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Metabolik Sindrome
Metabolik Sindrome
Kannel WB. In: Genest J, et al, eds. Hypertension: Physiopathology and Treatment. New York, NY: McGraw Hill;1977:888-910.
Perubahan Fisiologis Terkait Resistansi
Insulin (I)
Ganguan toleransi glukosa
- Impaired fasting glukose
- Impaired glukose tolerance
Ganguan metabolisme asam urat
- Palsma uric asid concentration
- Renal uric acid clearance
Perubahan Fisiologis Terkait resistensi
insulin (2)
Perubahan hemodinamik :
- Symphotettic nervous system activity
- Renal sodium retention
- Blood pressure(~50% of patient with
hypertention are insulin resistent )
Ganguan hemostatis
- Plasminigen activator inhibitor –I
- Fibrinogen
Disfungsi Endotel :
- Mononuclear cell adhesion
- Plasma concentration of celular
nadhesion molecules
- Plasma concentration of acymmetric
dimethyl arginine
- Endothelial-dependent vosodilation
Sistim reproduksi
- Polycystic ovary syndrome
The metabolik syndrome
Genes & evironment Interecting
ENVIRONMENT
Cardiovascular disease
The metabolik syndrome :
The epidemic strikes back !!!
High social & ekonomic infact
Globalozation
Modernization
migration
Morbidity &
Mortality
Metabolik
syndrome
Intervention/ Atherosclerosis
Control
Cardiovascular
disease
Treatment of obesity
Multiple risk reducer
Insulin resistence is linded to cardiovascular
disease
Hyperglycaemia
Hyperinsulinaemia
Hypertension
Dyslipidaemia
Decraesed fibrinolitic
INSULIN RESISTENCE Octivity ( PAI-1 )
Endothelial dysfunction
Inflammatory markers
Of a the rosclerosis
Mikroalbuminuria
Gangguan toleransi glukosa berkelanjutan ?
Normal TGT Diabetes
Tipe 2 komplikasi kematian
Tahap
Pencegahan Pencegahan
Pencegahan
primer Tertier
Skunder
The Cardiovascular Continuum of
ACS
Secondary
Coronary
Thrombosis
Events Arrhythmia and
prevention Stroke Loss of Muscle
Myocardial Remodeling
Ischemia
Ventricular
CAD Dilatation
Atherosclerosis Congestive
Heart Failure
Primary
prevention End-stage
Risk Factors
Dyslipidemia BP, DM,
( Dyslipidemia, Heart Disease
Insulin Resistance, Platelets,
Adapted from
Fibrinogen, etc) Dzau et al. Am Heart J. 1991;121:1244-1263
Kita Akan Fokus Pada…
Secondary
prevention
Myocardial
Ischemia Why primary
prevention ?
CAD
Atherosclerosis
Primary
prevention
Risk Factors
( Dyslipidemia, BP, DM,
Insulin Resistance, Platelets,
Adapted from
Fibrinogen, etc) Dzau et al. Am Heart J. 1991;121:1244-1263
Primary Prevention
Cost-effective
Less painful
Better quality of life
Easier to manage
But…..
No symptoms (low compliance)
“Investment”
1. Total cholesterol > 200 mg/dl
2. HDL-C < 40 mg/dl
3. Triglyceride > 150mg/dl
4. LDL-C:
Faktor Resiko LDL-C
³ 2 >130 mg/dl
HDL
TG
Adhesion Macrophage
Oxidized
Monocyte LDL-C molecule
LDL-C
Foam cell
CRP
Smooth muscle
cells
Tuzcu EM, Kapadia SR, Tutar E, et al. High Prevalence of Coronary Atherosclerosis in Asymptomatic Teenagers And Young Adults: EvidenceFrom
Intravascular Ultrasound. Circulation 2001;103:2705-2710
KERUSAKAN APA SAJA YANG BISA
DISEBABKAN OLEH PLAK?
Stroke
Coronary artery
• Plaque rupture
unstable angina Pulmonary embolism
Myocardial infarction (PE)
(MI) / heart attack
Deep vein
thrombosis (DVT)
KERUSAKAN APA SAJA YANG BISA
DISEBABKAN OLEH PLAK?
Stroke
Coronary artery
• Plaque rupture
unstable angina Pulmonary embolism
Myocardial infarction (PE)
(MI) / heart attack
Deep vein
thrombosis (DVT)
Atherosclerosis: Penyakit Sistemik
From a prospective analysis of 1886 patients aged 62 years, 810 patients were diagnosed with CAD as defined by a
documented clinical history of MI, ECG evidence of Q-wave MI, or typical angina without previous MI. (Adapted
from Aronow et al.)
Coronary Artery Disease (CAD):
Diagnosa Sering Terlambat
Murabito JM, Evans JC, Larson MG, et al. Prognosis After the Onset of Coronary Heart Disease. An Investigation of Differences In
Outcome Between the Sexes According To Initial Coronary Disease Presentation. Circulation 1993;88:2548-2555
Mortality from CVD and CHD in Selected Countries
Rate per 100,000 population (men aged 35–74 years)
1500
CVD deaths
CHD deaths
1000
500
0
Russia Poland Finland New England/ USA Italy Spain Japan
Zealand Wales
120
Diabetics
100
80
60
40
Non-diabetics
20
0
0 1 2 3
hypercholesterolaemia, smoking,
hypertension
Adapted from: Stamler, J. et al., Diabetes Care 1993; 16: 434-44
LDL-C: Primary target of therapy
LDL LDL
160 – 189 mg/dL >190 mg/dL
Sasaran:
LDL < 160 mg/dL
Faktor Risiko >2
LDL < 130 mg/dL LDL > 130 mg/dL
LDL LDL
130 – 159 mg/dL >160 mg/dL
Sasaran:
NCEP-ATP III Report. JAMA 2001;285:2486-2497 LDL < 130 mg/dL
Pencegahan Primer
Pada Pasien dengan > 2 Faktor Risiko
6 minggu
Bila sasaran LDL blm
Pemantauan respons tercapai, intensifkan
dan ketaatan berobat Tiap 4-6 bln obat hipollipidemik
atau rujuk ke
spesialis
Obati faktor rsisiko lipid
lainnya (TG / HDL)
NCEP-ATP III Report. JAMA 2001;285:2486-2497
PJK Atau Yang Disamakan
LDL < 100 mg/dL LDL > 100 mg/dL
• Berikan Statin
•Periksa ulang 3 bln
Sasaran:
LDL < 100 mg/dL
Visit: 1 2 3 4 5
Week: –4 –2 0 6 12
1.1
0 –0.7
–0.3
LSM change
–0.9
*** *** –2.8
***
–10 ***
–20 –19
–21
–30 –28
–32 ***
–37 –35
–40 ***
*** –41
–43
–50
LDL-C HDL-C TC TG nonHDL-C
†
ITT population by ‘as allocated’ treatment; **P<0.01, ***P<0.001 vs RSV
* 79
80 72
60
40
20 ***
10
Blood Preasure
Insulin sensitivity
Impaired Improved
Insulinaemia alycaemia
Susceptibility to thrombosis
Imflamation Markers
Abdominally Reduced Obesity
Obese (Hight Waist Hight Risk of coronary heart disease low (Low Waist measure ment)
Measurement) Despres JP, BMJ. 2001, 322. 716.20.
KESIMPULAN
Metabolik sindrom bukan satu penyakit
kumpulan fenomena klinis terkait resistensi
insulin
Metabolik sindrom risiko tinggi PKV
Intervensi terhadap metabolik sindrom termasuk
penurunan berat badan (perubahan gaya hidup,
obat) dapat menunda ataupun mencegah DM
tipe 2 serta menurunkan resiko PKV.
Pengidap Diabetes mempunyai resiko yg
disamakan dg penderita PJK.