Introduction

Improved understanding of the pathophysiology of cardiovascular disease and advances in cardiovascular care are two important factors that have contributed to the decline in cardiovascular event rates in Western populations over the last 50 years. Nevertheless, we still face a continuing burden of cardiovascular morbidity and mortality. The pathophysiology of cardiovascular disease is complex and multi-factorial, and a deeper understanding of the root causes of the risk factors that underlie atherosclerosis and the development of acute cardiovascular events is required before we can make substantial further progress in addressing them. It is clear, however, that the worldwide increasing prevalence of obesity, particularly abdominal obesity, is threatening to slow, or even reverse, the progress we have made so far. Abdominal fat is far from a metabolically inert storage depot. In contrast, intra-abdominal adipocytes are metabolically highly active and secrete a broad range of biologically active molecules. These substances, which include free fatty acids, plasminogen activator inhibitor-1, inflammatory mediators such as interleukin-6, and novel adipokines such as visfatin or resistin, have the potential to adversely influence cardiometabolic risk directly or indirectly through the promotion of insulin resistance and of an atherogenic, pro-thrombotic, inflammatory cluster of abnormalities that we often refer to as the metabolic syndrome. In addition, secretion of another probably critically important adipose tissue-derived protein, adiponectin, is markedly decreased in the setting of abdominal obesity. Evidence available suggests that the metabolic effects of adiponectin may confer protection against the development of type 2 diabetes and cardiovascular disease. A faculty of leading experts came together to consider the nature and magnitude of the clinical problem posed by abdominal obesity and its associated comorbidities in a symposium, entitled Abdominal Obesity and Cardiovascular Disease Risk: Adipose Tissue as a Metabolic and Endocrine Organ, and a Key Therapeutic Target, held on the occasion of the 14th European Congress on Obesity, in Athens, Greece, on 1 June 2005. Three speakers contributed to this state-of-the-art symposium. My own presentation reviewed the atherogenic and diabetogenic cluster of metabolic abnormalities, which often accompany abdominal obesity, and suggested simple approaches in clinical practice of identifying the abdominally obese patients at the highest cardiometabolic risk. Dr Michael Jensen, of the Mayo Clinic in the USA, described in detail the causes and physiological consequences of the profound disturbances in free fatty acid metabolism in abdominal obesity. We have known for decades that type 2 diabetes confers a very high risk of cardiovascular events and that most of these patients ultimately die of cardiovascular disease. The contribution of abdominal obesity to the excess cardiometabolic risk in this population was described by Dr Steven Haffner of the University of Texas Health Science Center, USA. The reviews arising from each of these presentations provide a useful snapshot of our current knowledge in this exciting field of research. However, if we are to manage abdominal obesity effectively, we must have accurate data on the prevalence of this condition in clinical practice as well as on its related health consequences. The International Day for the Evaluation of Abdominal Obesity (IDEA) was a worldwide survey of the prevalence of abdominal obesity in more than 170 000 patients consulting their primary care physicians in 63 countries. The fourth presentation outlined the rationale and design of this key study published here under the authorship of members of the IDEA Steering Committee. The symposium provided a timely and detailed exploration of the contribution of abdominal obesity to adverse cardiovascular outcomes. On behalf of our faculty, I hope you find the reviews arising from our presentations interesting and useful in your clinical practice.

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