metabolic syndrome: clinical perspective for best practice

CLINICAL PRACTICE

Metabolic syndrome: Clinical perspective for best practiceDarin Olde, MSN, APRN, FNP (Family Nurse Practitioner)1, Patricia Alpert, DrPh, MSN, APN, FNP, PNP, CNE,FAANP (Associate Professor)2,3, & Alona Dalusung-Angosta, PhD, APN, FNP, NP-C (Assistant Professor)2,4

1Silver Sage Center for Family Medicine, Reno, Nevada2Las Vegas School of Nursing, University of Nevada, Las Vegas, Nevada3First Med Health & Wellness, Las Vegas, Nevada4Advanced Urgent Care, Las Vegas, Nevada

KeywordsMetabolic syndrome; cardiovascular disease;

dyslipidemia; diabetes.

CorrespondenceAlona Dalusung-Angosta, PhD, APN, FNP, NP-C,

University of Nevada, Las Vegas School of

Nursing, 4505 Maryland Parkway Box 453018,

Las Vegas, Nevada 89154. Tel: 702-895-3360,

ext 1218 (work); Fax: 702-895-4807 (work);

E-mail: [email protected]

Received: July 2013;

accepted: January 2012

doi: 10.1002/2327-6924.12048

Abstract

Purpose: To explore current studies on metabolic syndrome (MetS), includingits complex pathophysiology and to describe the unique role of the advancedpractice nurse including management and ethical decision making utilizing acase study to exemplify salient points.Data sources: From original research articles extracted from nursing andmedical databases.Conclusions: MetS is a constellation of characteristics that increases the riskfor the development of diabetes and cardiovascular disease. The pathophysiol-ogy of MetS is not completely understood, but is thought to involve a complexinteraction between the environment, genetic susceptibility, insulin resistance,and abnormal adipose tissue function.Implications for practice: The role of the advanced practice nurse is appro-priate for early intervention and counseling of patients with MetS and thosewho are at risk, as well as addressing the ethical challenges that accompanytheir care.

Introduction

Metabolic syndrome (MetS) is a constellation of riskfactors that increase a person’s risk of developing car-diovascular disease (CVD). Also known as syndromeX, dysmetabolic syndrome, and insulin resistance syn-drome, MetS has been increasingly studied in recentdecades, partly because of increasing prevalence in theUnited States, and globally. Moreover, estimates suggestMetS confers twice the risk of developing coronary heartdisease (CHD) over the next 5–10 years, and the riskof developing type 2 diabetes mellitus (T2DM) is five-fold higher than the population without the syndrome(Alberti et al., 2009).

The purpose of this article is to (a) explore currentstudies on MetS including its complex pathophysiology,and (b) describe the unique role of the advanced practicenurse (APN) including management utilizing a case studyto exemplify salient points.

Review of literature

Definition, epidemiology, and prevalence

According to the diagnostic criteria of the NationalCholesterol Education Program Adult Treatment Panel

III (NCEP/ATP III), patients with MetS have at leastthree of five characteristics: elevated blood pressure (BP)≥ 130/85 mmHg or treatment for hypertension (HTN);atherogenic hypertriglyceridemia (TG ≥ 150 mg/dL) ordeficient high-density lipoprotein cholesterol (HDL-C <

40 mg/dL in males or <50 mg/dL in females) or treat-ment for either condition; impaired fasting glucose (≥100mg/dL) or treatment for hyperglycemia; and increasedabdominal waist circumference defined as ≥102 cm or40 inches for males and ≥88 cm or 35 inches for females(Alberti et al., 2009; Grundy et al. 2005; International Di-abetes Federation [IDF], 2006). Currently experts debatewhether or not MetS is a condition unto itself, or merelya cluster of independent clinical criterion. Those in thelatter group proposed treatment should focus on reduc-ing independent risk factors. To the contrary, Albertiet al. (2009) suggested a syndrome is appropriatelynamed as a clustering of factors that occur together moreoften than by chance alone. Moreover, in a 2008 meta-analysis review including 172,573 individuals, Grundy(2008) showed the relative risk for coronary events anddeath were associated with the syndrome, even after ad-justing for traditional CHD risk factors (cigarette smoking,hypertension, decreased HDL-C, family history of prema-ture CHD, and age). Grundy also suggested the syndrome

644 Journal of the American Association of Nurse Practitioners 25 (2013) 644–652 C©2013 The Author(s)C©2013 American Association of Nurse Practitioners

D. Olde et al. Metabolic syndrome: Clinical perspective for best practice

cannot be entirely explained by the presence of theserisk factors alone. He argued that by examining the clus-ter of characteristics, the focus changes to the underly-ing causes and lifestyle modifications to reduce long-termrisk. Much of this debate stems from disagreement amongexperts from the organizations that have established thecriteria used to diagnose MetS. For example, to make thediagnosis of MetS the IDF states the hallmark criterionis central obesity in addition to two other criteria; theWorld Health Organization (WHO) says the hallmark cri-terion must include impaired glucose (i.e., frank T2DM,impaired glucose tolerance, impaired fasting glucose, orinsulin resistance) in addition to two other criteria. Ac-cording to NCEP/ATPIII, as noted above, the diagnosis ofMetS is made if an individual exhibits three of the fivecriteria.

Although this debate continues, there is universal ac-ceptance among researchers and clinicians about the im-portance of reducing the incidence of CHD and T2DM.CHD remains the leading cause of death in the UnitedStates (American Heart Association [AHA], 2011a), fol-lowed by cerebrovascular diseases as the third leadingcause of death with diabetes mellitus as the seventh (Xu,Kochanek, Murphy, & Tejada-Vera, 2010).

Epidemiological studies based on NCEP waist circum-ference criterion indicate 34.5% of adults ≥20 years oldhave the syndrome in the United States (Ford, 2005).Using the IDF waist circumference cutoffs, the prevalenceincreases to 39%. It is estimated more than 64 millionAmericans have the syndrome and it may be presentin >40% of individuals 60 years of age or older (Ford,2005). Previous estimates from the 1988 to 1994 cohortof the National Health and Nutrition Examination Survey(NHANES) suggested the syndrome was less common, atapproximately 22%–25% of the population ≥20 yearsold (Park et al., 2003). But as the definition of MetSbecomes more consistent, and rates of obesity as wellas life span increases, these estimates need to be revisedupwards.

MetS is on the rise worldwide, and is thought to par-allel the increasing prevalence of obesity. About 34.2%of Americans are overweight (body mass index [BMI]25–29.9 kg/m2) and 33.8% are obese (BMI ≥ 30 kg/m2)according to 2007–2008 NHANES data (Flegal, Carroll,Ogden, & Curtin, 2010). Obesity is increasing in youngercohorts as well. According to Grundy (2008) data from1999 to 2004 suggested 16% of female and 18% ofmale children and adolescents were overweight. The1999–2000 NHANES estimates suggested the prevalencewas lower at 15% of children and adolescents in theUnited States being overweight (National Heart, Lung,and Blood Institute [NHLBI], 2010). Prevalence of theMetS is strongly correlated to both obesity and age, re-

gardless of gender or ethnicity. Early reports suggestedthe condition was more common in women than men,but some data suggested the margin of gender differenceis less than previously estimated (Grundy, 2008).

However, prevalence does change among men andwomen in specific ethnic groups, which has become in-creasingly studied in the last decade. Ford (2005) re-ported African American women had higher prevalencethan men at 33.8% and 21.6%, respectively. HispanicAmerican women also showed higher prevalence thanmen at 37.8% and 32.2%, respectively. However, Cau-casian men were more likely to have the syndrome thanwomen by a small margin at 36.0% and 35.4%, respec-tively. Internationally, Americans and Canadians had ahigher prevalence of the syndrome than many Europeanor Asian nations. Using NCEP-ATP-III criteria, Grundy(2008) estimated the prevalence of the syndrome amongEuropeans at approximately 25%, with less than 20%prevalence in Southeast Asia. As of yet, a lack of largeepidemiologic studies with adequate sample size substan-tially limited comparisons in other countries.

Emerging risk factors: Socioeconomicand environmental risk

Low adulthood socioeconomic status (SES) was asso-ciated with higher rates of MetS in numerous studies(Chichlowska et al., 2009; Loucks, Magnusson et al.,2007). However, there were conflicting results regardingthe association between gender and low SES in child-hood, and development of MetS as an adult. In largerstudies, the MetS was associated with low SES acrossthe life span with women, but less so for men. TheAtherosclerosis Risk in Communities (ARIC) study ex-amined life course SES and prevalence of the MetS inmore than 10,000 African American and Caucasian menand women and found significant correlations for bothCaucasian and African American women. Of both eth-nic groups, women with low SES in childhood, earlyadulthood, middle adulthood, or cumulatively, weremore likely to develop the syndrome than women withhigh SES (Chichlowska et al., 2009). Similarly, Loucks,Magnusson et al. (2007) found women aged 25–65 withincome below the poverty line were more likely to de-velop the syndrome than women with higher incomeratios even after adjusting for age, race/ethnicity, andmenopause status. Interestingly, income and educationwere not associated with the syndrome for males, or fe-male adolescents and older adults (age > 65 years).

Some authors suggested the higher prevalence of MetSamong women has to do with economic disparities be-tween men and women, particularly as a result of physi-cal attributes. Chichlowska et al. (2009) cited two studies

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Metabolic syndrome: Clinical perspective for best practice D. Olde et al.

that suggested obesity may affect economic trajectory forwomen more so than for men, particularly during ado-lescence and young adulthood (Gormaker, Must, Perrin,Sobol, & Dietz, 1993; Sargent & Blanchflower, 1994).The lower SES during this sensitive period of develop-ment was associated with increased prevalence of thesyndrome. It was also suggested women with low SESare more likely to be unemployed, a single parent, ordepressed (Thurston, Kubzansky, Kawaci, & Berkman,2005).

While smaller reports with limited samples showedconflicting data, theories linking cumulative economicchallenges and different environmental stressors are gain-ing momentum as a risk factor for the syndrome, par-ticularly for adult women. In the Coronary Artery RiskDevelopment in Young Adults study, childhood SES andearly family environment assessed through models thatmeasured depression, hostility, and poor quality of so-cial contacts, showed these factors were associated withmetabolic function (Lehman, Taylor, Kiefe, & Seeman,2005).

Environmental associations have been well docu-mented in the development of MetS. Cigarette smok-ing, excessive alcohol intake, and greater reliance onlow-cost, high-energy dense foods with fewer nutrientssuch as sugar, fat, or refined-grain foods were all relatedto higher prevalence of the MetS, or obesity (Loucks,Rehkopf, Thurston, & Kawachi, 2007). Empty caloriesand high-energy dense foods were shown to cost lesscompared to low-density foods, such as fruits and veg-etables, which may lead those with fewer economic re-sources to less desirable dietary choices. Similarly, thepositive correlation between depression and low SES iswell documented, and among this group smoking, alco-hol use, and sedentary lifestyles as well as less compli-ance with medication regimens all showed positive cor-relations. Loucks, Rehkopf et al. (2007) cited researchby Kawachi and Berkman (2003) indicating people withlow SES tend to live in environments with greater crimerates, fewer recreational opportunities, more fast foodrestaurants, liquor stores, and billboard advertisementsfor cigarettes, fast food, and alcohol—all of which are as-sociated with metabolic dysfunction or obesity. Finally,The U.S. Census Bureau showed the likelihood of beingcovered by health insurance increased with income alongwith the likelihood of seeking and receiving preventa-tive care for diseases such as hypertension, obesity, mixeddyslipidemia, and hyperglycemia. Surveys from the U.S.Census Bureau suggested poverty and number of peoplewithout health insurance increased from 2008 to 2009(DeNavas-Walt, Proctor, & Smith, 2009). As more andmore individuals struggle with current economic chal-

lenges, MetS is likely to increase concomitantly in theabsence of adequate attention and treatment.

Pathophysiology

Despite the substantial increase in research and clini-cal focus over the last two decades, the pathogenic in-teractions leading to MetS are still debated. Historically,insulin resistance was suspected as the underlying cause,and was initially incorporated as a diagnostic criterion. In-ternational focus lead to changes in the definition and di-agnostic criteria, but insulin resistance remains a predom-inant etiologic theory. More recently, research suggestedobesity, excess fat mass, or abnormal adipose metabolismwas the underlying cause (Grundy, 2007; Teran-Garcia &Bouchard, 2007). Both proposed mechanisms culminatein a proinflammatory and prothrombotic state associatedwith MetS as measured by serum inflammatory mark-ers and procoagulation biomarkers. The proinflammatoryand prothrombotic state sets the stage for endothelial dys-function and the development of CVD.

Abnormal adipose metabolism

Several authors suggested abnormal adiposemetabolism is the driving force behind the MetS viafour interrelated mechanisms: abnormal adipose tissuebiology, excess fat mass, high levels of visceral fat,and ectopic fat deposition (Teran-Garcia & Bouchard,2007). Adipose tissue produces and secretes hormones,including cytokines—also known as adipokines—freefatty acids (FFAs), prostaglandins, and angiotensinogen.Among the predominant adipokines implicated in MetSare leptin, adiponectin, and resistin as well as otheradipocyte products such as FFA, retinol binding protein4, and fatty-acid binding protein. As excess fat tissueaccumulates, adipocytes increase in size. The larger cellsexhibit greater rates of triglyceride synthesis, lypolysis,and FFA transmembrane flux. Numerous adipokines arereleased into the blood stream, such as leptin, resistin,adiponectin, tumor necrosis factor α, angiotensinogen,interleukin 6, C-reactive peptide, and others. Theseproinflammatory products affect endothelial cells andstimulate other inflammatory modulators.

Large omental adipocytes exhibit high rates of ly-polysis. The products of these cells enter hepatic cir-culation. Bjorntorp (1990) suggested higher concentra-tion of these products in hepatic circulation results inhepatic dysfunction as measured by insulin clearance,hepatic glucose, and very low-density lipoprotein (LDL)production. Other researchers suggested subcutaneousabdominal adipose tissue contributes in a similar fashion,

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and visceral adipocytes are not as large a contributor tohepatic dysfunction as initially thought (Teran-Garcia &Bouchard, 2007).

Ectopic fat deposition in nonadipose tissue, such as theliver, skeletal muscle, and pancreas, has also been impli-cated in insulin resistance. As adipocytes become moreinsulin resistant, researchers showed elevated rates ofserum FFA, and greater ectopic fat accumulation via mag-netic resonance spectroscopy, generating the “lipotoxic”effect. Researchers suggested ectopic fat accumulationmay be one mechanism by which organ systems lose in-sulin sensitivity (Lee et al., 1994; Seppala-Lindroos et al.,2002). This suggests excess calories, fat mass, ectopic fatdistribution, and the subsequent expulsion of FFA andadipokines may be how organ systems resist insulin.

Among the diagnostic criteria of MetS are elevated TGsor low HDL-C. But other cholesterol abnormalities are as-sociated with the syndrome, including a shift to smaller,denser, LDL cholesterol (LDL-C) particles. Smaller parti-cle LDL-C is more strongly related to coronary atheroscle-rosis and cardiovascular (CV) events than direct mea-sures of LDL-C. The smaller particle LDC-C may be moretoxic to endothelium, more mobile through endothelialbasement membranes, more adherent to endothelial cellwalls, are more susceptible to oxidation, and are more se-lectively bound to macrophages (Singh, Arora, Goswami,& Mallika, 2009). Hence, measuring LDL particle distri-bution may be more indicative of CV risk than a singlemeasure of LDL-C.

Insulin resistance

Insulin resistance has long been recognized as a defin-ing characteristic of the MetS. The extent to which itcauses the syndrome is uncertain (Grundy, 2007) becauseinsulin may have more endocrine functions than regulat-ing glucose into cells. Insulin also prevents lipolysis andstimulates the enzyme lipoprotein lipase. This enzyme isthought to prevent the release of FFA into circulation viacyclic AMP-dependent enzyme-hormone sensitive lipase.As more FFA are released into circulation, this inhibitsthe antilipolytic action of insulin (Singh et al., 2009). Hy-perinsulinemia may occur for several years with normalor near normal levels of fasting glucose. But as pancre-atic cells slowly lose the ability to produce insulin andlipoprotein lipase activity diminishes, lipolysis increases,further leading to the downward spiral of FFA release,ectopic fat deposition, endocrine organ dysfunction, andinsulin resistance. In later stages of the disease, DMT2 re-sults.

Grundy (2007) suggested metabolic susceptibility is animportant precursor to the development of MetS withexcess body fat leads the precursor. Susceptible risk fac-

Table 1 Commonly reported heritability estimates for components of the

metabolic syndrome

Phenotype Estimated heritability (%)

Body composition

BMI 25–60

Body fat 25–40

Abdominal obesity 40–55

Insulin/glucose

Fasting glucose 10–75

Fasting insulin 20–55

Insulin resistance of T2DM 46–90

Lipids

Triglycerides 25–60

LDL-C 25–60

HDL-C 30–80

Blood pressure

Systolic BP 20–70

Diastolic BP 10–50

Hypertension 50

Microalbuminuria 30

Argyropoulos et al. (2005).

tors include insulin signaling defects, adipose tissue disor-ders, as well as lifestyle and physical characteristics suchas physical inactivity, mitochondrial defects, aging, poly-genic variation, or drug use. Risk factors vary among dif-ferent ethnic groups, with different rates of heritability.Hence, genetic susceptibility is thought to be a substan-tial risk factor for MetS possibly explaining why certainethnic groups are more likely to exhibit metabolic dis-orders. Argyropoulos, Smith, and Bouchard (2005) re-ported BMI, body fat, and abdominal obesity have anestimated heritability of 25%–60%; insulin resistance orT2DM from 46% to 90%; LDL-C and triglycerides from25% to 60%; and hypertension of approximately 50%.Overall, the heritability of MetS is about 30% (for a com-plete list of commonly reported heritability estimates seeTable 1).

A patient with MetS

Health history

A 71-year-old Caucasian female, Ms. B, presented toa primary care clinic to establish care as her previousprovider retired. She was recently hospitalized for chestpain and was diagnosed with mild CHD after undergoinga battery of tests that were negative for acute pathology.A myocardial perfusion study showed mild ischemia ofthe apex, anterior wall, and lateral wall without acutestenosis or obstruction. At discharge she was advised tofollow up with a primary care provider. In addition toher diagnosis of mild CHD her past medical history indi-cated diagnoses of osteoarthritis in her left knee, essential

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Table 2 Ms. B’s fasting lipid profile

Lab test Result Normal range Unit

Chemistry panel

Sodium 135 135–145 mmol/L

Potassium 4.1 3.6–5.5 mmol/L

Chloride 98 96–112 mmol/L

CO2 26 20–33 mmol/L

Glucose 98 65–99 mg/dL

BUN 13 8–22 mg/dL

Creatinine 0.8 0.5–1.4 mg/dL

GFR >90 >90 mL/min/1.73

Calcium 9.6 8.4–10.2 mg/dL

Aspartate amino-tran 32 12–45 U/L

Alanine amino tran 31 2–50 U/L

Alkaline phosphatase 96 30–99 U/L

Bilirubin total 0.5 0.1–1.5 mg/dL

Albumin 3.9 3.2–4.9 g/dL

Total protein 7.2 6.0–8.2 g/dL

Globulin 3.0 1.9–3.5 g/dL

Albulin/globulin ratio 1.3 g/dL

Lipid panel

Total cholesterol 192 100–200 mg/dL

Triglycerides 176 H 0–150 mg/dL

HDL-C 52 40–59 mg/dL

LDL-C 105 H <100 mg/dL

Unit key: mmol/L, milimoles/liter; mg/dL, milligram/deciliter; mL/min,

milliliter/minute; U/L, units/liter; g/dL, grams/deciliter; H, indicates abnor-

mally high levels.

hypertension, dyslipidemia, and gastroesophageal reflux.She underwent hemorrhoidectomy, hysterectomy, andvaginal vault repair secondary to urinary incontinence.In 2009, she had bilateral intraocular lens transplantfor cataracts and esophageal dilation on two separateoccasions.

Ms. B’s parents lived into their 70s. Her mother diedfrom complications related to diabetes and her father diedof heart failure and CHD. Her review of systems wasnoncontributory.

Physical examination

Ms. B presented as a morbidly obese female in no acutedistress. Her weight was 224 pounds, and height was 5′2′ ′,with a BMI of 41 kg/m2. Abdominal exam showed centraladiposity. Her waist circumference was approximately 43inches. Extremity range of motion was limited becauseof excessive adipose tissue. Varicose veins were noted inbilateral lower extremities. Her BP at presentation was150/90 mmHg, and fasting lipid profile results were ele-vated (see Table 2). All other exam findings were unre-markable. Given these objective findings, Ms. B met thediagnostic criteria for MetS.

Table 3 Diagnoses and plan of care

Diagnosis Plan

Morbid obesity Dietary referral

(metabolic syndrome) Exercise (cardiac rehab referral)

TSH, free T4

Hypertension, uncontrolled Dietary referral (DASH diet)


Add: atenolol 50 mg, 1 tab, PO QD

Return to office 1 month

Dyslipidemia, uncontrolled Dietary referral


Add: nicotinic acid 500 mg QHS

Return to office 1 month (increase

nicotinic acid as tolerated)

Repeat CMP, fasting lipids 3 months

Coronary heart disease Dietary referral

Exercise (cardiac rehab referral)

Continue aspirin

Preventive care/education Education regarding new

medications, side effects, timing,

adverse reactions

Education regarding signs of

myocardial ischemia

Education regarding importance of

diet/exercise in disease prevention,

treatment

Depression screen

Sleep apnea screen

Family therapist referral

Table 4 DASH diet recommendations

Servings per day based on caloric needs

1600 2000 2600

Food Calories Calories Calories

Grainsa 6 6–8 10–11

Vegetables 3–4 4–5 5–6

Fruits 4 4–5 5–6

Fat free or low fat milk

products

2–3 2–3 3

Lean meats, poultry, and

fish

3–6 6 or less 6

Nuts, seeds, and legumes 3 per week 4–5 per week 1

Fats and oils 2 2–3 3

Sweets and added 0 <5 per week ≤2

aWhole grains are recommended formost grain servings as a good source

of fiber and nutrients.

NHLBI. (2006). Your guide to lowering your bloodpressurewithDASH.U.S.

Department of Health and Human Services (NIH Publication No. 06-5834).

Management of MetS in primary care

The management plan for patients with MetS, such asMs. B, includes pharmacological and nonpharmacologicaltreatment for HTN, CHD, dyslipidemia, and obesity. Theseare presented in Tables 3–7.

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Table 5 Soluble fiber and total fiber amounts (in grams) for various foods

Soluble fiber Total fiber

Whole-grain cereals—1/2 cup cooked (except where noted)

Barley 1 4

Oatmeal 1 2

Oatbran 1 3

Psyllium seeds, ground (1 tbsp) 5 6

Fruit—1 medium (except where noted)

Apple 1 4

Banana 1 3

Blackberries (1/2 cup) 1 4

Citrus (orange, grapefruit) 2 2–3

Nectarine 1 2

Peach 1 2

Pear 2 4

Plum 1 1.5

Prunes (1/4 cup) 1.5 3

Legumes—1/2 cup cooked

Black beans 2 5.5

Kidney beans 3 6

Lima beans 3.5 6.5

Navy beans 2 6

Northern beans 1.5 5.5

Pinto beans 2 7

Lentils (yellow, green, orange) 1 8

Chick peas 1 6

Black-eyed peas 1 5.5

Vegetables—1/2 cup cooked

Broccoli 1 1.5

Brussels sprouts 3 4.5

Carrots 1 2.5

National Heart, Lung, and Blood Institute. (2005). Your guide to lowering

your cholesterol with TLC.U.S. Department of Health andHuman Services

(NIH Publication No. 06-5235).

tbsp, tablespoon.

Table 6 Lowering LDL-C with dietary changes

Change LDL-C

Saturated fat Decrease to less than 7% of calories 8%–10%

Dietary cholesterol Decrease to less than 200 mg/day 3%–5%

Weight reduction Lose 10 pounds if BMI ≥ 25 5%–8%

Soluble fiber Add 5–10 g/day 3%–5%

Plant sterols/stanols Add 2 g/day 5%–15%

Total LDL reduction 20%–30%

National Heart, Lung, and Blood Institute. (2005). Your guide to lowering

your cholesterol with TLC.U.S. Department of Health andHuman Services

(NIH Publication No. 06-5235).

An important challenge of the therapeutic relationshipis inspiring behavior change. APNs are in the unique posi-tion to encourage patients to make changes. Motivationalinterviewing (MI) and frequent follow-up is one strategyfor helping patients rationalize the need for care by ex-ploring and removing ambivalence. MI technique is a col-laborative, patient-centered approach of guiding patients

Table 7 Self care requisites, deficits and nursing agency

Requisites Potential deficits Nursing agency

Universal Diet Dietary referral/education

� Calorie control

� Portion control

� Saturated fat excess

� Fiber deficiency

� Stanol/sterols

limitations

� Dairy portions

� Cholesterol excess

� Salt excess

� Vitamin D deficiency

Exercise/activity Cardiac rehabilitation

� Mobility constraints

or exercise

equipment

referral physical therapy

� Access to walkways

� Knowledge deficit

Developmental Environment Support group/community

� Temperature

constraint

involvement/education

� Sunlight limitation

� Activity limitations

Social interactions Social network/peer group

� Loss of peer group interaction

� Family/friend loss

Generativity

� Life stage regression Psychotherapy referral

Psychological

� Age-related decline Support group/depression

screen

Health deviation Sleep disturbances

Pain/osteoarthritis

Obesity

Hypertension

Dyslipidemia

Vitamin D deficiency

GERD

Obstructive sleep apnea

screening

Cognitive behavioral sleep

training

Depression screen

Vitamin deficiency screening

Diet/physical therapy referral

GERD, gastroesophageal reflux.

to elicit and strengthen motivation for change (Miller& Rollnick, 2009). MI has been utilized in a variety ofhealthcare settings and it has been shown to promote be-havior change and improve lifestyle choices among pa-tients. This behavioral approach can be used during pri-mary care visits because it is easy to learn, it is brief, andit focuses on the patient’s concerns. This is an ideal ap-proach for patients with MetS such as Ms. B who is mor-bidly obese.

Weight loss strategy involves lifelong changes tolifestyle, behavior, and dietary practices. Among thechallenges for obese patients is building motivation forchange; this is particularly challenging for Ms. B, who dis-likes the concept of exercise. She refused suggestions to

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engage in vigorous activity, mostly because of her kneepain. The APN assessed Ms. B’s level of readiness to en-gage in physical activity and realized she would needfurther encouragement and assistance. Physical activityreduces the risk of MetS, but patients like Ms. B re-quire referral to a cardiac rehabilitation center for exer-cise stress testing so her capacity and safety for exercisecan be determined. Overall, supervised exercise trainingthrough cardiac rehabilitation is safe, effective, and canimprove her metabolic disorder. Studies assessing adher-ence to cardiac rehabilitation showed greater adherenceif patients begin the program early in the recovery phaseof CHD. Asking Ms. B to attend cardiac rehabilitation wasnot realistic because she lives part-time with both her sonin California and her daughter in northern Nevada. Shewas also not motivated to exercise because of knee pain,even if the pain subsides when she increased the fre-quency of her activity. She expressed enjoying leisurelywalks near the beach on the boardwalk when she is inCalifornia. At her daughter’s residence the weather is lessfavorable, with hot summers and cold winters, which re-ally limits her activity.

She also requires a dietary referral to help her improveall lipid parameters, BP, and weight. While dietary re-ferral is optimal Ms. B’s living arrangements may not beideal for prescribed meal preparation. Her son or daugh-ter prepares most meals. Her son being a chef, preparesmeals higher in calories and while Ms. B reported eatingsmaller portions her son and his girlfriend plan and createall of the meals in his home. Her daughter, on the otherhand, prepares meals suggested by the patient, which isreported to be healthier. In spite of being conscious ofgood eating practices she is not able to lose weight.

Each step in the MI process is implemented at everyprimary care visit and a follow-up discussion should oc-cur to address the change process. Focusing on improv-ing the quality and duration of life is another strategy.These strategies involve empathy, encouragement, part-nership, and development of coping skills (Rollnick &Miller, 1995). Combining this approach with the MI mayenhance behavioral change and encourage Ms. B to makehealthy lifestyle choices.

Pharmacologic treatment

Regarding medications, according to Grundy et al.(2005) the first line antihypertensive agents for MetS pa-tients include angiotensin converting enzyme (ACE) in-hibitors that lowers BP by inhibiting the production ofangiotensin II. Ms. B was on an ACE inhibitor, which hasthe added benefit of improving glucose metabolism andinsulin sensitivity. In a large clinical trial, ACEs demon-strated the ability to delay new onset T2DM (Pepine &

Cooper-Dehoff, 2004). If ACE inhibitors are not toler-ated, patients may be switched to angiotensin receptorblockers. Other studies revealed vasodilating β-blockers(nebivolol, labetalol, and carvedilol) helped modestlylower BP through its nitric oxide derived vasodilatationproperties. It also improved dyslipidemia by attenuatingFFAs release from adipose tissue in patients with MetSparticularly those with a history of CHD (Deedwania,2011). Further findings indicated some of these newer β-blockers have a beneficial effect on insulin resistance andadipokines. For instance, nebivolol’s sympaticomimeticeffect elevates plasma adiponectin in hypertensive over-weight patients and Celiprolol, with both β-1 antagonistand β-2 agonist lowers leptin in dyslipidemic patientswithout changing body weight (Westerink & Visseren,2011). Ms. B was already on three classes of antihyper-tensive medications (angiotension receptor blocker, di-uretic and calcium channel blocker) with poor BP controlso further antihypertensive treatment is in order. Reeval-uation of her current antihypertensive medications canhelp the APN determine if her current medications arebeing used for maximum benefit. Perhaps she would ex-perience greater BP control with the addition of one ofthe newer β-blockers that may confer greater controlwith added pleiotropic effects as an added benefit.

To treat her dyslipidemia, Ms. B was on a statin. Withher recent diagnosis of mild CHD, her therapeutic goal forLDL-C was set at 100 mg/dL. Because her fasting lab re-sults showed her LDL-C was still slightly elevated at 107mg/dL, her triglycerides were elevated to 176 mg/dL andshe was on the upper limit of her statin, she requiredan additional agent. Ordinarily, nicotinic acid would beadded to Ms. B’s therapeutic regimen. In addition to thelipid lowering effects (i.e., lowers LDL and triglyceridesand raises HDL [Scott et al., 2009]), the literature sug-gested niacin reduces markers of inflammation includingC-reactive protein, fibrinogen, and lipoprotein associatedwith phospholipase A2 (Kuvin et al., 2006; Miranda, De-Fronzo, Califf, & Guyton, 2005). A recent randomizedclinical trial suggested statins had better pleiotropic bene-fits compared to nicotinic acid. Those on the combinationof a statin and niacin had a small risk for strokes (Wise,2011). In light of this new finding adding nicotinic acidto Ms. B’s medication regimen may not be ideal; thosewho cannot tolerate statins are, however, candidates forniacin therapy. Because Ms. B was reluctant to take moremedications, a frank discussion needs to occur to identifywhich pharmacological measures are realistic for her.

In people with MetS already engaged in dietary andphysical activity measures, but need an additional treat-ment to reduce their risk for CVD, can be consideredcandidates for combination drug therapy. In a recentstudy of 143 participants on gemfibrozil, niacin, and

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cholestyramine added to dietary and physical activity reg-imens had significant decrease of the prevalence of MetScompared to those on the triple drug therapy alone.Those in the triple therapy alone group did, however,also exhibit some benefit (Kraswki, Devendra, Carter, &Whitney, 2011). While a need for additional studies usingmedication combinations hold promise for MetS patientslike Ms. B, this study demonstrates the power of combi-nation therapy.

Follow-up office visit

Ms. B required education and counseling of her medi-cation regimen and side effects, as well as how and whento take her medications. A depression and anxiety screenwas initiated because if present, this may potentially pre-vent adherence with her healthcare plan. Because shewas not clinically depressed a referral to seek counselingwas not made. A discussion of willingness to see a fam-ily counselor with her family to help incorporate lifestyleand behavior modifications was pursued to no avail. Fi-nally, ongoing monitoring of her BP, medication toler-ance, weight management (i.e., assessing BMI and waistcircumference), and laboratory tests were completed.

Consideration for future follow-up office visits

Helping Ms. B to become more physically active isan important component to remain independently liv-ing in the community. Initiating MI when she returns forfollow-up visits is important to keep her thinking abouthow she can increase her physical activity and may moti-vate her to obtain a CV assessment to determine her toler-ance and risk stratification given her CHD. Assessing hercommitment to increase activity can easily be overlookedespecially because she is an older adult. Ms. B admittedshe enjoyed leisure walks near the beach and noticed lessknee pain when she was more physically active so theAPN needs to build on to her enjoyable activities usingMI techniques.

Ms. B is not able to lose weight even if she perceivedher diet was healthy. Exploring portion size with her isa reasonable next step. Assess for “portion distortion.”This misperception is not uncommon today with the in-crease in food portion sizes over the past two to threedecades. Educate her about the difference between por-tion and serving sizes and provide her with strategies shecan use, such as using a smaller plate, reading labels forthe number of serving seizes. Offer her reference for serv-ing sizes of various foods, that is, a serving of rice is 1/2cup; a serving of fruit is medium size; and a serving ofprotein is the size of a deck of cards. Additionally, edu-

cation about sodium restriction is crucial. Studies showsodium reduction of 1800 mg/day lowers systolic BP by 5mmHg and diastolic BP by 2.7 mmHg (AHA, 2011b). Thenew sodium recommendation for all adults and childrenis 1500 mg/day (AHA, 2011b). Advise Ms. B to cut backon her sodium intake equal or less than 1500 mg/day tohelp lower her BP.

When beginning to work on these types of strategiesfrequent follow-up with Ms. B is important to realize pos-itive results. While having her return to the office morefrequently may be prohibitive for many reasons, remain-ing in contact via the phone or e-mail may be alterna-tive ways to conduct follow-up assessments between of-fice visits.

Conclusion

MetS is a constellation of CV risk factors that occurtogether more often than not, and confers an increasedrisk for the development of CHD and DMT2. The patho-physiology of MetS is not completely understood, but isthought to involve a complex interaction between the en-vironment, genetic susceptibility, insulin resistance, andabnormal adipose tissue function. Environmental con-tributors and the obesity epidemic are increasing, whichsuggests the incidence and prevalence of the syndromewill change concomitantly. Patients like Ms. B representthe complexity of both the disease process and treat-ments. The psychosocial implications for treatment areequally important in treating the disease, as are strate-gies for successful long-term behavior modification. Fam-ily systems, as well as larger environmental influencesneed to be included to adequately address the self-careneeds of patients with MetS.

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