To mark the first anniversary of Cardiovascular Endocrinology, a mini symposium was held in Manchester, UK on 14 March 2013 to coincide with the annual Diabetes UK national professional conference. The symposium explored the historical aspects of the intersection of endocrinology and cardiovascular disease and provided updates in the basic science and therapeutics for cardiometabolic disease.
Andrew Krentz, MD, FRCP
Editor-in-Chief Cardiovascular Endocrinology; Senior Director of Scientific Services, Profil Institute for Clinical Research, San Diego, USA; Visiting Professor of Medicine, Bedfordshire & Hertfordshire Postgraduate Medical School, UK.
Hormonal homeostasis and the heart
In his introductory presentation, Prof Krentz paid tribute to the pioneering studies of Ernest Starling who, during a few short years at the start of the 20th century codescribed the first hormone ‘secretin’, coined the word ‘hormone’ and described the celebrated Frank–Starling principle of heart contractility. The profound influence of endocrine disorders on cardiovascular function is well recognized. In the space of a generation, classic endocrinology has been superseded by the appreciation that fat, the gut, and the heart also function as bona fide endocrine organs in their own right. A brief review of the effects of adipocytokines as regulators of metabolic and vascular function was followed by consideration of the metabolic contractile coupling as a promising therapeutic target in heart failure. An update on recent pharmacological advances focused on the glucagon-like peptide-1 agonists and the partial fatty acid oxidation inhibitors; these two classes share the intriguing ability to simultaneously improve aspects of vascular and metabolic function. This observation points to bidirectionality in metabolic vascular disorders with the prospect of novel therapeutic approaches.
Martin Rutter, MD, FRCP
Senior Lecturer in Cardiometabolic Medicine, Institute of Human Development, University of Manchester, UK; Honorary Consultant Physician, Manchester Royal Infirmary, UK.
Low testosterone and cardiovascular disease: the case for causality
The male and female reproductive organs are considered classic components of the endocrine system. Although it is well recognized that sex hormones can modulate cardiovascular health, the influence of sex steroid hormones on vascular physiology remains incompletely delineated. A close association between low androgen levels in men and a heightened risk of cardiometabolic disease is now well established. However, the directionality of cause and effect remains uncertain. In his lecture, Dr Rutter focused on the mounting evidence implicating adult male hypogonadism with an increased risk of atherosclerotic cardiovascular disease. Using the causality criteria proposed by the eminent epidemiologist Sir Austin Bradford Hill, Dr Rutter examined the relationship under the following headings: strength of association; consistency; specificity; temporal relationship; dose–response; biological plausibility; coherence; reversibility through experiment; and analogy. Given the increasing recognition of male hypogonadism in clinical practice allied to growing enthusiasm for testosterone replacement therapy, definitive prevention studies are urgently required.
Tony Heagerty, MD, FRCP, FMedSci
Professor of Medicine & Head of the Cardiovascular Research Group, Institute of Human Development, University of Manchester, UK; President of the British Hypertension Society.
Adipokines and vascular tone
Fat-derived adipocytokines have emerged as important mediators of metabolic–vascular interactions. Obesity is associated with disturbances of adipocytokine physiology that are implicated in the well-documented increase in the risk of atherothrombotic disease that accompanies excess adiposity. It is now apparent that adiponectin and leptin secreted by the perivascular tissues may influence local and regional vascular reactivity, the latter effect being known as vasocrine signalling. Professor Heagerty presented data from his laboratory demonstrating that exaggerated arteriolar contractility in response to noradrenaline is abolished following removal of perivascular fat. Moreover, recent studies on obese individuals show rapid and marked improvement in the vascular responses of resistance vessels after bariatric surgery. Of note, this improved vascular reactivity was observed with relatively modest degrees of weight loss. The latter observation is reminiscent of the rapid improvements in glucose metabolism described after surgically induced weight reduction in which novel hormonal modulators have been implicated.
Conflicts of interest