Académique Documents
Professionnel Documents
Culture Documents
1998: WHO defines metabolic syndrome 2001: NCEP defines metabolic syndrome and gives
ICD code
Diagnostic Criteria
WHO (1999) NCEP ATPIII (2002)
IDF Consensus
Central obesity: For Asian populations, 90 cm in men and 80 cm in women Plus any two of the following :
raised TG level: 150 mg % or specific t/t for this lipid abnormality reduced HDL-C: <40 mg% in males and <50 mg% in females or specific t/t for this lipid abnormality raised BP: 130/85 mmHg or t/t of previously diagnosed HTN raised fasting plasma glucose (FPG) 100 mg% or previously diagnosed type 2 DM
CVD Mortality Increased in the Metabolic Syndrome: Kuopio Ischaemic Heart Disease Risk Factor Study
Cumulative Hazard, %
15
10
Metabolic Syndrome:
YES
5 0
NO
4 6 8 Follow-up, y
1 0
1 2
Prevalence of CHD by the Metabolic Syndrome and Diabetes in the NHANES Population Age 50+
25% 20% 15% 10% 5% 0%
% of Population =
CHD Prevalence
No MS/No DM 54.2%
MS/No DM 28.7%
DM/No MS 2.3%
DM/MS 14.8%
p<0.001
n=6055
0
n=690 IGT
n=158
n=135
G<140 mg/dL
Different Components of the Metabolic Syndrome Predict Diabetes: San Antonio Heart Study Risk of Type 2 Diabetes per Unit Change in Risk Trait
Levels
FPG per mg/dl SBP per mm Hg HDL-C per mg/dl decrease BMI per kg/m2 2% 4%
8%
7%
0%
2%
4%
6%
8%
10%
prevalence of CAD and hypertriglyceridaemia were higher in the middle income group (NS) The relative odds ratio for diabetes and impaired glucose tolerance increased significantly with increase in income while hypercholesterolaemia, hypertension and CAD showed no significant changes. Analysis revealed that higher social class had a strong association with the components of the metabolic syndrome
8%
6%
70
Age, years
Ford ES et al. JAMA 2002;287:356-359.
Hyperleptinemia Sympathomimetic activity Sodium retention High intra-myocellular lipids Sub-clinical inflammation (CRP) Low levels of serum adiponectin Lipodystrophies Sleep Apnea
Endothelial dysfunction
Metabolic Syndrome
Prothrombotic state (fibrinogen, Factor VIIa, fibrinolytic activity)
Insulin Resistance
Hyperinsulinaemia
Hyperuricemia
Central obesity
Type 2 Diabetes
Diabetes Care 1998;21(2):310314. Williams G, Pickup JC. Handbook of Diabetes. 2nd Edition, Blackwell Science. 1999.
Hypertension Microalbuminuria
HDL cholesterol
Triglycerides
Free fatty acids Interleukin-6 PAI (plasminogen activator inhibitor) Leptin Tumor necrosis factor Resistin Angiotensinogen cytokines (tumor necrosis factor) adiponectin
Central Obesity
each other not allowing appreciable increase in the value of BMI, therefore BMI does not reflect adiposity accurately in Asian Indians.
The Ashwell Shape Chart to assess Syndrome X - based on waist circumference and height
In patients with established CVD, assess risk with detailed physical activity
history and/or an exercise test, to guide prescription.
Encourage resistance training 2 d/wk. Advise medically supervised programs for high-risk patients (eg, recent ACS
or revascularization, CHF).
simple sugars should be limited. Increase whole grains Increase fruits and vegetables Eat fish 1-2 times per week
Fat
Margarine Cottonseed Shortening Chicken fat
Saturated Poly
19% 27% 28% 31% 41% 52% 66% 32% 54% 28% 22% 12% 4% 4%
Mono
49% 19% 44% 47% 47% 44% 30%
Safflower
10%
77%
13%
Sunflower
11%
69%
20%
62% 9% 61%
Peanut
19%
33%
49%
ATP III LDL-C Goals and Cutpoints for TLC and Drug Therapy
Insulin resistance
Metformin & Thiazolidinediones
Hypertension
No class of antihypertensive drugs has been identified as being uniquely efficacious in patients with metabolic syndrome.
Prothrombotic State
AHA currently recommends use of aspirin prophylaxis in metabolic syndrome when their 10year risk for CHD is10%.
Proinflammatory State
AHA and CDC guidelines for measurement of CRP in clinical practice suggest that measurements should be limited to individuals assessed to be at intermediate risk (10-year risk for CHD 10% - 20%). No specific therapies beyond lifestyle therapies
fasting glucose) Fasting insulin/proinsulin levels Homeostasis model assessment for insulin resistance (HOMA-IR) Insulin resistance by Bergman Minimal Model Elevated free fatty acids (fasting and during OGTT)
elevated TG and non-HDL-C and low HDL) Apolipoprotein B Small LDL particles Triglycerides/HDL-C ratios
Proinflammatory state Elevated hs-CRP Elevated inflammatory cytokines (IL-6) Low levels of adiponectin
Prothrombotic state Fibrinolytic factors (PAI-1) Clotting factors (fibrinogen) Hormonal factors Corticosteroid axis Polycystic ovary syndrome
The value of treating atherogenic dyslipidemia beyond LDL-lowering therapy The efficacy of treating insulin resistance for reducing the risk of CVD A better understanding of the relationship between a proinflammatory state and the
metabolic syndrome and the efficacy of intervention on this state for the prevention of both CVD and diabetes
Conclusions
The metabolic syndrome is a term for a constellation of risk factors that increase the risk of developing both ASCVD and type 2 DM The syndrome is strongly associated with the presence of abdominal obesity. Weight reducton, lowering the levels of LDL-C, and blood pressure management are primary targets for risk reduction
Lifestyle interventions are the initial therapies recommended. If not sufficient, then drug therapies for individual risk factors Considerable additional research is needed to better refine the most appropriate therapies for individuals with the metabolic syndrome.