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PROFIL LIPID DARAH

Oleh :
dr. Aulia Syavitri D.

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PROFIL LIPID

pemeriksaan untuk menentukan :

 Tipe

 Kadar
Lipid darah
 Distribusi

Terutama :

Kolesterol Kondisi resiko


Trigliserida
kardiovaskuler
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PENGANGKUTAN KOLESTEROL

KOLESTEROL ditranspor oleh LIPOPROTEIN


Lapisan luar yg larut dalam air
lapisan dalam yg larut lemak

LIPOPROTEIN
berbentuk sferis
bervariasi pada : ukuran, densitas, komposisi

Chylomicrons
very low density lipoprotein (VLDL)
low density lipoprotein (LDL)
high density lip[oprotein (HDL)

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Density Cla Diameter % % % %
(g/mL) ss (nm) protein cholesterol phospholipid triacylglycerol

>1.063 HDL 5–15 33 30 29 4

1.019–1.063 LDL 18–28 25 50 21 8

1.006–1.019 IDL 25–50 18 29 22 31

VLD
0.95–1.006 30–80 10 22 18 50
L
Penamaan Lipoprotein :

Tergantung pada derajad densitasnya.


Lipoprotein terutama mengandung TRIGLISERIDA dan protein

Chylomicron hanya mengandung 2% protein

VLDL hanya mengandung 5% protein

LDL mengandung 21% protein

HDL mengandung > 50%protein

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Chylomicron lipoprotein yg membawa kolesterol & fat lainnya
masuk ke dalam tubuh dari usus halus & membawanya
ke sel/jaringan

VLDL membawa kolesterol hasil absorpsi makanan &


trigliseri dan kolesterol yg diproduksi tubuh (liver)
ke sel tubuh.
saat di sirkulasi VLDL melepas kandungannya, dan
proteinnya berubah shg menjadi LDL

Trigliserida lipid utama yg terkandung dalam Chylomicron, VLDL,


LDL, & HDL

LDL ¾ kolesterol darah terkandung dlm LDL


LDL membawa kolesterol dari liver ke jaringan

HDL HDL menangkap kelebihan kolesterol tubuh & membawanya


kembali ke liver untuk dirubah menjadi BILE, 8
shg HDL mengurangi kadar kolesterol dalam darah
GUIDE LINES OF CHOLESTEROL LEVEL
TOTAL CHOLESTEROL
< 200 mg /dl Desirable
200-239 Borderline high
≥ 240 High
LDL-CHOLESTEROL
< 100 Optimal
100-129 Near or above optimal
130-159 Border line high
160-189 High
≥ 190 Very high
HDL- CHOLESTROL
< 40 Undesirable
≥ 60 Desirable
TRIGLYCERIDE
< 150 Normal
150-199 Border line high
200-499 High
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≥ 500 Very high
NCEP ATPIII, 2001
RASIO LDL/HDL

RESIKO RASIO LDL/HDL


PRIA WANITA
Sangat 1 1,5
rendah
Rata-rata 3,6 3,2
Sedang 6,3 5,0
Tinggi 8 6,1

NCEP ATP, 2001

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PROSEDUR PERSIAPAN PEMERIKSAAN LIPID

 persiapan : puasa ± 8 jam

(bila tidak puasa, kadar trigliserida

setelah makan akan meningkat tinggi)

 sampel : darah vena tanpa antikoagulan

(kemudian, di laboratorium diproses

untuk menjadi serum)

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CARDIAC MARKER
OF
CORONARY HEART DISEASE

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ISCHEMIC HEART DISEASE

is caused by an imbalance between


the myocardial blood flow and
The metabolic demand of the myocardium.

Reduction in coronary blood flow


is related to progressive atherosclerosis
with increasing occlusion of coronary arteries.

Blood flow can be further decreased


by superimposed events such as
vasospasm,
thrombosis, or
circulatory changes

leading to hypoperfusion.
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Factors reducing coronary blood flow include:

Decreased aortic diastolic pressure

Increased intraventricular pressure and myocardial contraction

Coronary artery stenosis,


which can be further subdivided
into the following etiologies:
Fixed coronary stenosis
Acute plaque change (rupture, hemorrhage)
Coronary artery thrombosis
Vasoconstriction

Aortic valve stenosis and regurgitation

Increased right atrial pressure 15


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KRITERIA Dx. IMA (WHO)

2 diantara :

1. chest pain khas


2. perubahan ECG
3. perubahan enzim jantung

The American College of Cardiology (ACC) and


the European Society of Cardiology (ESC)
Meredefinikan Kriteria Dx IMA

Cardiac marker adalah yg terpenting


dalam menegakkan Dx IMA

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According to these bodies, AMI is now defined as a typical rise and
fall of biochemical markers (eg, troponin, creatine kinase–MB
[CK-MB]), with at least one of the following:

Ischemic symptoms

New pathologic Q waves on ECG

Ischemic ECG changes (ST-segment elevation or depression)

Coronary artery intervention

Pathologic findings of AMI

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Creatine Kinase-MB Isoenzymes

Dx AMI :

2 serial elevations above the diagnostic cutoff level or


a single result more than twice the upper limit of normal.

Although CK-MB is more concentrated in the myocardium


(approximately 15% of the total CK),
it also exists in skeletal muscle.
The cardiospecificity of CK-MB is not 100%.
False-positive elevations occur in a number of clinical settings,
including trauma, heavy exertion, and myopathy.

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CK-MB

first appears 4-6 hours after symptom onset,

peaks at 24 hours,

returns to normal in 48-72 hours.

Its value in the early and late (>72 h) diagnosis of AMI is limited.
However, its release kinetics can assist in diagnosing reinfarction
if levels rise after initially declining in the time period after AMI.

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Relative index, CKMB, and total CK

the ratio of CK-MB (mass)/total CK X 100


can assist the clinician in differentiating false-positive elevations
of CK-MB arising from skeletal muscle.

Ratio <3 is consistent with a skeletal muscle source.


Ratios >5 are indicative of a cardiac source.
Ratios 3 - 5 represent a gray zone.

No definitive diagnosis can be established without serial


determinations to detect a rise.
The diagnosis of AMI must not be based on an elevated
relative index alone.
The relative index is only useful when both the total CK and
the CK-MB levels are increased.
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Creatine kinase-MB isoforms
CK-MB1 and CK-MB2.

CK-MB2 is the tissue form and initially is released from


the myocardium after MI.
It is converted peripherally in serum to the CK-MB1 isoform.
This occurs rapidly after symptom onset.

analyzed using high-voltage electrophoresis.


Automated analyzers with rapid turnaround times are available.
The ratio of CK-MB2/CK-MB1 is calculated.
Normally, the tissue CK-MB1 isoform predominates;
thus, the ratio characteristically is less than 1.
A result is positive if CK-MB2 is elevated and the ratio is more than 1.7

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CK-MB2

is detected in serum within 2-4 hours after onset and


peaks at 6-9 hours.

It is an early marker for AMI.

sensitivity of 92% at 6 hours after symptom onset compared with


66% for CK-MB and
79% for myoglobin.

The major disadvantage of this assay is that it is relatively


labor intensive for the laboratory.

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Myoglobin

an early marker of MI.


It is a heme protein found in skeletal and cardiac muscle.
Its low molecular weight accounts for its early-release profile.

typically rises 2-4 hours after onset of infarction,


peaks at 6-12 hours, and
returns to normal within 24-36 hours.

Rapid myoglobin assays are available,


but overall they suffer from lack of cardiospecificity.
Serial sampling every 1-2 hours can increase the sensitivity
and specificity.
A rise or delta of 25-40% over 1-2 hours is strongly suggestive of AMI.
In most studies, myoglobin only achieved a 90% sensitivity for AMI.
The negative predictive value of myoglobin is not high enough
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to exclude the diagnosis of ACS
Cardiac troponins

The troponins are regulatory proteins found in :


skeletal and cardiac muscle.

The 3 subunits that have been identified include


troponin I (TnI),
troponin T (TnT), and
troponin C (TnC).

the skeletal and cardiac subforms for TnI and TnT are distinct,
and immunoassays have been designed to
differentiate between them.

This explains the unique cardiospecificity of the cardiac troponins.


Skeletal TnI and TnT are structurally different.
No cross-reactivity occurs between skeletal and
cardiac TnI and TnT with the current assays. 26
Studies on the release kinetics of the cardiac troponins :
they are not early markers of myocardial necrosis.

They appear in serum within 4-8 hours after symptom onset,


(similar in timing to the release of CK-MB)
however, they remain elevated for as long as 7-10 days post-MI.

An elevated troponin level


enabled risk stratification of patients with ACS and
identified patients at high risk of adverse cardiac events
(ie, death, MI) up to 6 months after the index event.

Sensitive/cardiospecific,
and provide prognostic information for patients with ACS.
They have become the cardiac markers of choice for patients
with ACS.
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Lactate dehydrogenase:

The LDH has been supplanted by other tests.


It begins to rise in 12 to 24 hours following MI,
peaks in 2 to 3 days,
gradually dissipating in 5 to 14 days.

Measurement of LDH isoenzymes is necessary


for greater specificity for cardiac injury.
There are 5 isoenzymes (1 through 5).
Ordinarily, isoenzyme 2 is greater than 1,
but with myocardial injury, this pattern is "flipped" and
1 is higher than 2.

LDH-5 from liver may be increased


with centrilobular necrosis from passive congestion
with congestive heart failure following ischemic myocardial injury.
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Aspartate aminotransferas (AST)/
Serum glutamic oxalo acetic acid (SGOT)

SGOT is an enzyme that is also released with myocardial


Infarction

SGOT rises to a maximum at 24 hours &


Declines to normal levels at about 48 hours postinfarction

However, it is not specific to cardiac disease in that it may


Reflect disease of
the lung
liver, or
skeletal muscle
Therefore, it is not a reliable marker & is now rarely used
In diagnosis
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What Is the Best Marker ?

The best marker depends on the time from onset of symptoms.


The earliest markers are myoglobin and the CK-MB isoforms.

CK-MB and troponins are ideal in the intermediate


period of 6-24 hours.
(the troponins are not early markers)

Only 35% of patients with NSTEMI have (+) troponins


at baseline evaluation.
One of the medicolegal pitfalls for the clinician is to mistakenly
rule out NSTEMI on the basis of a single negative determination
of troponin in the early 3- to 6-hour time frame after symptom onset.

The troponins are recommended for evaluation of patients who present


more than 24 hours after symptom onset.

Lactic dehydrogenase (LDH) isoenzymes no longer are 30

recommended and should be abandoned.


Table . Time of measurement cardiac marker

Base
2-4 h 6-12 h 12-24 > 24 h
line
h

Early
(CKMB
X X X
isoforms,
myoglobin)
Intermediate
(CK-MB, TnI, X X X X
TnT)
X
Late
(TnI, TnT) 31
Troponin
CK
10 LDH
SGOT
Relative
Enzyme
activity

0
0 24 48 72 96 120 144
hours from onset of symptoms 32
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