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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
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
2
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
3
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
4
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
5
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
6
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)
7
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
8
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
9
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
10
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.
11
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
32
Used with permission from John Foreyt, PhD,
NLA Lipid University.
12
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
13
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
14
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
15
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)
16
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
17
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
18
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.
19
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
20
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
21
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
22
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
23
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 ?