dr. Khomimah Sp.

PD,K-EMD
§ Pencegahan Primer bertujuan Kriteria dan klasifikasi ASCVD
mencegah Onset Baru Atherosclerosis
Cardiovascular Disease (ASCVD).
§ Pencegahan sekunder : mencegah
kejadian ASCVD ulang
§ ASCVD: coronary heart disease (CHD),
stroke, and other atherosclerotic
vascular diseases.
§ ASCVD Penyebab Utama Kematian di
dunia (Bonow et al. 2002).
§ Untuk menurunkan beban ASCVD
dunia, harus menurunkan onset baru
ASCVD
 Table 5
Major Coronary Artery Disease Risk Factors (10 [EL 4], 11 [EL 4],
12 [EL 4], 13 [EL 4], 14 [EL 2], 15 [EL 4], 16 [EL 2], 17 [EL 4],
Tabel Major Coronary Artery Disease Risk Factors
18 [EL 2], 19 [EL 2], 20 [EL 4], 21 [EL 3])

Major risk factors Additional risk factors Nontraditional risk factors

Advancing agea,d Obesity, abdominal obesityc,d Elevated lipoprotein (a)
High total serum cholesterol Family history of hyperlipidemiad Elevated clotting factors
levela,b,d Small, dense LDL-Cd Inflammation markers (hsCRP;
High non–HDL-Cd Apo Bd Lp-PLA2)
High LDL-Ca,d LDL particle number Hyperhomocysteinemia
Low HDL-Ca,d,e Fasting/postprandial Apo E4 isoform
Diabetes mellitusa,b,c,d hypertriglyceridemiad Elevated uric acid
Hypertensiona,b,c,d PCOSd
Cigarette smokinga,b,c,d Dyslipidemic triadf
Family history of CADa,d,g
Abbreviations:
Abbreviations: CHD,
apo,coronary heart disease;
apolipoprotein; CAD, LDL-C, low-density
coronary artery lipoprotein cholesterol.
disease; HDL-C, high-density lipoprotein cholesterol; hsCRP,
ahighly
Major sensitive
independent risk factors are high low-density lipoprotein cholesterol, polycystic
C-reactive protein; LDL-C, low-density lipoprotein cholesterol; Lp-PLA ovary syndrome, cigarette smoking, phos-
, lipoprotein-associated
2
hypertension (blood pressure ≥140/90 mm Hg or on hypertensive medication), low high- density lipoprotein cholesterol (<40 mg/dL),
pholipase A2; PCOS, polycystic ovary syndrome.
family
a Riskhistory of coronary artery disease (n male rst-degree relative younger than 55 years; in female rst-degree relative younger than
factors identified
≥55 years). Subtract in theifFramingham
1 risk factor Heart
the person has study.
high high-density lipoprotein cholesterol
b Risk factors identified in the MRFIT study (Multiple Risk Factor Intervention Trial).
b(≥60
c Riskmg/dL) (10 [EL 4], 11 [65 years), and age (men ≥45; women EL 4]).
factors identified in the INTERHEART study.
cd Framingham risk scoring is applied to determine 10-year risk (10 [EL 4]). Coronary artery disease risk equivalents include diabetes
andRisk factors
clinical identified in
manifestations guidelines and
of noncoronary position
forms statementsdisease
of atherosclerotic (National Cholesterol
(peripheral Education
arterial Program Adult
disease, abdominal aortic Treatment
aneurysm,
Panel III, American
and carotid artery disease)Association of Clinical Endocrinologists Polycystic Ovary Syndrome Position Statement, American
Association of Clinical Endocrinologists Insulin Resistance Syndrome Position Statement, American Diabetes
Association Standards of Care 2009, American Diabetes Association/American College of Cardiology Consensus
Statement on Lipoprotein Management in Patients with Cardiometabolic Risk).
e Elevated high-density lipoprotein cholesterol is a negative risk factor.
f Hypertriglyceridemia; low high-density lipoprotein cholesterol; and small, dense low-density lipoprotein cholesterol.
Jacobson et al NLA Dyslipidemia Recommendations - Part 1 6 5 Journal of Clinic

smooth muscle proliferation. The proliferation of smooth to be a better predictor

muscle cells creates a fibrous cap or plaque.43 As the plaque which may, at least in p
matures and atherogenic particles continue to infiltrate,
between the non–HDL
lipid-rich areas form within the fibrous plaque.41 Inflamma-
tion triggers processes that weaken the fibrous cap and
levels of atherogenic p
make the plaque susceptible to rupture.44 Thus, atherogenic both LDL-C and trigly
lipoproteins play important roles in the initiation of athero- (non–HDL-C is the s
sclerosis, progression to a mature plaque and, eventually, rich lipoprotein chole
plaque instability and rupture. When plaque rupture occurs, components.
subendothelial components are exposed to the blood, and
luminal thrombosis occurs, which, if sufficiently large, 2. Reducing elevated le
can occlude arterial flow. Atherosclerotic plaque rupture lower ASCVD risk
is generally the proximal cause of acute atherogenic choleste
coronary syndromes (eg, myocardial infarction, unstable sumed to result from
angina).45–48 through multiple m
Epidemiologic studies have demonstrated a strong
drug therapies.
relationshipFigure
between4serum cholesterol between
Relationship levels andpercent
increasedreduction in total
Figure 2 Log-linear relationship between serum cholesterol and
ASCVD risk, and, conversely,
cholesterol low rates
and percent of ASCVD
reduction in are
coronary heart disease Numerous clinical
coronary heart disease (CHD) mortality from the Multiple Risk 49–53
associated with low levels
(CHD) incidence. of 8cholesterol (Fig. 2). The lowering therapies have
Factor Intervention Trial (N 5 356,222).8,50
importance of LDL-C in ASCVD is corroborated by the
the incidence of ASC
existence of familial hypercholesterolemia (FH), an auto-
and that this relationship is evident in those with and somal codominant genetic disorder characterized by very of LDL-C and non–H
64
without hypertriglyceridemia.31–37 HDL-C). Genetic
high levels of LDL-C (and LDL mutations thatand
particles) result in increased circu-
early Examinations of on-tre
Atherosclerosis has been described as a lipid-driven ASCVD. lating
54,55 levels of
In patients triglycerides
with and triglyceride-rich
FH, the removal of apo lipopro- pared with coronary h
inflammatory disorder of the arterial wall.38–41 Atherogenic B–containing teinlipoproteins
cholesterolby(eg, variantsapheresis
lipoprotein associated has with lipoprotein dies of primary preven
 in grou
life.56,101
maintain
periods
(averagin
greater r
1% to
approach
lifetime
Many
designed
guide de
predict in
Figure 7 Major CV event risk according to LDL-C and non– event.3,9
HDL-C levels achieved with statin therapy in a meta-analysis of importan
statin trials.97 CI, confidence interval; CV, cardiovascular; HR, ularly by
preexisti
Ø Kelainan metabolisme lipid - peningkatan maupun penurunan fraksi lipid
dalam plasma.
✦Kolesterol total (K- total)⬆
✦Kolesterol LDL (K-LDL)⬆
✦Trigliserida (TG)⬆
✦Penurunan kolesterol HDL (K-HDL)⬇‍‍
Ø Peran penting dalam proses aterosklerosis
Dislipidemia primer - kelainan genetik
ü dislipidemia sedang
✦ hiperkolesterolemia poligenik
✦ dislipidemia kombinasi familial
ü Dislipidemia berat
✦ hiperkolesterolemia familial
✦ dislipidemia remnan
✦ hipertrigliseridemia primer.
Dislipidemia Sekunder, penyebab
✦ Diabetes melitus
✦ Hipotiroidisme
✦ Penyakit hati obstruktif
✦ Sindroma nefrotik
✦ Obat-obat yang ⇑ kolesterol LDL
✦ ⇓ kolesterol HDL (progestin, steroid
anabolik, kortikosteroid, beta-blocker)
1. Perokok aktif (IC) 7. ! LP > 90 cm atau " LP > 80
cm (IC)
2. Diabetes (IC)
8. Disfungsi ereksi
3. Hipertensi (IC)
9. Aterosklerosis atau abdominal
4. Riwayat keluarga dengan PJK aneurisma(9)
dini (IC) Riwayat keluarga 10. Manifestasi klinis hiperlipidemia
dengan hiperlipidemia (IC)(8) (Xanthelasma / Xanthoma)
5. Penyakit ginjal kronik (I C) 11. Obesitas IMT ≥ 25 kg/m2
6. Penyakit inflamasi kronik(IC) (Asia) (10)
12. ! ≥ 40 tahun " ≥ 50 tahun,
atau menopause
 Klasifikasi kadar Kolesterol & Trigliserida
(mg/dL)

1. Total kolesterol
2. Kolesterol LDL
3. Trigliserida
4. Kolesterol HDL
5. Non HDL (Total Kol-HDL)
6. Lipoprotein (a)
7. Apo B
8. Rasio Apo B/Apo a
9. Rasio Non-HDL C/HDL-C

Kol. LDL (mg/dl) =

Kol. total – Kol. HDL – TG/5

Tidak berlaku pada:

§ TG > 400 mg/dl
§ dislipidemia Frederickson type III
§ fenotip Apo E2/2
1. Score Chart
2. Framingham Score
3. Pooled Cohort Equations (ASCVD score)
§ memperkirakan risiko 10 tahun kedepan kejadian ASCVD
§ Komponen: JK, usia, kol. total, kol. HDL, TD sistolik, ras, terapi untuk
hipertensi, riwayat DM dan merokok(15)
§ http://www.cardiosource.org/science-and-quality/practice- guidelines-
and-quality-standards/2013-prevention guideline-tools.aspx.

§ Estimasi risiko berdasarkan skor tersebut tidak berlaku pada kelompok

high dan very high risk
§ Target dan komponen yang akan diterapi
 § :10-year risko fatal cardio vascular
disease(CVD)in populations at high
CVD risk based on the following risk

Downloaded from http://eurheartj.oxfordjournals.org/ by guest on November 29, 2016

factors: age, gender, smoking, systolic
blood pressure, and total cholesterol.
To convert the risk of fatal CVD to risk
of total (fatal + nonfatal) hard CVD,
multiply by 3 in men and 4 in women,
and slightly less in old people.
§ Note: the SCORE chart is for use in
people without overt CVD, diabetes,
chronic kidney disease, familial
hypercholesterolaemia or very high
levels of individual risk factors
because such people are already at
high-risk and need intensive risk
factor advice.
ESC/EAS Guidelines
 number, small dense LDL, fasting/postprandial experiencing a coronary event in the presence of

Table 5
A. Identifications risk factors
Major Coronary Artery Disease Risk Factors (10 [EL 4], 11 [EL 4],
12 [EL 4], 13 [EL 4], 14 [EL 2], 15 [EL 4], 16 [EL 2], 17 [EL 4],
Tabel Major Coronary Artery Disease Risk Factors
18 [EL 2], 19 [EL 2], 20 [EL 4], 21 [EL 3])

Major risk factors Additional risk factors Nontraditional risk factors

Advancing agea,d Obesity, abdominal obesityc,d Elevated lipoprotein (a)
High total serum cholesterol Family history of hyperlipidemiad Elevated clotting factors
levela,b,d Small, dense LDL-Cd Inflammation markers (hsCRP;
High non–HDL-Cd Apo Bd Lp-PLA2)
High LDL-Ca,d LDL particle number Hyperhomocysteinemia
Low HDL-Ca,d,e Fasting/postprandial Apo E4 isoform
Diabetes mellitusa,b,c,d hypertriglyceridemiad Elevated uric acid
Hypertensiona,b,c,d PCOSd
Cigarette smokinga,b,c,d Dyslipidemic triadf
Family history of CADa,d,g
Abbreviations: CHD, coronary
Abbreviations: heart
apo, disease; LDL-C,
apolipoprotein; low-density
CAD, lipoprotein
coronary cholesterol.
artery disease; HDL-C, high-density lipoprotein cholesterol; hsCRP,
a Major independent risk factors are high low-density lipoprotein cholesterol, polycystic
highly sensitive C-reactive protein; LDL-C, low-density lipoprotein cholesterol; ovary syndrome,
Lp-PLA cigarette smoking, hypertension (blood pressure
2, lipoprotein-associated phos-
≥140/90 mm Hg or on hypertensive medication), low high- density lipoprotein cholesterol (<40 mg/dL), family history of coronary artery disease (n male rst-
pholipase A2; PCOS, polycystic ovary syndrome.
degree relative
a Riskyounger than 55 years; in female rst-degree relative younger than ≥55 years). Subtract 1 risk factor if the person has high high-density
factors identified in the Framingham Heart study.
lipoproteinb cholesterol
Risk factors identified in the MRFIT study (Multiple Risk Factor Intervention Trial).
b(≥60 mg/dL) (10 [EL 4], 11 [65 years), and age (men ≥45; women EL 4]).
c Risk
c Framingham
factors identified in the INTERHEART study.
risk scoring is applied to determine 10-year risk (10 [EL 4]). Coronary artery disease risk equivalents include diabetes and clinical
d Risk factors identified
manifestations of noncoronary forms in guidelines anddisease
of atherosclerotic position statements
(peripheral (National
arterial Cholesterol
disease, abdominalEducation Program
aortic aneurysm, and Adult
carotidTreatment
artery disease)
Panel III, American Association of Clinical Endocrinologists Polycystic Ovary Syndrome Position Statement, American
 § Evaluasi fator risiko mayor yang lain
§ Kondisi yang dikaitkan dengan risiko tinggi dan sangat tinggi
18 Journal of Clinical Lipidology, Vol -, No -, - 2015

Table 7 Major
Major risk Factors
risk factors for ASCVDASCVD
* Table High or very
9 High- or veryHigh riskpatient
high–risk patients group
groups
1. Age Quantitative risk scoring is not necessary for initial risk
Male $45 y assessment in patients with the following conditions:*
Female $55 y ! Diabetes mellitus, type 1 or 2
2. Family history of early CHD† ! Chronic kidney disease, stage $3B
,55 y of age in a male first-degree relative or ! LDL-C $190 mg/dL: severe hypercholesterolemia
,65 y of age in a female first-degree relative phenotype, which includes FH
3. Current cigarette smoking ! ASCVD
4. High blood pressure ($140/$90 mm Hg, or on blood ASCVD, atherosclerotic cardiovascular disease; FH, familial hyper-
pressure medication) cholesterolemia; LDL-C, low-density lipoprotein cholesterol.
5. Low HDL-C *Patients in these categories are all at ‘‘high’’ or ‘‘very high’’ risk for
Male ,40 mg/dL an ASCVD event and should be treated accordingly.
Female ,50 mg/dL
ASCVD, atherosclerotic cardiovascular disease; CHD, coronary heart
disease; HDL-C, high-density lipoprotein cholesterol.
ASCVD risk assessment and treatment goals
*Levels of non–high-density lipoprotein cholesterol and low- based on risk category
density lipoprotein cholesterol are not listed, because these risk Journal of Clinical Lipidology, Vol -, No -, - 2015
factors are used to assess risk category and treatment goals for athero- In addition to lipoprotein lipid levels, ASCVD risk
12 Journal of Clinical Lipidology, Vol -, No -, - 2015
Kriteria asesmen risiko ASCVD, target terapi kolesterol aterogenik, kadar yang
dipertimbangkan
Table 3 Criteria for ASCVD risk assessment, untukcholesterol,
treatment goals for atherogenic diterapi and levels at which to consider drug therapy
Treatment goal Consider drug therapy
Non–HDL-C, mg/dL Non–HDL-C, mg/dL
Risk category Criteria LDL-C, mg/dL LDL-C, mg/dL
Low ! 0–1 major ASCVD risk factors ,130 $190
! Consider other risk indicators, if known ,100 $160
Moderate ! 2 major ASCVD risk factors ,130 $160
! Consider quantitative risk scoring ,100 $130
! Consider other risk indicators*
High ! $3 major ASCVD risk factors ,130 $130
! Diabetes mellitus (type 1 or 2)† ,100 $100
B 0–1 other major ASCVD risk factors and

B No evidence of end-organ damage

! Chronic kidney disease stage 3B or 4‡

! LDL-C of $190 mg/dL (severe hypercholesterolemia)x
! Quantitative risk score reaching the high-risk thresholdjj
Very high ! ASCVD ,100 $100
! Diabetes mellitus (type 1 or 2) ,70 $70
B $2 other major ASCVD risk factors or
{
B Evidence of end-organ damage

For patients with ASCVD or diabetes mellitus, consideration should be given to use of moderate or high-intensity statin therapy,
irrespective of baseline atherogenic cholesterol levels.
Journalcholesterol.
ASCVD, atherosclerotic cardiovascular disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein of Clinical Lipidology, Vol -, No -, - 2015
*For those at moderate risk, additional testing may be considered for some patients to assist with decisions about risk stratification. See Tables 4
 Klasifikasi Kadar
Non–HDL-C dan LDL-C
Kolesterol dan Trigliserida

Target terapi Kol. non-HDL dan Kol. LDL

Journal of Clinical Lipidology, Vol -, No -, - 2015

 courage TGbut
tematically, lowering
felt that(Table
it was18).
appropriate to look at the totality

urnals.org/ by guest on November 29, 2016

1.7 mmol/L (150 mg/dL). 258 HTG can have different causes
Table 9 Recommendations for lipid analyses as of the evidence. Indeed, the task force accepts that the choice of
able 17), treatment
among which its polygenic
targets nature isofmost
in the prevention important
cardiovascular any given target goal for LDL-C may be open to debate given the
relation to CVD prevention. Table 18 Recommendations for drug treatments of
disease continuous nature of the relationship between LDL-C reduction
hypertriglyceridaemia
and reduction in risk. Particular consideration was given to results
Recommendations Class a Level b Ref c from systematic reviews confirming the dose-dependent reduction
LDL-C is recommended as the
Recommendations
in CVD with LDL-C lowering; the greater Class a
the Levelreduction,
LDL-C b
Ref c
Possible
Table 17 primary targetcauses of hypertriglyceridaemia
for treatment.
I A 64, 68 the greater the CV risk reduction.65,66 The benefits related to
Drug treatment should be 63
TC should be considered as a LDL-C reduction
considered are not
in high-risk specific
patients withfor statin
IIa therapy.B No 261, level
262
Genetic predisposition
treatment target if other analyses IIa A 64, 123 of LDL-C
TG >2.3below
mmol/Lwhich benefit ceases or harm occurs has been
(200 mg/dL).
are not available. defined.
Obesity Statin treatment may be
Non-HDL-C should be considered There is considerable individual variability in the LDL-C re-
Type 2 diabetes IIa B 103 considered as the first drug of 61
as a secondary treatment target. sponse tofor
dietary andCVD
drug 263,
choice reducing risktreatments, IIbwhich is B traditionally
taken to support a tailored 264
Alcohol consumption
ApoB should be considered as a in high-risk individuals with approach to management. Total
secondary treatment target, when IIa B 103, 124 CV hypertriglyceridaemia.
risk reduction should be individualized, and this can be
Diet high in available.
simple carbohydrates
more specific if goals are defined. The use of goals can also
Renal disease
HDL-C is not recommended as a In high-risk patients with TG
III A 92, 93 aid patient – doctor communication. It is judged likely that a
target for treatment. >2.3 mmol/L (200 mg/dL) despite
Hypothyroidism goalstatin
approach mayfenofibrate
treatment, facilitate adherence
may to treatment,
IIb C although261–264
The ratios apoB/apoA1 and thisbeconsensus opinion has not been fully tested. For all these
Pregnancy (physiological triglyceride
non-HDL-C/HDL-C are notconcentrations double during the considered in combination with
III B 103 reasons
statins.the European Task Force retains a goal approach to
third trimester)
recommended as targets for
treatment. lipid management and treatment goals are defined, tailored
Paraproteinaemia and autoimmune disorders such as systemic lupus
to the total CV risk level. There is also evidence suggesting
erythematosus CVD ¼ cardiovascular disease; TG ¼ triglycerides.
Apo ¼ apolipoprotein; HDL-C ¼ high-density lipoprotein-cholesterol; LDL-C ¼ that
a lowering LDL-C beyond the goals that were set in
Class of recommendation.
Multiple low-density
medications including: the
lipoprotein-cholesterol; TC ¼ total cholesterol. b
Levelprevious
of evidence.EAS/ESC guidelines is associated with fewer
• Corticosteroids
a
Class of recommendation. CVD
c events.
Reference(s)
126
Therefore,
supporting it seems appropriate to reduce
recommendations.
b
Level of especially
• Oestrogens, evidence. those taken orally
c
Reference(s) supporting recommendations. LDL-C as low as possible, at least in patients at very high
• Tamoxifen ESC/EAS Guidelines
CV risk.
• Antihypertensives: adrenergic beta-blocking agents (to a different
§ Target kolesterol non-HDL adalah 30 mg/dL di atas target kolesterol LDL.

§ target kolesterol LDL bagi pasien dengan risiko sangat tinggi adalah ˂70 mg/dL

§ maka target untuk kolesterol non-HDL adalah ˂100 mg/dL.

§ target kolesterol non-HDL untuk pasien dengan risiko tinggi adalah ˂130 mg/dL.

§ Target ini sesuai dengan konsentrasi kolesterol VLDL pada pasien yang mempunyai
konsentrasi TG >150 mg/dL.

§ Konsentrasi kolesterol VLDL “normal” yang besarnya ˂30 mg/dL adalah konsentrasi
kolesterol VLDL ketika
§ Prinsip strategi intervensi
1. Selalu pertimbangkan tingkat risiko KV total
2. Semua pasien, kecuali risiko rendah, dan kadar Kol. LDL pre terapi
<100 mg/dL, perlu mendapat intervensi perubahan gaya hidup.
3. Intervensi farmakologis, obat penurun lipid:
§ terhadap target primer, pada pasien Kadar awal Kol.- LDL di atas target terapi.
§ terhadap target sekunder (kolesterol non-HDL) hanya dilakukan pada pasien
dengan tingkat risiko tinggi dan sangat tinggi yang target kolesterol LDL- nya
telah tercapai sementara konsentrasi TG masih di atas 200 mg/dL.

§ Intervensi kolesterol LDL

§ Pertimbangkan adanya penyebab sekunder peningkatan kolesterol LDL

PEDOMAN TATALAKSANA DISLIPIDEMIA DI INDONESIA, PERKI 2013
Pengaruh Perubahan Gaya Hidup
Terhadap Kadar Lipid
Obat-obat Hipolipidemik(17)

Klasifikasi Statin menurut ACC/AHA 2013 berdasarkan

kemampuan menurunkan K-LDL(15)
PILIHAN OBAT UNTUK DISLIPIDEMIA
 • CONTOH : simvastatin, atorvastatin, rosuvastatin
PILIHAN OBAT UNTUK DISLIPIDEMIA
• Mekanisme : Inhibitor HMG CoA reduktase, mengganggu
konversi HMG CoA menjadi mevalonate
STATIN • first liner untuk menurunkan LDL
• Jika tidak toleran terhadap statin, direkomendasikan
pemakaian ezetimibe, inhibitor PCSK9, atau bile acid
sequestrant monoterapi

• CONTOH : Ezetimibe
• Mekanisme : menghambat ambilan kolesterol dari
INHIBITOR ABSORPSI diet dan kolesterol empedu tanpa mempengaruhi
KOLESTEROL absorpsi nutrisi yang larut dalam lemak
• Dosis ezetimibe yang direkomendasikan adalah 10
mg/hari dan harus digunakan bersama statin

• CONTOH : alirocumab, bococicumab, dan

evolocumab
INHIBITOR PCSK9
• Mekanisme : menghambat degradasi reseptor LDL à
menurunkan konsentrasi kolesterol LDL plasma
 • CONTOH : kolestiramin, kolesevelam, dan kolestipol
PILIHAN OBAT UNTUK DISLIPIDEMIA
BILE ACID SEQUESTRAN
• Mekanisme : mengikat asam empedu (bukan kolesterol) di usus
sehingga menghambat sirkulasi enterohepatik dari asam empedu
dan meningkatkan perubahan kolesterol menjadi asam empedu di
hati

• CONTOH : fenofibrate, gemfibrozil

FIBRAT • Mekanisme : peningkatan katabolisme TG oleh lipoprotein lipase,
berkurangnya pembentukan kolesterol VLDL, dan meningkatnya
pembersihan kilomikron.

• CONTOH : evacetrapib
• Mekanisme : Cholesteryl ester transfer protein berfungsi membantu
INHIBITOR CETP transfer cholesteryl ester dari kolesterol HDL kepada VLDL dan LDL
yang selanjutnya akan dibersihkan dari sirkulasi melalui reseptor
LDL di hepar.
 PILIHAN OBAT UNTUK DISLIPIDEMIA
PUFA OMEGA 3 • Mekanisme : berinteraksi dengan PPAR dan
menurunkan sekresi apoB

• Tindakan aferesis ditujukan bagi pasien dengan

HoFH atau HeFH berat.
Aferesis
kolesterol LDL • kolesterol LDL dan Lp(a) dibuang dari plasma
selama dilakukan sirkulasi ekstrakorporeal setiap
1 atau 2 minggu sekali.
 Stage 5 CKD (or on dialysis) is indeed a very high-risk condition patients at high or very high risk for developing CVD, recommenda-

oaded from http://eurheartj.oxfordjournals.org/ by guest on November 29, 2016

in which different factors influence outcome; results from RCTs tions are summarized in Table 30.
of lipid-altering therapies have not provided convincing evidence
of reduced CVD events in such patients.
In the 4D trial (Die Deutsche Diabetes Dialyse studie) involving a Table Rekomendasi
30 Recommendationsmanagemen lipid
for lipid management in
cohort of 1200 patients with diabetes on haemodialysis, atorvastatin PGK sedang-berat
patients with moderate to severe chronic kidney disease
had no positive effect on the primary composite endpoint of
CVD.395 The results from AURORA (A study to evaluate the Use Recommendations Class a Level b Ref c
of Rosuvastatin in subjects On Regular haemodialysis: an Assess- Patients with stage 3–5 CKD have
ment of survival and cardiovascular events), involving 2776 patients to be considered at high or very I A 388–392
on haemodialysis, show that rosuvastatin lowered LDL-C as ex- high CV risk.
pected but had no significant effect on the composite CVD end- The use of statins or statin/
point.396 The neutral results question the benefits of statins in ezetimibe combination is indicated
I A
393,
these very high-risk patients with poor outcomes. in patients with non-dialysis- 394, 397
dependent CKD.
In the SHARP study397 simvastatin and ezetimibe combination
therapy was associated with lower risk for major atherosclerotic In patients with dialysis-dependent
CKD and free of atherosclerotic
events (coronary death, MI, non-haemorrhagic stroke or any revas- III A 395, 396
CVD, statins should not be
cularization) compared with placebo in persons with CKD stage initiated.
3A– 5. The trial did not have sufficient power to assess the effects In patients already on statins,
in the primary outcome separately in dialysis and non-dialysis pa- ezetimibe or a statin/ezetimibe
Dosis yang lebih rendah dipertimbangkan untuk populasi di Asia. Data didasarkan pada studi
combination at the time of dialysis
ALERT1 4D2, AURORA3, SHARP4 tients, but there was no good statistical evidence that the propor- initiation, these drugs should be
IIa C
tional effects in dialysis patients differed from those seen in
continued, particularly in patients
patients not on dialysis; in general, CV risk was much lower in the
Penyesuaian dosis statin pada PGK95
patients in the SHARP trial compared with those of the AURORA
with CVD.
In adult kidney transplant recipients
and 4D trials, reflected in the lower event and mortality rates. treatment with statins may be IIb C
A cost-effectiveness analysis of statins for primary CVD preven- considered.
tion in CKD398 showed that statins reduced absolute CVD risk in
patients with CKD but that the increased risk for rhabdomyolysis, CKD ¼ chronic kidney disease; CV ¼ cardiovascular.
a
and competing risks associated with progressive CKD, partly offset b
Class of recommendation.
Level of evidence.
these gains. A systematic review of the benefits and harms of statins c
Reference(s) supporting recommendations.
in patients with a functioning kidney transplant included 3465 pa-
tients, free of CHD, from 22 studies. The authors concluded that
statins may reduce CV events, although treatment effects were im-
ESC/EAS Guidelines
f dyslipidae-
Table 25 Summary of dyslipidaemia in metabolic
syndrome and in type 2 diabetes
ome
Dyslipidaemia in MetS represents a cluster of lipid and lipoprotein
e world and abnormalities including elevation of both fasting and postprandial TG,
will increase apoB, and small dense LDL and low HDL-C and apoA1.
Despite sig- Non-HDL-C or apoB are good surrogate markers of TRLs and remnants
lessen CVD and are a secondary objective of therapy. Non-HDL-C <3.4 mmol/L
orbidity and (<130 mg/dL) or apoB <100 mg/dL is desirable in those at high-risk,
and <2.6 mmol/L (<100 mg/dL) and <80 mg/dL, respectively, in those at
2DM). It has
very high-risk.
-old person
Increased waist circumference and elevation of TG seems to be a simple
difference is
tool to capture the high-risk subjects with MetS.
ndependent
Atherogenic dyslipidaemia is one of the major risk factors for CVD in
f CVD, even people with type 2 diabetes.
sk between
ubstantially
apoB ¼ apolipoprotein B; CVD ¼ cardiovascular disease; HDL-C ¼ high-density
een diabetes lipoprotein-cholesterol; LDL-C ¼ low-density lipoprotein-cholesterol; MetS ¼

Downlo
betes per se metabolic syndrome; TG ¼ triglycerides; TRLs ¼ triglyceride-rich lipoproteins. ESC/EAS Guidelines
Figure Risk of major cardiovascular events by low-density lipoprotein cholesterol (LDL-C) and non–high-density
lipoprotein choles- terol (non-HDL-C) categories. Data markers indicate hazard ratios (HRs) and 95% confidence
intervals (CIs) for risk of major cardio- vascular events. Results are shown for 4 categories of statin-treated
patients based on whether or not they reached the LDL-C target of 100 mg/dL and the non–HDL-C target of 130
mg/dL. HRs were adjusted for sex, age, smoking, diabetes, systolic blood pressure, and trial. Taken from
Boekholdt SM et al. with permission. Copyright ! (2012) American Medical Association. All rights reserved.
Journal of Clinical Lipidology, Vol -, No -, - 2015
§ Figure 10 Hazard ratios for coronary heart
disease across quintile of non–high-density
lipoprotein cholesterol (non-HDL-C), apolipopro-
tein (apo) B, HDL-C, and apo A1.
 life.56,
mainta
period
(avera
greate
1% to
approa
lifetim
Ma
design
guide
predic
Figure 7 Major CV event risk according to LDL-C and non– event.
HDL-C levels achieved with statin therapy in a meta-analysis of impor
statin trials.97 CI, confidence interval; CV, cardiovascular; HR, ularly
hazard ratio; LDL-C, low-density lipoprotein cholesterol; non– preexi
HDL-C, non–high-density lipoprotein cholesterol; Ref, referent. likelih
Journal of Clinical Lipidology (2015) - , –
- -
§ Langkah 1. Identifikasi masalah pada pasien
§ Langkah 2. Melakukan penghitungan risiko kardiovaskular, klasifikasi
kelompok risiko dan pilihan terapi
§ Langkah 3. Pemberian edukasi

§ Langkah 4. Pemantauan dan evaluasi

ALUR 1 ALUR 2.
(ATP III) ACC/
AHA
2013
§ Dislipidemia –kelainan metabolism lemak yang ditandai:

§ Kol Total, Kol. LDL, dan TG meningkat dan atau Kol HDL turun

§ Bersifat Atherogenic –meningkatkan risiko PKV

§ Kol. LDL dan Kol. Non-HDL merupakan target pencegahan ASCVD

§ Langkah: Identifikasi risiko, stratifikasi risiko, dan Target terapi

§ Modifikasi gaya hidup dan atau Obat hipolipidemik yang optimal dan sesuai
target terapi