2023+OMA临床实践声明：肥胖和高血压.pdf

Obesity Pillars 8(2023)100083Available online 7 August 20232667-3681/2023 The Authors.Published by Elsevier Inc.on behalf of Obesity Medicine Association.This is an open access article under the CC BY-NC-ND license(http:/creativecommons.org/licenses/by-nc-nd/4.0/).Obesity and hypertension:Obesity medicine association(OMA)clinical practice statement(CPS)2023 A R T I C L E I N F O Keywords Adiposopathy High blood pressure Hypertension Obesity A B S T R A C T Background:This Obesity Medicine Association(OMA)Clinical Practice Statement(CPS)provides an overview of the mechanisms and treatment of obesity and hypertension.Methods:The scientific support for this CPS is based upon published citations,clinical perspectives of OMA authors,and peer review by the Obesity Medicine Association leadership.Results:Mechanisms contributing to obesity-related hypertension include unhealthful nutrition,physical inac-tivity,insulin resistance,increased sympathetic nervous system activity,renal dysfunction,vascular dysfunction,heart dysfunction,increased pancreatic insulin secretion,sleep apnea,and psychosocial stress.Adiposopathic factors that may contribute to hypertension include increased release of free fatty acids,increased leptin,decreased adiponectin,increased renin-angiotensin-aldosterone system activation,increased 11 beta-hydroxysteroid dehydrogenase type 1,reduced nitric oxide activity,and increased inflammation.Conclusions:Increase in body fat is the most common cause of hypertension.Among patients with obesity and hypertension,weight reduction via healthful nutrition,physical activity,behavior modification,bariatric sur-gery,and anti-obesity medications mostly decrease blood pressure,with the greatest degree of weight reduction generally correlated with the greatest degree of blood pressure reduction.1.Introduction Beginning in 2013,the Obesity Medicine Association(OMA)created and maintained an Adult“Obesity Algorithm”(i.e.,educational slides and eBook)that underwent yearly updates by OMA authors and was reviewed and approved annually by the OMA Board of Trustees 1.This current OMA Clinical Practice Statement(CPS)regarding obesity and hypertension was derived from extensive updates to the content of the 2021 OMA Adult Obesity Algorithm.This CPS is one of a series of OMA CPSs designed to assist clinicians in the care of their patients with the disease of obesity.2.Obesity and high blood pressure/hypertension Hypertension can be defined as arterial blood pressure readings that,when persistently elevated above ranges established by medical orga-nizations,adversely affect patient health 2.For this discussion,high blood pressure refers to the physiologic measurement of the blood flow force on arteries,while hypertension refers to the disease of persistent high blood pressure.2.1.Blood pressure measurements Blood pressure measurements can be affected by many factors.A key for potentially actionable longitudinal assessment and treatment of high blood pressure is consistency in how blood pressure is measured,with recognition that blood pressure can be affected by:White-coat hypertension:Some patients may experience an increase in blood pressure due to anxiety and stress before and dur-ingencounters with the clinician.Such patients may benefit from home blood pressure(BP)monitoring and/or ambulatory BP moni-toring(ABPM)2.Masked hypertension:Some patients have normal blood pressure measurements in the clinician office,but elevated blood pressure upon ambulatory blood pressure monitoring or home blood pressure monitoring.Patients with masked hypertension are at risk for car-diovascular disease 3.Overstimulation:Patients should avoid caffeine,energy drinks,de-congestants,physical exercise,stressful situations,full bladder,and/or smoking for at least 30 minutes prior to BP measurement.For example,if a patient arrives to the medical office after experiencing frustration due to anxiety-producing traffic,then the patient should be given the opportunity to calm down in a quiet room for 30 mi-nutes or longer.Patients with full bladder,4 and/or who feel the need to urinate,may have increased blood pressure and should void prior to having blood pressure taken.Some patients with acute pain(e.g.,immediately after a phlebotomy stick)or discomfort may also experience transient increased blood pressure;the high blood Contents lists available at ScienceDirect Obesity Pillars journal homepage: https:/doi.org/10.1016/j.obpill.2023.100083 Received 6 August 2023;Accepted 6 August 2023 Obesity Pillars 8(2023)1000832pressure due to acute pain should resolve once the pain and/or discomfort resolves.On first measurement date,blood pressure should optimally be measured in both arms by repeated values separated by at least 1 min,with a record of the values and respective arms(left and right).Longitudinally,future BP measurement might best be measured on the same arm previously recorded as having the highest BP measurement.Patients should have clothing removed from the arm,be seated with feet flat on the floor(i.e.,not crossed),relaxed and quiet for 510 minutes prior to BP measurement.Crossed legs may increase blood pressure 5.During the BP measurement,the patient should not talk,nor should the patient be asked questions(including medical questions)during the time blood pressure is being assessed.Blood pressure should be obtained by trained medical personnel using a properly validated and calibrated blood pressure measure-ment device.The cuff should be placed on around the skin of the upper arm(i.e.,not over clothing).The cuff type and size should be appropriate for the patient arm size 6.If blood pressure is taken by a manual cuff(i.e.,sphygmomanometer):o The cuff should be placed one inch above the elbow bend,with the center of the cuff(often identified with a marker)aligned with the brachial artery,as found by palpation.o The cuff should be inflated until the radial pulse is no longer felt.o The cuff is then slowly deflated until the pulse is felt again.This number reading(mmHg)on the mercury column is the approxi-mate systolic blood pressure.o After deflating the cuff,and after waiting another 15 seconds,the bell of the stethoscope is placed over the brachial artery.o The cuff is then inflated 30 mmHg above the previous systolic blood pressure reading.o The cuff is then deflated(again)at 2 mmHg per second or beat.o The first of at least two regular beats is the systolic blood pressure.o When the beat disappears entirely,this is the diastolic blood pressure.o After obtaining BP readings,the cuff should be deflated,removed,and the systolic and diastolic BP should be recorded(in mmHg)immediately.2.2.Differential diagnosis of hypertension Among the more important considerations in evaluating high blood pressure in patients with obesity is ensuring an accurate diagnosis.While the adiposopathic effects of increased body fat are the most common cause of hypertension,simply because a patient has obesity does not negate the need to be mindful of other potential secondary causes that include 7:Pheochromocytoma Primary hyperaldosteronism Hypercortisolism Hyperthyroidism Renal artery stenosis Kidney diseases Side effects of concomitant therapies Familial or genetic syndromes That said,overweight and obesity clearly increases the risk of hy-pertension 810.As with obesity itself,hypertension is a chronic dis-ease that represents a major risk factor for cardiovascular disease(CVD),which is the most common cause of mortality among patients with obesity and hypertension 11.In the United States,hypertension is present in over 40%and 25%of individuals with obesity and over-weight,respectively.Over 70%of individuals with hypertension have overweight or obesity 12,13.When implementing comprehensive management of obesity,standards of care include healthful nutrition,physical activity,behavior modification,and medical treatment(e.g.,anti-obesity medications and/or bariatric procedures)14,15.Regarding medications,it is best to avoid obesogenic medications,and instead select pharmacotherapy that not only improves the body composition of patients,but also improves the health of patients,with control of blood pressure being a key health metric 16.Table 1 de-scribes ten takeaways from this current OMA CPS regarding obesity and hypertension.Fig.1 illustrates how positive caloric balance may lead to increase body fat storage.If during the process of body fat storage,adipocyte proliferation is impaired resulting in pathogenic adipocyte hypertrophy,then this may lead to“sick fat disease”(adiposopathy),as well as“fat mass disease.”The ensuing deranged endocrine and immune responses,as well as pathogenic physical forces,all may contribute to obesity complications such as an increase in blood pressure.3.Conceptually,how does the“fat mass disease”of obesity contribute to hypertension?Fig.2 illustrates how obesity may lead to fat mass disease.The increased body fat of obesity may result in pathogenic physical forces Table 1 Ten takeaway messages:obesity and hypertension.The disease of obesity may promote the development of hypertension,which is a major risk factor for cardiovascular disease.See text for details.1.The disease of obesity may promote an increase in blood pressure,which if persistent,leads to the metabolic disease complication of hypertension.2.Over 70%of individuals with hypertension have overweight or obesity.Hypertension is a major risk factor for cardiovascular disease(CVD);CVD is the most common cause of mortality among patients with obesity and hypertension.3.Patients with obesity and hypertension should optimally undergo comprehensive obesity management(e.g.,healthful nutrition,physical activity,behavior modification,and/or anti-obesity medications/bariatric procedures)14 as well as global CVD risk reduction(e.g.,optimal control of blood pressure,blood lipids,blood glucose,and smoking cessation)2.4.In addition to unhealthful food intake contributing to positive caloric balance,increased dietary sodium and saturated fats can also increase blood pressure.Conversely,nutritional interventions that contribute to healthful weight reduction and reduced sodium intake can help prevent and treat hypertension,especially when accompanied by routine physical activity and behavior modification.5.Obesity and“fat mass disease”can contribute to sleep apnea,kidney and renal vessel compression,perivascular adipose tissue(restricting blood vessel wall expansion)and increased cardiac output all of which can increase blood pressure.6.Mechanisms contributing to obesity-related high blood pressure include unhealthful nutrition,physical inactivity,insulin resistance,increased sympathetic nervous system activity,renal dysfunction,vascular dysfunction,heart dysfunction,increased pancreatic insulin secretion,sleep apnea,and psychosocial stress.7.Adiposopathic factors that may contribute to high blood pressure include increased release of free fatty acids,increased leptin,decreased adiponectin,increased renin-angiotensin-aldosterone system activation,increased 11 beta-hydroxysteroid dehydrogenase type 1,reduced nitric oxide activity,and increased inflammation.8.Bariatric surgery(e.g.,gastric bypass and sleeve gastrectomy)can produce clinically meaningful reduction in both blood pressure and body weight.9.Especially when accompanied by clinically meaningful weight reduction,many anti-obesity medications such as glucagon like peptide-1(GLP-1)receptor agonists(e.g.,semaglutide and liraglutide),GLP-1 and glucose-dependent insulinotropic peptide receptor agonist(e.g.,tirzepatide),and some bariatric procedures,decrease blood pressure.Some adrenergic anti-obesity agents may initially increase blood pressure(i.e.,sympathomimetics such as phentermine)with possible longer-term reduction in blood pressure(compared to baseline)after weight reduction.10.Unless the medication has blood pressure raising effects(i.e.,some adrenergic agents),the degree of reduction with anti-obesity medications generally correlates to the degree of weight reduction.T.L.Clayton et al.Obesity Pillars 8(2023)1000833contributing to biomechanical/structural abnormalities,which in turn can lead to sleep apnea,kidney and renal vessel compression,restriction of arteriole wall expansion,and increased cardiac output all that contribute to high blood pressure and the disease of hypertension 810,18.4.Conceptually,how does the“sick fat disease”(adiposopathy)of obesity cause hypertension?Independent of increased adiposity,high blood pressure can be caused by rare conditions such as pheochromocytoma,primary hyper-aldosteronism,hypercortisolism,hyperthyroidism,renal artery stenosis,kidney diseases,side effects of concomitant therapies,and familial or genetic syndromes 7.That said,increased body fat is by far the most common cause of hypertension.Estimates suggest the essential hyper-tension is attributable to increased adiposity in 78%in men and 65%in women 12,19 Other reports suggest up to 80%of essential hyperten-sion is attributable to increased adiposity 20.Anatomically,if during positive caloric balance proliferation and differentiation of adipose tis-sue is impaired in subcutaneous adipose tissue,then the energy overflow Fig.1.Obesity,adiposopathy(sick fat disease),fat mass disease,and obesity complications.An increase in body fat can ultimately lead to endocrine/metabolic and biomechanical/structural abnormalities,potentially leading to complications such as increased blood pressure 17.Fig.2.Fat mass disease and hypertension.Increased body fat leading to biomechanical and structural abnormalities(i.e.,“fat mass disease”)may lead to hy-pertension through promotion of sleep apnea,kidney/renal vessel compression,perivascular adipose tissue,and increased cardiac output(heart rate x stroke volume)810,17,18.T.L.Clayton et al.Obesity Pillars 8(2023)1000834may result in fat deposition within and/or around other body tissues,such as the liver,muscle,and pancreas potentially contributing to“fatty liver”and“fatty muscle”and lipotoxicity leading to insulin resistance 21.This energy overflow may also increase fat deposition in the visceral region,as well as increase fat surrounding the blood vessels(i.e.,perivascular fat),heart,and kidney 21.An increase in the volume and activity of fat depots surrounding the arterial blood vessels,heart,and kidney may not only contribute to biomechanical dysfunction,but these fat depots may have pathogenic local and systemic immune and endocrine effects that contribute to high blood pressure 22.In short,Fig.3 illustrates how adiposopathic complications of obesity may lead to functional adiposopathy,or“sick fat disease,”resulting in immuno-pathies,endocrinopathies,and increased circulating free fatty acids,all that may contribute to high blood pressure 810,18.5.Nutrition and blood pressure Fig.4 describes various mechanisms accounting for obesity-related hypertension.Among these mechanisms includes unhealthful nutri-ti