Obesity and difficult-to-treat arterial hypertension.

Abstract

Hypertension and obesity frequently coexist. While hyper-tension is the ‘old’ disease with well-established, albeitchanging, guidelines for its investigation and management,the growing prevalence and severity of obesity presents newcomplexities. These are often in terms of varying types ofpresentation, assessment of diverse but important associ-ated clinical risks, and management of increasing numbersof patients with raised blood pressure.Obesity is associated with more severe hypertension, aneed for an increased number of anti-hypertensive medica-tions, and an increased likelihood of never achieving bloodpressure control (1). It is not just obesity, as defined bybody mass index, that is important, but also fat distributionhighlighted by, e.g., recent English data which have shownthat men with a raised waist circumference are more thantwice as likely to have high blood pressure as those with awaist circumference of 102 cm or less (51% compared with23%) (2). This pattern was similar for women in that 42%of those with a raised waist circumference had high bloodpressure, compared with 15% of those with a waist cir-cumference of 88 cm or less (2). The interplay betweenobesity and blood pressure remains poorly recognized. Forexample, a search for the terms ‘obesity’ and ‘obstructivesleep apnoea’ in the UK National Institute for Health andClinical Excellence (NICE) guidelines (published in 2006(3) and updated in 2011 (4)) identifies only one ‘hit’ andthat relates to Cushing’s syndrome.Last year, the European Association for the Study ofObesity (EASO) and the European Society for Hyperten-sion produced a joint statement on obesity (5) and‘difficult-to-treat’ arterial hypertension. This consensusdocument highlighted the growing clinical importance ofthis combination to all clinicians.Thirty years ago, it was thought that hypertension inobese individuals was driven by circulating volume expan-sion and increased cardiac output, rather than increasedperipheral resistance. However, it is now known that thepathophysiology is complex, involving adipocytokines (6),insulin resistance, neuroendocrine dysfunction, nutritionalfactors associated with obesity (such as high fat, a highsodium diet (7), and possibly fructose consumption (8)) aswell as increased levels of physical inactivity. The EASOconsensus statement considers ‘known knowns’ and‘known unknowns’ (9).What is known? The starting point for detection andclinical care of hypertension in the obese individual is theability to measure blood pressure accurately. The need forlarge cuff diameters for obese patients was recognized anddetailed in the 1980s and yet, even today, this message hasfailed to permeate into clinical care. 45% of automatedblood pressure devices assessed in 2010 failed to mentionthe need for an appropriate cuff size (10), and a recentaudit of hospital blood pressure devices found that nearly90% of the aneroid devices had only one cuff size available,suggesting that ‘miss-cuffing’ may be a serious cause ofinaccurate blood pressure measurements (11).Lifestyle interventions are the mainstay of obesity man-agement programmes and are also advocated in the preven-tion and treatment of arterial hypertension, but it isinteresting that they are rarely adequately addressed inhypertension guidelines. Furthermore, anti-obesity drugsare known to lead to clinically meaningful reductions inblood pressure – especially in previously hypertensive sub-jects. However there are few approved pharmacologicalagents, and many have, or have had, unwanted effects onincreasingheartratethatmayoffsetthepotentialbenefitsof