Yellon3,
  5. M S Marber1
  1. 1Cardiovascular Division, King's College London BHF Centre of Research Excellence, The Rayne Institute, St Thomas’ Hospital, London, UK
  2. 2Division of Cardiovascular Sciences, Mayo Clinic, Rochester, Minnesota, USA
  3. 3Department of Medicine, The Hatter Cardiovascular Institute, University College London, London, UK
  1. Correspondence to Dr Aung Myat, Cardiovascular Division, British Heart Foundation Clinical Research Training Fellow, King's College London BHF Centre of Research Excellence, The Rayne Institute, St Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH, UK; aung.myat{at}

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The diabetes pandemic

In 2012 an estimated 371 million people had diabetes and of those about a half were undiagnosed. That number is set to expand to 552 million by 2030. Type 2 diabetes mellitus (T2DM) constitutes 85–95% of all diabetes in high income nations and may account for an even greater proportion in their low and middle income counterparts (figure 1). As a global pandemic, diabetes claimed the lives of 4.8 million people in 2012, half of whom were below the age of 60 years.w1 The predominant cause of morbidity and mortality in diabetes is cardiovascular disease, with at least a twofold excess risk of developing a multitude of vascular pathologies including ischaemic heart disease, different stroke subtypes, peripheral arterial disease, and heart failure.w2 w3 Indeed, as many as 80% of T2DM patients will develop and possibly die from macrovascular complications.w3 Such stark findings have led many to regard diabetes as a coronary heart disease risk equivalent, to a level at which non-diabetic individuals with a previous history of acute coronary syndrome (ACS) would reside.

Figure 1

The International Diabetes Federation Diabetes Update 2012. Diabetes has become a truly global pandemic. Urbanisation, changes in lifestyle, and improvements in healthcare systems combine to increase an individual's risk of acquiring the condition. Reproduced with permission from the International Diabetes Foundation.

For many years this enhanced cardiovascular risk was thought to be a solely atherosclerosis driven process characterised by endothelial cell dysfunction, oxidative stress, vessel remodelling, impaired vasodilatation, and subendothelial plaque formation. Latterly the concept of the vulnerable patient emerged to highlight the complex interplay between a constellation of deleterious processes spearheaded not only by the vulnerable vessel/plaque but also by vulnerable blood constituents and a vulnerable myocardium; together these processes shift an individual towards a greater susceptibility to developing cardiovascular complications.w4 w5 It …

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  • Contributors AM wrote the manuscript in its entirety. All authors were involved in conception, design, appraising and revising the manuscript critically for important intellectual content. All authors have seen and given approval of the final version of the manuscript for submission.

  • Funding MSM and AM are supported by the Department of Health via the National Institute for Health Research comprehensive Biomedical Research Centre award to Guy's & St Thomas’ NHS Foundation Trust in partnership with King's College London and King's College Hospital NHS Foundation Trust. AM also acknowledges financial support from the British Heart Foundation via a Clinical Research Training Fellowship (grant number FS/11/70/28917).

  • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. DMY reports receiving research grant support from Bristol-Myers Squibb and Merck Sharp and Dohme to investigate the potential cardioprotective effect of incretins in animal models. AM, SRR, BJG and MSM: none declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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