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NCNP 2016

Metabolic Syndrome: It’s a short trip to

Cardiovascular Disease

Joyce L. Ross, MSN, CRNP, CS, FPCNA, FNLA

President National Lipid Association

Diplomate Accreditation Council for Clinical Lipidology

Certified Clinical Lipid Specialist

University of Pennsylvania Health System – Retired

jlr@joycerossnp.com

484-614-5027

Disclosures

Speakers Bureau:

AstraZeneca

Abbott/AbbVie

Sanofi/Regeneron

Amgen

Amarin

Consultant:

Amarin

Learning Objectives At the end of this session the participant will be able to:

• Recall that multiple risk factors contribute to

development of cardiovascular disease

• Discuss the relationship of metabolic syndrome and its

components to the development of cardiovascular

disease

• State the role of the healthcare team in reducing

cardiovascular risk

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Diagnosis of metabolic syndrome

(MetSyn)

Defined as

any pathophysiologic dysfunction that results in a loss of metabolic control of homeostasis in the body

Components of the syndrome

discussed in terms of risk factors and defining levels

Spectrum of CHD Risk: Risk Is More Than

Elevated LDL-C

Expert Panel. JAMA 2001;

Grundy et al. Circulation 2005; 112:2735-52.

Metabolic

Syndrome

The end of the

LDL-C only era

Waist Circumference

Low levels of HDL-C

Elevated BP

Elevated TG

Elevated Fasting

Glucose

Adopted from: Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA

2001;285:2486-2497

Central adiposity + Lack of physical activity + Genes =

Metabolic syndrome/insulin resistance

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Integrated Perspective on CV

Risk Factors and Atherosclerosis

CV

Disease

Ross R. N Engl J Med. 1999;340:115-26.

Oxidative Stress & Inflammation

Endothelial Dysfunction

Ross R. N Engl J Med. 1999;340:115-26.

Mason RP and Jacob RF

Clinical Identification of the Metabolic Syndrome

(NCEP 2005)*

Elevated waist circumference

Men 40 in (102 cm)

Women 35 in (88 cm)

TG 150 mg/dL†

HDL-C

Men <40 mg/dL†

Women <50 mg/dL†

BP 130/85 mm Hg†

Fasting glucose 100 mg/dL†

*Diagnosis is established when 3 of these factors are present. †Patients must either meet the indicated criteria OR be on drug treatment for that factor.

NCEP=National Cholesterol Education Program

BP=Blood Pressure National Institutes of Health. May 2001. NIH Publication No. 01-3670.

Grundy SM, et al. Circulation. 2004;109:551-556.

Grundy SM, et al. Circulation. 2005;112:2735-2752.

0

1

2

3

4

CVD*

CHD†

0 1 2 3 4 5

Mo

rta

lity h

aza

rd r

atio

Number of Metabolic Syndrome Criteria

*Adjusted for age, sex, race or ethnicity, education, smoking status, non–HDL-C,

recreational/nonrecreational activity, white blood cell count, alcohol use, prevalent heart disease, and

stroke †Similar adjustments except for prevalent stroke

Ford ES. Atherosclerosis 2004;173:309-314

Metabolic Syndrome: Risk of Death

CHD=Coronary heart disease, CVD=Cardiovascular disease

Risk is Proportional to the Number of ATP III Criteria

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Role of Insulin Resistance and

Compensatory Hyperinsulinemia

Genetics Environment

Insulin Resistance

Hyperinsulinemia

Glucose Uric Acid Dyslipidemia Hemodynamic Hemostatic

Metabolism

elevated TG

increased PP Lipemia

decreased HDL

small, dense LDL

LDL Oxidation

Coronary Heart Disease

Decreased clearance

Sympathetic Response Sodium retention & Increased BP

Increased PAI I & fibrinogen

Increased Glucose Levels = diabetes

American Journal of Epidemiology 2000; 152(10): 897-907Sakkinen PA, Wahl P, Cushman M, et al

The Damage from components of

metabolic syndrome assert their

influence on the

Ross, J 2005

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Glucose Metabolism

• Insulin resistance caused by abdominal

obesity may lead to the development of risk

factors for CHD1

• Abdominal adiposity and insulin resistance

may independently affect hemostatic

variables2

• Most people with MetSyn DO NOT have Diabetes !

1. Wilson PWF, et al. Arch Intern Med. 1999;159:1104–1109.

2. Meigs JB, et al. JAMA. 2000;283:221–228.

Dyslipidemia

Dyslipidemia is a major risk factor for CHD, the

leading cause of death in the United States1

The World Health Organization estimates that

dyslipidemia is associated with >50% of global

ischemic heart disease cases and >4 million deaths

per year2

Two components of dyslipidemia are directly related to

risk factors for metabolic syndrome, and one indirectly

affects it.

1. Smith DG. Am J Manag Care. 2007;13:S68-S71. 2. World Health Organization.

The World Health Report. 2002;4:47-97.

2. Jacobson et al, 2016 NLA Part 2 recommendations for Patient Centered Care

CHD = coronary heart disease.

Causes of Lipid Disorders

Primary and Secondary Causes Primary are related to genetics

Secondary may be related to medical disorders, and medications, that effect specific parameters of the lipid profile

Metabolic endocrine

Diabetes

Thyroid disease

Renal

Hepatic

Ross, J 2005

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TG (the Rodney Dangerfield of

Cholesterol) and Non-HDL

Patients with triglycerides 200 mg/dL

LDL cholesterol: primary target of therapy

Non-HDL cholesterol: secondary target of therapy

Non HDL-C = total cholesterol – HDL cholesterol

Example: TC 270 minus HDL 50 = 220 non-HDL-

C - Should not be higher than 30 points than LDL

goal.

- If LDL goal 130, non HDL goal = < 130

NCEP ATP III. JAMA. 2001;285:2486-2497

Jacobson et al, 2016 NLA Part 2 recommendations for Patient Centered Care

Atherogenic Changes Associated with

Triglycerides Low HDL-C

Increased VLDL

Remnants

Coagulation changes

Increased PAI-1

Increased fibrinogen

Increased Chylomicron Remnants

Small dense

LDL particles

HYPERTRIGLYCERIDEMIA

Vascular Biology Working Group

Risk of CHD by Triglyceride Level:

The Framingham Heart Study

Castelli WP. Am J Cardiol. 1992;70:3H-9H.

0.0

0.5

1.0

1.5

2.0

2.5

3.0

50 100 150 200 250 300 350 400

Rel

ativ

e ri

sk

Men

Women

n=5,127

Triglyceride level (mg/dL)

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Hypertension in Metabolic Syndrome

Insulin resistance in metabolic syndrome is associated with hypertension

Increase in sympathetic nervous system (SNS) activity plays a key role

Causes of Secondary Hypertension

Medical Conditions

Chronic kidney disease

Primary hyperaldosteronism

Renovascular disease

Chronic steroid therapy

Cushing’s syndrome

Pheochromocytoma

Aortic coarctation

Thyroid or parathyroid disease

Sleep apnea

Drugs

NSAIDS

Oral contraceptives

Adrenal steroids

Sympathomimetics

Cyclosporine or tacrolimus

Erythropoietin

Ephedra, mu huang, bitter orange

Cocaine or amphetamines

Alcohol

Chobanian AV et al. JAMA. 2003;289:2560-2572

NSAIDS=Non-steroidal anti-inflammatory drugs

Treatment Approach to Metabolic

Syndrome

Kendall DM, Harmel AP. The metabolic syndrome, type 2 diabetes, and cardiovascular disease:

understanding the role of insulin resistance. Am J Manag Care. 2002;8(Suppl 20):S635-S653

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Risk Reduction Therapy

Risk Behavior % Mortality – 10 years

Smoke Cessation 35 – 45 %

LDL Reduction to goal 25 – 35 %

BP management to goal 10 – 15 %

ASA 10 %

ACE Inhibitor Use 20 – 30 %

Weight Loss 20 %

Exercise 20 %

Grundy 9/2000

Involve the patient

Enhanced communication improves patient

adherence, outcomes, and satisfaction

Barrier PA et al. Mayo Clin Proc. 2003;78:211-4.

Patient-centered

approach facilitates

identification of risk

conditions

Provider-centered

approach may lead to

missed diagnoses and

poor adherence

Therapeutic Lifestyle Interventions

Weight reduction

– enhances LDL-C lowering

– reduces metabolic syndrome risk factors

Increased physical activity

reduces VLDL levels, raises HDL-C, lowers LDL-C levels

lowers blood pressure

reduces insulin resistance

Dietary carbohydrate restrictions

periodic assessments of dietary changes

Metabolic Syndrome and Subclinical Atherosclerosis

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1. Wing RR, et al. Arch Intern Med. 1987;147:1749–1753.

2. Goldstein DJ. Int J Obes. 1992;16:397–415.

3. Thomas PR, ed. Weighing the Options. 1995.

Health Benefits of Weight Loss

Weight loss of 5%–10% in obese individuals with type 2

diabetes, hypertension or dyslipidemia resulted in:

Improved glycemic control1

Reduced blood pressure2

Improved lipid profile2

“Several studies demonstrate that small losses...help

reduce obesity-related comorbidities and that

improvements in these risk factors persist with

maintenance of these modest weight losses.”3

— Institute of

Medicine

TLC Teaching Tips:

The Four F’s for a Healthier Diet

Fiber: More whole grain products, dietary fiber

Fruits and vegetables: Dietary sources of antioxidants

Fish and plant sources of omega-3 fatty acid intake shown to reduce CHD death

Fluids: before and during the meal

Adopted from NLA Lipid University, Dr. Penny Kris-Etherton

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Alcohol and CHD

There is a “U-shaped” curve

One drink lowers CHD risk vs. risk in teetotalers

Increasing amounts lead to increasing total mortality

No difference between red and white wine in ecological,

epidemiological studies

Resveratrol in red wine may ⟶ CV benefits via ↓ LDL

oxidation, ↑ nitric acid, or by changes in thrombogenicity,

ischemia, or vascular tone1

1. Opie LH, et al. Eur Heart J. 2007;28:1683-1693.

Relative risk alcohol consumption and

the risk of CHD

Corrao G, et al. Prev Med. 2004;38:613-619.

One drink equals:

•12 oz beer

• 4 oz wine

•1.5 oz 80 proof spirits

10 g alcohol equates to:

• 1 shot liquor

• 1 regular can beer

• 1 glass table wine

•1 drink/day females

•2 drink/day males

Address the Obesity Epidemic via

Small Changes Approach*

Small changes are more feasible to achieve and maintain than

large changes

2000 more steps/day (expends extra 100 kcal)

Simple food substitutions (Replace regular 12-oz soda with

diet soda, ↓ caloric intake 150 kcal)

Small changes can impact body weight regulation

Slight energy discrepancy (higher intake + lower output)

has created an “energy gap” → weight gain

Average energy gap in adults is

~ 100 kcal/day

* Report of the Joint Task Force of the American Society for Nutrition, Institute of Food Technologists, and

International Food Information Council; Endorsed by the American Dietetics Association, the American Heart

Association and the American Cancer Society

Hill JO. Am J Clin Nutr. 2009;89:477-484.

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National Weight Control Registry: Important Behaviors

of Successful Long-Term Weight Management

Self-monitoring

Diet: record food intake daily, limit certain foods or food quantity

Weight: check body weight >1x/week

Low-calorie, low-fat diet

Total energy intake: 1300–1400 kcal/day

Energy intake from fat: 20%–25%

Eat breakfast daily

Regular physical activity: 2500–3000 kcal/week (e.g., walk 4 miles/day)

Klem ML et al. Am J Clin Nutr. 1997;66:239. McGuire MT, et al. Int J Obes Relat Metab Disord.1998;22:572. 31

“If exercise could be purchased in a pill,

it would be the single most widely

prescribed and beneficial medicine in

the nation.”

—Dr. Robert Butler,

former Director National Institute of Aging

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Used with permission from John Foreyt, PhD,

NLA Lipid University.

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Strategies for Exercise

Specific counseling advice such as a detailed exercise

prescription may help1 - Use acronym FIT with patients

Frequency

Intensity

Time (duration)

Suggest incorporating lifestyle activities

Climbing stairs

Walking

Gardening

Housework

View as ongoing process in behavioral change2

1. Swinburn BA, et al. Am J Public Health. 1998;88:288-291.

2. Wee CC. JAMA. 2001;286:717-719. FIT = Frequency Intensity Time

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Lipid Therapy Options

for Dyslipidemia

1. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497. 2. Zetia® (ezetimibe)

[package insert]. Merck/Schering-Plough Pharmaceuticals. North Wales, PA; 2008.

3. Lovaza™ (omega-3-acid ethyl esters) capsules [package insert]. Reliant Pharmaceuticals. Durham, NC; 2007.

Drug Class LDL-C HDL-C TG Key Limitations

Statins1 ↓ 18%–55% ↑ 5%–15% ↓ 7%–30% Myositis, ↑ LFTs

Bile acid

sequestrants1 ↓ 15%–30% ↑ 3%–5% No effect or ↑ Upper/lower GI complaints

(eg, constipation)

Nicotinic acid1 ↓ 5%–25% ↑ 15%–35% ↓ 20%–50% Flushing, hyperglycemia,

hyperuricemia/gout

Fibric acid

derivatives1 ↓ 5%–20% ↑ 10%–20% ↓ 20%–50% Upper GI complaints,

myopathy

Cholesterol-

absorption

inhibitors2

↓ 18% ↑ 1% ↓ 8%

↑ LFTs in combination with

statins; lack of outcomes

data

Omega-3

fatty acids3* ↑ 45% ↑ 9% ↓ 45%

↑ LDL-C; lack of outcomes

data

* Based on use in patients with very high TG levels (≥500 mg/dL).

HMG CoA

Reductase

Inhibitors

(Statins)

Competitiv

e Inhibition

Cholesterol

production

Expression

of LDL

receptors

LDL,

VLDL,

and IDL

particles

LDL-C

Lowering

Acetyl CoA

HMG-CoA

Mevalonate

Cholesterol

production

Statins

VLDL=Very Low Density

Lipoprotein

IDL

HMG-CoA reductase inhibitors

wwwlipid.org

Taking a walk on the Cytochrome P450

Pathway

Ross J 2004

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Dose Efficacy of Statin-Based

Therapies for LDL-C Reduction (%)1

Dose Efficacy in STELLAR1*

Drug 10 mg 20 mg 40 mg 80 mg

CRESTOR® (rosuvastatin calcium 46 52 55

Lipitor® (atorvastatin calcium) 37 43 48 51

Pravachol®

(pravastatin sodium)

20 24 30 *

Zocor® (simvastatin) 28 35 39 46

•VytorinTM (ezetimibe 10 mg/simvastatin)* reduces LDL-C by 46% to 59%2*

•Data derived from the prescribing information for Vytorin

Mechanism of Action

The mechanism by which the fibrates lower lipid levels is unknown

May act through interactions with the hepatic peroxisome proliferator activated receptors (PPARs) which regulate gene transcription of enzymes involved in lipid synthesis and secretion

Fibrates bind specifically to a PPAR alpha isozyme, which is found largely in the liver and which regulates fatty acid oxidation, increasing lipoprotein lipase levels which, in turn, enhances clearance of triglyceride rich lipoproteins.

Fibric Acid Derivatives

TG

HDL

VLDL

ApoB

LDL

ApoB

Fibric Acid

Derivatives

(Fibrates) Liver

Fibric Acid Derivatives

Wwwlipid.org

Activate

PPAR

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Fibric Acid Derivatives – Cont’d

Lipoprotin Effects:

• Increase/decrease LDL

• Decrease TGs

• Increase HDL

Fenofibrates are much more efficacious and safer than previous

triglyceride lowering medication

• Fenofibrate decreases TGs 32 - 53 %, HDL increased by 2

- 26 %

• Gemfibrozil decreased TG’s 31 - 35 %, HDL increased by

6 - 10 %

Omega-3 Fatty Acids (FA)

Mechanism of action:

Unclear mechanism; reduces hepatic VLDL-TG

synthesis and/or secretion and enhances TG

clearance from circulating VLDL

Lipoprotein effect:

Reduces VLDL

Reduces TGs

44 Bays HE. Am J Cardiol. 2007;99(Suppl 6A):35C–43C.

Ingredients for TG lowering

Eicosapentaenoic acid (EPA) and docosahexaenoic

acid (DHA) have TG lowering

Alpha-linoleic acid does not have CV benefits

Role in therapy:

Prescription omega-3 FA products approved for

severe hypertriglyceridemia (≥ 500 mg/dL):

Lovaza® both EPA and DHA

Vascepa® EPA only

Omega-3 Fatty Acids (FA)

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www.puritan.com

www.naturesbounty.com 46 NLA Lipid University

PCSK9 Inhibitors

Approved by the FDA to reduce LDL-C

Proprotein convertase subtilisin/kexin 9 (PCSK9) inhibition is a novel therapeutic approach in patients with elevated LDL-C.

PCSK9, a secretory cell surface receptor regulator, binds to cell surface LDL receptor (R) and promotes its degradation.

By inhibiting binding of PCSK9 to LDLR, PCSK9 inhibitors increase the number of LDLRs available on the cell surface to clear LDL particles, thereby lowering LDL-C levels

PCSK9 Inhibition

To date, several PCSK9 inhibitors have been developed and proven to be efficacious in clinical studies.

Recently Praluent, (alirocumab) and Repatha™ (evolocumab), fully human monoclonal antibody to PCSK9, were approved by the FDA as adjunct therapy to diet and maximally tolerated statin therapy for the treatment of adults with HeFH or clinical ASCVD who require additional LDL-C lowering

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PCSK9 Inhibitors

Injectable

Given q 2 weeks to 1 month apart

Very favorable side effect profile

Currently long term outcome data is not available

HTN Key Facts

Persons > age 50

SBP is a more important cardiovascular risk factor

than DBP

Starting at 115/75

CVD risk doubles for each increase of 20/10 mmHg

Normotensive patients at age 50

90% lifetime risk of developing hypertension

Chobanian AV, et al. JAMA 2003;289:2560-72

Key Message

Thiazide diuretics recommended as initial therapy for most patients

Certain high-risk conditions are compelling indications for other drug classes

Most patients require 2 or more drugs to reach BP goal

If BP is > 20/10 mmHg above goal

initiate therapy with 2 agents either as fixed-dose combination or separately

Chobanian AV, et al. JAMA 2003;289:2560-72

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Hypertension and Medicine

Evaluate other sources

Cold and flu medicines that contain

decongestants are one of several classes of

medicine that can cause blood pressure to

rise

Others include NSAID, steroids, diet pills,

birth control pills, and some antidepressants

Choice of BP Meds is dependent on causative

factor

Heart Rate Renin/Ang/Aldo – CCB – Beta Blocker Renal/Endothelium

Diuretics

Oldest and least expensive class of drugs used to treat

hypertension

Help the kidneys eliminate sodium and water from the body

This process decreases blood volume, so the heart has less to

pump with each beat, which in turn lowers blood pressure.

Loop diuretics, act on the part of the kidney tubules called the

loop of Henle, block sodium and chloride from being

reabsorbed from the tubules into the bloodstream.

Thiazide diuretics act on another portion of the kidney tubules

to stop sodium from re-entering circulation.

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Anti-adrenergics

Anti-adrenergics lower blood pressure by

limiting the action of the hormones

epinephrine and norepinephrine

thereby relaxing the blood vessels and

reducing the speed and force of the heart’s

contractions

This class includes a variety of different

agents that work in slightly different ways

Calcium-channel blockers

Slow the movement of calcium into the smooth-

muscle cells of the heart and blood vessels

This weakens heart muscle contractions and

dilates blood vessels, lowering blood pressure

Because calcium-channel blockers also slow nerve

impulses in the heart, they are often prescribed for

arrhythmias

Common side effects of calcium-channel blockers

are headache, edema, heartburn, bradycardia, and

constipation

ACE Inhibitors

Introduced in 1981, have proved widely effective

in treating hypertension

These agents prevent the kidneys from retaining

sodium and water by deactivating angiotensin-

converting enzyme, which converts inactive

angiotensin I to the active angiotensin II

Angiotensin II raises blood pressure by triggering

sodium and water retention and constricting the

arteries

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Reduce blood pressure in most patients and produce fewer side

effects than many other classes

In addition, protect the kidneys of patients with diabetes and

kidney dysfunction and the hearts of patients with congestive

heart failure

Most common side effects are a reduced sense of taste and a dry

cough

Rarely, difficulty breathing because of a swelling of the lips,

tongue, and throat can occur

Can also cause potassium retention; therefore, patients with poor

kidney function require caution

Because these drugs can cause fetal abnormalities, women who

are pregnant or trying to get pregnant should not take them

Angiotensin-receptor blockers (ARB)

Approved for treating hypertension since 1995, blocks

angiotensin II from constricting the blood vessels and

stimulating salt and water retention

Because highly effective and well tolerated by most people

who take them, these medications are well utilized

Do not produce any of the traditional side effects of other

antihypertensive medications, and less likely than ACE

inhibitors to cause a cough

In addition, like ACE inhibitors, they benefit patients with

diabetes, congestive heart failure, or both

Case Study

Typical patient with MetSyn

Age: 59 years male with no known history of CAD

Adopted. no information about family history

HTN for 5 years

BP: 149/76 mm Hg

Treated with ACE and beta blocker

Impaired fasting glucose for 2 years

Smoker – 42 year pack history

Moderate exercise

No particular Diet

Ht: 6'0", Wt: 185 lbs, Waist: 37"

Lab results

TC: 196 mg/dL

LDL-C: 135 mg/dL

HDL-C: 39 mg/dL

Triglycerides: 155 mg/dL

Glucose: 142

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Assessing Traditional Risk Factors

Age *

Family history of premature CAD

HDL cholesterol

HTN *

Smoking *

Old way - With 2 or more traditional risk factors go on to do a Framingham assessment now - current ACC/AHA guidelines to decide how aggressively to treat LDL

http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof

AHA/ACC Focus on ASCVD Risk Reduction using

4 statin benefit groups (those who would benefit most from treatment)

• Individuals with clinical ASCVD

Individuals with primary elevations of LDL-C >190 mg/dL

Individuals 40 to 75 years of age with DM and without ASCVD with LDL-C 70-189mg/dL

Individuals without clinical ASCVD or DM who are 40 to 75 years of age with LDL-C 70-189 mg/dL and an estimated 10 year ASCVD

risk of 7.5% or higher

Stone NJ, et al. 2013 ACC/AHA Blood Cholesterol Guideline

NCEP ATP III Summary. JAMA. 2001;285:2486-2497

Risk Factor Defining Level

Abdominal obesity Waist Circumference Men >102 cm (>40 in) Women >88cm (>35 in)

Triglycerides 150 mg/dL

HDL-C Men <40 mg/dL Women <50 mg/dL

Blood Pressure 130/85 mmHg

Fasting Glucose 110 mg/dL

Multiple Risk Factors

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Considerations and Challenges

HTN is uncontrolled with multiple medications Change or increase dose?

Impaired fasting glucose: Is he really a hidden diabetic? Order a 2 hour glucose tolerance test

Get hemA1c

Needs to quit smoking

LDL level is above goal of < 70 Add statin to reduce LDL levels and decrease risk of

cardiovascular event

Intensity of Statin Therapy

*Individual responses to statin therapy varied in the RCTs and should be expected to vary in clinical practice. There might be a biologic basis for a less-than-average response.

†Evidence from 1 RCT only: down-titration if unable to tolerate atorvastatin 80 mg in IDEAL (Pedersen et al).

‡Although simvastatin 80 mg was evaluated in RCTs, initiation of simvastatin 80 mg or titration to 80 mg is not recommended by the FDA due to the increased risk of myopathy, including rhabdomyolysis.

High-Intensity Statin Therapy Moderate-Intensity Statin

Therapy Low-Intensity Statin

Therapy

Daily dose lowers LDL-C on average, by approximately ≥50%

Daily dose lowers LDL-C on average, by approximately 30% to <50%

Daily dose lowers LDL-C on average, by <30%

Atorvastatin (40†)-80 mg Rosuvasatin 20 (40) mg

Atorvastatin 10 (20) mg Rosuvastatin (5) 10 mg Simvastatin 20-40 mg‡ Pravstatin 40 (80) mg Lovastatin 40 mg Fluvastatin XL 80 mg Fluvastatin 40 mg bid Pitavastatin 2-4 mg

Simvastatin 10 mg Pravastatin 10-20 mg Lovastatin 20 mg Fluvastatin 20-40 mg Pitavastatin 1 mg

Take Home Messages

Metabolic Syndrome (MetSyn) represents a constellation of

clinical findings associated with increased risk for diabetes and

CHD

Increasing obesity, physical inactivity and insulin resistance are

associated with increased triglycerides

Patients with MetSyn often have normal LDL-C values but

elevated levels of apoB containing lipoproteins

Mixed dyslipidemia (low HDL-C, high TG and increased

numbers of small LDL-P) is common in the metabolic

syndrome and diabetes

Understanding the pathophysiology of MetSyn helps us to

identify treatment targets for the prevention of CVD

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We have our work cut out for us

Many to work with who need our care and expertise

ARE YOU UP & READY TO MEET THE CHALLENGE ?