Dyslipidemia Update by DR Sarma

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O ALMIGHTY
Tallee ninnu dalanchi pustakamu
chaetan boonitin neevu naa
ullambanduna nilchi jrumbhanamugaan
uktul su sabdambul
sobhillan balkumu naadu vaakkunan
sampreetin, Jaganmohinee
pullaabjaakshee Saraswatee Bhagavatee
poornaendu bimbaanana
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O! Almighty, the Goddess of Wisdom!
We start this learning process, keeping
YOU in our inner hearts, please shower
Your kind blessings on all of us and ensure
What ever we speak is eloquent
What ever we discuss is pertinent
What ever we learn is relevant.
May we be blessed with the best wisdom !
O! ALMIGHTY
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Dr.Sarma RVSN, M.D., M.Sc (Canada)
Consultant in Medicine and Chest,
# 3, Jayanagar, Tiruvallur 602 001
98940 60593, 2766 0593

Visit us at : www.drsarma.in
Dyslipidemias-
Practice Approach
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CD ROM Available
The contents of my todays presentations
are made available in a CD-ROM format
This CD, in addition, contains my talks on
Asthma, COPD, Hypertension, ECG, CAD
Dyslipidemias, Diabetes, Osteoporosis
Dr.Sarma@works 6
The Almighty
Pardons and Grants me heaven
Even if I don't know a single letter about
Crutz Feld Jacobs Disease
Tsutsugamushi Fever
Criggler Nazzar Syndrome
South American equine encephalitis and
Many and much more rarer topics
BUT .
Dr.Sarma@works 7
The Almighty
Will drag me to hell and will not pardon
My ignorance of even the minute details of HT, DM
My indifference to apply the current knowledge
My negligence in screening for Lipids, DM, HT, LVH
My despondency about preventing TOD and ACS
My inadequacy in maintaining my patients
Normotensive, Euglycemic, Eulipidemic
(This is applicable to all common diseases)
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National Cholesterol
Education Program - NCEP
Adult Treatment Panel III
(ATP III) Guidelines -2002
Updated October 2004
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The Good, Bad, Ugly and Deadly
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Two Types of Lipids
LIPIDS IN BLOOD
TOTAL CHOLESTEROL TRIGLYCERIDES (TG)
GOOD CHOLESTEROL
HDL 1 and HDL 2
BAD CHOLESTEROL
LDL, VLDL (TG), Lp(a)
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Lipoprotein
TG, EC
Phospholipids
Free Cholesterol
(Hydrophilic)
Apoproteins A,
B, C, E, (a)
(Amphiphatic)
Lipids or Fats
(Hydrophobic)
Size < RBC
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Lipoproteins
EC TG
Apoprotein boat
Apo A I and A II for HDL Apo B100 for LDL
Apo B100+C+E for VLDL, IDL Apo B100+Apo(a) for Lp(a)
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Good, Bad, Ugly & Deadly
C
TG
B 100 + E +C
C
TG
B 100
C
T
G
A I, A II
HDL LDL
VLDL
C
TG
B 100+ (a)
Lp(a)
TG
GOOD BAD
UGLY DEADLY
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All are the terrorists !!
Apolipoprotein B
Non-HDL-C
Measurements
TG-rich lipoproteins
VLDL VLDLR IDL LDL SDL
Highly atherogenic
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Particle size & Density
Chylomicrons
<< 1.006
VLDL
< 1.006
IDL
< 1.019
LDL
< 1.063
Small LDL
< 1.085
HDL
< 1.210
Atherogenicity increases as density increases
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LIPIDS ESTIMATED
TOTAL CHOLESTEROL (TC) TRIGLYCERIDES (TG)
HDLc LDLc VLDLc Chylomicrons VLDL
Lipid Profile Report
PP Fasting
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Normal Lipid Profile
Total Cholesterol < 200
TG Ugly Lipid < 150
Bad Cholesterols LDL < 100
HDL Good cholesterol > 50
VLDL is Ugly TG 5 < 30
Lp(a) Deadly cholesterol < 20
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How to interpret Lipid Profile Report?
A. Total Cholesterol
HDL Cholesterol (Soldiers) - Good
Non HDL Cholesterol (Culprits)
LDL Cholesterol Bad fellows
Lipoprotein(a) Deadly fellows
VLDL Cholesterol (1/5 of TG)- Ugly
B. Triglycerides 150
100
150
50
200
20
30
Normal Lipid Profile
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Interpret this Lipid Profile Report
B. Triglycerides
150
140
190
50
240
20
30
Hyper cholesterolimia LDL, HDL, TG, Lp(a) - N
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70
150
50
200
20
60
Hyper triglyceridemia TG, HDL, LDL, Lp(a) - N
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85
135
25
160
20
30
Low HDL : HDL, LDL, TG, Lp(a) - N
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75
155
45
200
50
30
High Lipoprotein(a) : Lp(a) , HDL, LDL, TG - N
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95
175
25
200
20
60
High Lipoprotein(a) : HDL, TG, LDL, Lp(a) - N
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B. Triglycerides
250
120
210
50
260
40
50
Combined Dyslipidemia : TCLDLTG Lp(a)
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Dyslipidemic Triad

A. Isolated High LDL 32.90%
B. Isolated low HDL 21.35%
C. Isolated high TG 10.45%

IHJ, 2000, 52: 173-177
Am J Med, 1998, vol 105(1A), 48S-56S
LDL
HDL
TG
The Triad
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Indian Dyslipidemic Triad

IHJ, 2000, 52: 173-177
Am J Med, 1998, vol 105(1A), 48S-56S
Lp(a)
HDL
TG
The Indian Triad
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Indian Dyslipidemia
Low HDL 39.2%
High TG 32.5%
Lp(a) excess 28.6%

High LDL 10.8%
Normal Lipids 23.5%
Am J C 2001;88(suppl) 9N-13N; 22N
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Look at the risks
Low HDL + High LDL +
LP(a) excess > 30 mg% +
LP(a) excess > 30 mg% + LDL high ++
LP(a) excess > 30 mg% + low HDL +++
LP(a) excess > 30 mg% + Incr. tHCy ++++
LP(a) excess + Incr. tHCy + low HDL +++++
Circulating lipids are one aspects
Tissue lipid content is more important

J. Atherosclerosis : Hopkins PN, 1997 17, 2792
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Intestinal Cholesterol Absorption
Bays H et al. Expert Opin Pharmacother 2003;4:779-790.
Intestinal
epithelial cell
Biliary
cholesterol
Dietary
cholesterol
Luminal
cholesterol
Micellar
cholesterol
Bile
acid
Cholesteryl esters
Free
cholesterol
excretion
uptake
ACAT
ABCG5
ABCG8
(esterification)
MTP
CM
Through
lymphatic
system to
the liver
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Lymph Enterocyte Intestinal
Lumen
Cholesterol Absorption
Cholesterol
NPC1L1
Cholesteryl
Ester
ABCG5/G8
ACAT
Ezetimibe
Avasimibe
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Lumen
Triglyceride Absorption
2 Fatty Acid
+
Monoglyceride
DGAT
Triglyceride
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CE
A-I
CE
A-I
CE
A-II A-II
HDL 1 HDL 2 HDL 3
APO A I
Atheroprotective
Alcohol increases
Athero-neutral
The soldiers
The soldier-like
HDL Sub types
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LIVER
Reverse Cholesterol Transport
MF in Vascular
Endothelium
Free Chol.
L CAT
Enzyme
UEC
EC
HDL
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HDL Metabolism and
Reverse Cholesterol Transport
Liver
ABC1 = ATP-binding cassette protein 1; A-I = apolipoprotein A-I;
CE = cholesteryl ester; FC = free cholesterol;
LCAT = lecithin:cholesterol acyltransferase;
SR-BI = scavenger receptor class BI
Mature HDL
CE
A-I
CE
CE
FC FC
LCAT
F
C
Bile
SR-BI
A-I
ABC1
Macrophage
Nascent
HDL
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B
SRA
Mature HDL
Role of CETP in HDL Metabolism
A-I
Liver
CE
CE
FC
FC
LCAT
FC
Bile
SR-BI
A-I
ABC1
Macrophage
CE
CETP = cholesteryl ester transfer protein
LDL = low-density lipoprotein
LDLR = low-density lipoprotein receptor
VLDL = very-low-density lipoprotein
LDLR
VLDL/LDL
CETP
Nascent HDL
CE
Torcitrapib
X
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Hyperlipidemias
Secondary 95%
Primary 5%
Familial & genetic
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Secondary Hyperlipidemia
LDL Cholesterol TG
Nephrotic syndrome. Obesity
Hypothyroidism Diabetes
Obstr. liver disease Uremia
Anorexia nervosa Alcoholism, Smoking
Acute Int. Porphyria Oral contraceptives
Progestogens Beta blockers
Thiazides Pregnancy
Anabolic steroids Steroids, Thiazides
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Clinical Action
Presence of secondary causes of Hyperlipidemia
Order for full lipid profile (LP) HT also
Presence of hyperlipidemia increased TG or EC
Investigate for all secondary causes
For all above 20 years once in every 5 years
For those above 45 yrs once in 2 years
For those with already known lipid abnormality
follow-up every 3-6 months
Extended Lipid profile includes Homocysteine,
LP(a), SD-LDL, ALP, Apo A and Apo B, hS-CRP
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Clinical Photoes
Tuberous xanthoma.
Flat-topped, yellow, firm tumor
Xanthelasma. Multiple, longitudinal, creamy-
orange, slightly elevated papules on eyelids .
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Clinical Photoes
Tendinous xanthomas. Large sub-
cutaneous tumors adherent to the
Achilles tendons.
Papular eruptive xanthomas. Multiple,
discrete, red-to-yellow confluent papules
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Evaluation
1. History of eruptive xanthomas, Abd. pain
2. H/o wt. gain, DM, estrogens, Alcohol, Ex.
3. Fasting Lipid profile (TC, LDL, HDL, TG)
4. OGTT, TSH, Liver & Renal Function tests
5. CHD assessment by ECG, TMT, Angio
6. Risk factor assessment, Family H/o P.CHD
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The Weapons in our hand
Diet and Exercise (Life Style)
Drug therapy
1. HMG
Co A Reductase Inhibitors
2. Fibric Acid derivatives
3. Nicotinic Acid
4. Ezetimibe
5. Bile Acid binding Resins (BAR)
6. Probucol
HMG is Hydroxy Methyl Glutaryl

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New Treatments
Drug therapy
1. Colesevelam (BAR)
2. Phytosterols
3. Avasimibe ACAT inhibitor
4. Torcetrapib CETP inhibitor
5. Drugs decreasing Apo B synthesis
6. Selective LDL apopheresis

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Therapeutic Lifestyle Changes - TLC
Nutrient Recommended Intake
Saturated fat < 7% of calories
PUFA fat Up to 10% of calories
MUFA fat Up to 20% of calories
Total fat 2535% of calories
Carbohydrate 5060% of calories
Fiber 2030 grams per day
Protein Approx. 15% of calories
Cholesterol Less than 200 mg/day
DIETARY THERAPY
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Our dietary fats
SFA (saturated) meet and diary products,
coconut oil, Kernel, Ghee, Butter, Palm oil,
Trans fatty acids in vanaspati, chocolates
confectionaries, baked, deep fat fried food
MUFA (N1) Olive oil, Gingili oil
PUFA (N6) Soya, Sun Flower oil, GN oil
PUFA (N3) Fish oils Twice a wk 76% CAD
Legumes, fruits, olive oil all cause mortality
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Treatment of LDLc
High LDLc
Therapeutic Lifestyle Change
Add on drug - EZ , Niacin, BAR
Therapy of Choice: Statin
Drug Therapy
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Statins Mechanism of Action
1. Reduce hepatic cholesterol synthesis (HMG CoA),
2. lowering intracellular cholesterol,
3. Upregulation of LDL receptor and
4. the uptake of non-HDL from circulation.
LDL receptormediated
hepatic uptake of LDL
and VLDL remnants
Serum VLDL remnants
Serum LDL-C
Cholesterol
synthesis
LDL receptor
(BE receptor)
synthesis
Intracellular
Cholesterol
Apo B
Apo E
Apo B
Systemic Circulation Hepatocyte
LDL
Serum IDL
VLDL
R

VLDL
HMGCoA
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Time course of Statin effects
* Time course established
Days Years
LDL-C
lowered*
Inflammation
reduced
Vulnerable
plaques
stabilized
Endothelial
function
restored
Ischemic
episodes
reduced
Cardiac events
reduced*
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HMG CoA Reductase
Inhibitors (Statins)
Statin Dose Range
Lovastatin 2080 mg
Pravastatin 2040 mg
Fluvastatin 2080 mg
Simvastatin 2080 mg
Atorvastatin 1080 mg
Rosuvastatin 520 mg
Cerivastatin 0.40.8 mg
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Atorvastatin
211 mg/dl*
Simvastatin
219 mg/dl*
-60%
-50%
-40%
-30%
-20%
-10%
0%
LDL-C Lowering - Statin Dose
Adapted from Jones P et al. Am J Cardiol 1998;81:582-587.
Daily Dose
10 mg
20 mg
40 mg
80 mg
16% with
3 Titrations
13
%
38%
46%
51%
54%
28%
35%
41%
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HMG CoA Reductase Inhibitors (Statins)
Common side effects
Headache, Myalgia, Fatigue, GI intol. Flu-like symptoms
Increase in liver enzymes serious problems are very rare
Occurs in 0.5 to 2.5% of cases in dose-dependent manner
Myopathy occurs in 0.2 to 0.4% of patients
Rare cases of Rhabdomyolysis
We can reduce this risk by
Cautiously using statins in impaired renal function
Using the lowest effective dose
Cautiously combining statins with fibrates
Muscle toxicity requires the discontinuation of statin
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Short falls of Statins
Effectiveness and community impact are to be improved
Rebound increase in lipids and of events after
withdrawal of statin Rx.
High rate of discontinuation by patients
Differences in the efficacy of different statins
They reduce only endogenous lipids Individual variation
Modest effect on TG and HDL, No effect on Lp(a)
No effect on chylomicrons; escape phenomenon
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Lumen
Ezetimibe
Cholesterol
NPC1L1
Cholesteryl
Ester
ABCG5/G8
ACAT
Ezetimibe
X
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Dual Inhibition
Duodenum
Jejunum
Ileum
CM
apoB48
Liver
CM
Remnant
apoB48
VLDL
apoB100
Ezetimibe
X
LDL
apoB100
X
Statin
Colon
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Ezetimibe Efficacy (10 + 10 = 80)
Ballantyne CM et al. Circulation 2003;107:2409-2415.
Atorvastatin
40 mg
(n=66)
20 mg
(n=60)
10 mg
(n=60)
53%
37%
42%
45%
54%
P < 0.01
80 mg
(n=62)
-60%
-50%
-40%
-30%
-20%
-10%
0%
Ezt + Ator
10+10 mg
(n=65)
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Bile Acid Resins: Mechanism of Action
Net Effect - LDL-C
Gall Bladder
LDL Receptors
VLDL and LDL removal
Cholesterol 7- hydroxylase
Conversion of cholesterol to BA
BA Secretion
Liver
BA Excretion
Terminal Ileum
Bile Acid
Enterohepatic Recirculation
Reabsorption of
bile acids
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Bile Acid Resins (BAR)
Major actions
Reduce LDLc by 1530%
Raise HDLc by 35%
May increase TG
Side effects
GI distress / constipation / nausea
Decreased absorption of other drugs
Contra indications
Dysbetalipoproteinemia,
Biliary Obstruction
Raised TG (especially >400 mg/dL)
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Bile Acid Resins
Drug Dose Range
Cholestyramine 416 g
Colestipol 520 g
Colesevelam 2.63.8 g

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Treatment of HDLc
Low HDLc
Add on drug - Finofibrate
Therapy of Choice : Niacin
Drug Therapy
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Causes of Low HDL
Smoking
Obesity (visceral fat), Physical inactivity
Very high Carbohydrate diet
Type II Diabetes
Hyper-triglyceridemia
Drugs like beta-blockers, androgenic steroids
and androgenic progestins
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Nicotinic Acid Mechanism of Action
Liver
Circulation
HDL
Serum VLDL
results in reduced
lipolysis to LDL
Serum LDL
VLDL
Decreases hepatic production of VLDL and of apo B
VLDL
secretion
Apo B
Hepatocyte Systemic Circulation
Mobilization of FFA
TG
synthesis
VLDL
LDL
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Effect of Niacin on Lipoproteins
Adapted from Knopp RH. N Engl J Med 1999;341:498-511..
0 1 g / d 2 g / d 3 g / d
Baseline
-15%
12.5%
25%
-30%
HDL-C with Niaspan

TG with Niaspan

TG with crystalline niacin
LDL-C with Niaspan

LDL-C with crystalline niacin
35%
HDL-C with crystalline niacin
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Nicotinic Acid
Products available
Immediate-release, 24 g/d, Sustained Release 3 g /d
Extended-release (Niaspan
) 12 g/d
Best agent to raise HDL-C
Reduces coronary events
Adverse effects
Flushing, itching, headache (immediate-release, Niaspan
)
Hepatotoxicity, GI (sustained-release)
Activation of peptic ulcer
Hyperglycemia and reduced insulin sensitivity
Contraindications
Active liver disease or unexplained LFT elevations
Peptic ulcer disease
Coronary heart disease and HDL-C
Framingham Heart Study
Gordon, Castelli et al. Am J Med 1977; 62: 707714
0
50
100
150
200
R
a
t
e
/
1
0
0
0

<25 2534 3544 4554 5564 6574 75+
HDL-C (mg/dl)
Women
Men
Relative risks of MI
3.21
3.78
1.00
2.41
Low HDL cholesterol
<47 mg/dl
High HDL cholesterol
47 mg/dl
Low total cholesterol
<212 mg/dl
High total cholesterol
212 mg/dl
Stampfer, Sacks et al. N Engl J Med 1991; 325: 373381
The Physicians Health Study
HDL-C vs LDL-C
as a predictor of CHD risk
*Men aged 5070 Gordon, Castelli et al. Am J Med 1977; 62: 707714
100 mg/dl 160 mg/dl 220 mg/dl
0
0.5
1
1.5
2
2.5
3
Risk of CAD over 4
years of follow-up*
LDL-C
85 mg/dl
65 mg/dl
45 mg/dl
25 mg/dl
CHD RR
HDL-C
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LDL cholesterol is primary target of therapy
Weight reduction and increased physical activity
(if the metabolic syndrome is present)
Non-HDL cholesterol is secondary target of
therapy (if triglycerides 200 mg/dL)
Consider nicotinic acid or fibrates
(for patients with CHD or CHD risk equivalents)
Management of Low HDLc
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Treatment of TG
High TG
Add on drug Statin, Niacin
Therapy of Choice : Fibrate
Drug Therapy
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Triglycerides
TG Level Classification Treatment
< 150 mg% Normal TG No Rx.
150 to 200 mg% Borderline high Diet alone
201 to 500 mg% High Diet + drugs
> 500 mg% Very high Diet + Intensive Rx
NCEP 2004 Guidelines by expert panel on TG
Fenofibrate
Mode of Action
Enhances the activity of lipoprotein lipase
Reduces hepatic fatty acid synthesis
Inhibits HMG co-enzyme A reductase activity
Reduces the CETP activity
Increases the LCAT activity
Increases the production of Apo AI and Apo A II
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Fibric Acid Derivatives
Major actions
Lower TG 2050%,VLDL synthesis
Raise HDL-C 1020%
LDL (TG is N), LDL (TG is )
Increase the SDL particle size (less athero)
Side effects
Dyspepsia, gallstones, myopathy, Abn. LFT
Contraindications
Severe renal or hepatic / biliary disease
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Fibric Acid Derivatives
Drug Dose
Clofibrate 1000 mg BID
Bezafibrate 200 mg BID
Gemfibrozil 600 mg BID
Fenofibrate 200 mg OD
Fenofibrate micronized 160 mg OD
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Treatment of LDL + TG
Combined
Add on drug Niacin, BAR
Therapy of Choice : Statin + Fibrate
Drug Therapy
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Da Col PG et al. Curr Ther Res Clin Exp 1973;53:473-482.
Statin + Fibrate
-60
-50
-40
-30
-20
-10
0
10
20
30
Simva +
Gemfibrozil
50%
39%
16%
22%
41%
28%
Ator or Simva +
Fenofibrate
230 332
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191 166
LDL
TG
HDL
LDL
TG
HDL
P
e
r
c
e
n
t

C
h
a
n
g
e

34
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Statin + Fibrate Precautions
Use statin alone for non-HDL-C goals
Use fish oils or niacin rather than fibrates
Keep the doses of the statin and fibrate low
Dose the fibrate in the AM and the statin in the PM
Avoid (or cautiously use) combo in renal impairment
Teach the patient to recognize muscle symptoms
Discontinue therapy if muscle symptoms are present
and CK is >10 times the upper limit of normal
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Probucol
1. Probucol (Lorelco) 500mg b.i.d with food
2. Third line drug erratic effect on LDL & HDL
3. Lowers Cholesterol and the only drug which
regresses xanthomas
4. It is an antioxidant of LDL
5. Diarrohea, flatulence, nausea, increases QTc
6. Can be combined with BAR
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The Three Canons
LDL - STATIN
DYSLIPIDEMIA
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How do we treat ?
Increased LDL Statins +/- EZ
Increased TG Fibrates
Decreased HDL Niacin
Increased Lp(a) Niacin
Increased LDL + TG Statin + Fibrate
LDL + HDL Statin + Niacin
TG + HDL Fibrate + Niacin
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Summary of Drug choice
Lipid abnormality type First choice Additional Remarks
LDL Statin Ezetimibe Myopathy
TG Fibrate Niacin CHO intake
HDL Niacin Fibrate Exercise
LDL + TG Statin + Fibrate Niacin Myo risk
LDL + HDL Statin + Niacin Fibrate Exercise
TG + HDL Fibrate + Niacin Statin Exercise
LDL + TG + HDL Statin + Fibrate E, N, BA, FO Myo risk
Atherogenecity of small, dense LDL
SDL is highly atherogenic. It
Generates free radicals
Increases trans endothelial filtration
Increases susceptibility to oxidation
Reduces affinity for the LDL receptor
Increased binding to intimal proteoglycan
Formation of pro-aggregators / vasoconstrictors
Impaired in vivo ED independent of HDL, LDL, TG
Circulation, 2000, 102: 716-721
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Lp(a) or Littlea
Similar to LDL molecule
Apo B + additional Apo a attached by S=S bond
Primary determinant is genetic
Normal value 20 mg %, > 30 high risk
It competes with plasminogen because of its
structural similarity and so interferes with
plasmin synthesis and thrombolytic pathway
Nicotinic acid, ? Bezafibrate, Estrogens it
This ALP or phenotype B is present and
seen in most often
Insulin resistant individuals
Diabetics
Obese persons
Sedentary life style
More prevalent in India
Apo A I Apo B will be < 1
Phenotype B or ALP
0
10
20
30
40
50
60
70
80
90
100
20 40 60 80 100 120 140 160 180 200 220 240 260 280 300 500
Phenotype A
Phenotype B
% Cumulative
frequency
TG (mg/dL)
Cumulative Distribution of TG Levels
Phenotypes A and B
Austin M et al. Circulation. 1990;82:495-506.
20 25 30 35 40 45 50 55 60 65 70 75 80
Phenotype A
Phenotype B
% Cumulative
frequency
HDL-C (mg/dL)
100
90
80
70
60
50
40
30
20
Cumulative Distribution of HDL levels
Phenotypes A and B
Austin M et al. Circulation. 1990;82:495-506.
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Homocysteine
Normal value is up to 10 mols./L
Folic acid, Vitamin B
6
and B
12
are essential for
the normal transulfuration and remethylation
cycles
Excess of homocystine generates oxidative
stress on the cell membranes. DNA and protein
denaturation through ROS formation
Folic acid 5 mg/ day + Vit. B
6
and B
12
are to be
given on regular basis
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Summary of Drug choice
Lipid abnormality type Advised Rx. Remarks
Homocysteine Folic acid

B
6
+ B
12
helps
Small dense LDL Statin + Fibrate Aggressive Rx.
Little a or LP(a) Niacin Statin no effect
Phenotype B Under research DM, Obesity
in Phenotype A Under research Aerobic exercise
87
www.drsarma.in
Some Brand Names
Drug class Brand name
Atorvastatin TG-TOR, Storvas, Avastin, Atcor

Simvastatin Sim, Simvotin, Simcard, Simvas
Atorvastatin + Ezetimibe TG -Tor EZ, Storvas EZ,
Ezetimibe Ezedoc, Ezee, Ezet
Fenofibrate Lipicard, Fibrate, Finolip, Stanlip
Gemfibrozyl Lopid, Lipizyl, Normolip, Losterol
Niacin Niasyn, Nialip, Nicocin
Dr.Sarma@works
88
Atherosclerosis and IR and DM
Hypertension
Obesity
Hyperinsulinemia
Diabetes
Hypertriglyceridemia
Small, dense LDL
Low HDL
Hypercoagulability
Insulin
Resistance
Atherosclerosis
Dr.Sarma@works
89
Elevated TG
Elevated VLDL
Reduced HDL-C
Increase in SD-LDL
Decrease in Apo A I
Increase in Apo B
Ratio of Apo B / Apo 1 > 2
Dyslipidemia in IR and DM
All Diabetics must be given STATIN
Dr.Sarma@works
90
Diabetes Treatment and Lipids
Type Rx used Effect on lipids
1. Insulin Favourable
2. Metformin Mildly favourable
3. Sulfonylureas Not favourable
4. Glitazones Favourable
5. Acarbose No effect
Dr.Sarma@works
91
Hypertension Treatment and Lipids
Type Rx used Effect on lipids
1. Diuretics Unfavourable
2. Indapamide Mildly favourable
3. ACEi and ARB Very favourable
4. Betablockers Unfavourable
5. Ca channel blockers No effect
Dr.Sarma@works
92
Web Resources on Lipids
www.lipidsonline.org
www.hypertensiononline.org
www.ncbi.nlm.nih.gov
www.univbaylore.org
93
www.drsarma.in
Announcements
1. Purpose, Men behind
2. Our emphasis and topics
3. Frequency, timings
4. Very informal - Interactive
5. Funds, sponsors, venues
6. Let us know you correctly
7. Feed back, make friends
www.drsarma.in
94
CD ROM Available
The contents of my todays presentations
are made available in a CD-ROM format
This CD, in addition, contains my talks on
Asthma, COPD, Hypertension, ECG, CAD
Dyslipidemias, Diabetes, Osteoporosis
www.drsarma.in
95
Visit us at: www.drsarma.in

96
www.drsarma.in
It is time for
Coffee Break

Dyslipidemia Update by DR Sarma

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Dyslipidemia Update by DR Sarma

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