fasting lipid profile

1. DYSLIPIDEMIA
PROF DR FARHAT BASHIR

2.  28 year old female referred for FH/O premature
cardiac death. Her 21 year old brother died
suddenly after a race. Autopsy revealed a
completely occluded left coronary artery. Non-
smoke, no H/O hypertension and diabetes mellitus.
 Height 5’8”, weight 166lb, pulse 72 beats/ min, BP
120/75 mmHg,
 Thickened Achilles tendon, corneal arcus
 FBG 80 mg/dl, AST and ALT N, BUN 10 mg/dl, Cr 0.8
mg/dl,
 TC 440mg/dl, LDL 385, TG 100, HDL 55

3. LIPIDS AND CARDIOVASCULAR
DISEASE
 Dyslipidemia(abnormal plasma
lipoproteins are a major modifiable risk
factor for cardiovascular disease.
 They contribute to the development of
atherosclerosis
 Elevated total cholesterol
 Elevated LDL
 Elevated TG
 Low HDL

5. LIPIDS AND ATHEROSCLEROSIS
 Atherogenic LDL, IDL lipoprotein(a) and
possibly chylomicron remnants contribut
to development of atherosclerosis
 Increased plasma concentration and
reduced diameter favor sub-endothelial
accumulation of these lipoproteins.
 Following oxidation these lipoproteins are
no longer cleared by normal mechanism.

6.  The LDL molecules enter the sub-endothelial
space.
 Trigger a self-perpetuating inflammatory
response to form foam cells, hallmark of
atherosclerosis
 HDL removes cholesterol from the tissues to
liver where it is metabolized and excreted in
bile.
 Low HDL levels are often associated with TG
elevation which also predisposes to
atherosclerosis

7. RESPONSE TO INJURY
HYPOTHESIS

8. PROGRESSION OF
ATHEROSCLEROSIS

9.  HIGH LDL LEVELS ARE A LEADING CAUSE
OF CORONARY HEART DISEASE
 SHOULD BE THE MAIN TARGET OF ANT
CHOLESTEROL LOWERING REGIMEN

10. ETIOLOGY
PRIMARY
 Single/multiple gene
mutation
 Resulting in disturbance
of LDL, HDL and TG,
production orclearance.
 Suspected in patients
with- premature heart
disease, family history of
atherosclerosis, serum
cholesterol>240mg/dl,
physical signs of
hyperlipidemia.
SECONDARY
 Sedentary lifestyle
 Diet
 Hypothyroidism
 Pregnancy
 Cholestatic liver disease
 Drugs
 ART
 Thiazide diuretic
 Beta blocker
 Hormones
 Nephrotic syndrome
 Anorexia
 Porphyria
 hyper[parathyroidism

11. SPECIFIC DYSLIPIDEMIA
 HIGH LDL>190mg/dl
 Genetic disorder
 Monogenic familial hypercholesterolemia
 Familial defective apolipoproteinB-100 (Apo
B)
 Polygenic hypercholesterolemia
 Family testing to detect affected relatives

12.  HIGH TRIGLYCERIDES
 Overweight and obesity
 Physical inactivity
 Cigerrete smoking
 Alcohol
 High carbohydrate diet
 Disease-type 2 Diabetes mellitus, CKD, nephrotic
syndrome.
 Drugs-steroids, estrogens, retinoids, beta
blockers.

13.  LOW HDL<40mg/dl
 Elevated TG
 Overweight and obesity
 Physical inactivity
 Type 2 diabetes
 Cigerette smoking
 High carbohydrate intake
 Drugs-beta blockers, anabolic steroids,
progestational agents.

14. COMPLICATIONS
 Atherosclerosis
 Hypertension
 Ischemic heart disease
 Stroke
 Retinopathy
 Nephropathy
 Fatty liver, NASH

22. INDICATION FOR FLP
 Total lipid profile/ fasting lipid profile
 Screening for primary / secondary
prevention of cardiovascular disease
 Investigations of patients with clinical
features of lipid disorder
 Testing relatives with single gene defects
causing dyslipidemia

27. MANAGEMENT OF HYPERLIPIDEMIA IN CVD PATIENTS
 lipid profile in all patients should be established
 lipid-lowering therapy before discharge
 Lifestyle modifications
 daily physical activity
 weight management
 dietary therapy

28. • Reduce intake of saturated and trans-unsaturated fat to less
than 710%of total energy
• Reduce intake of cholesterol to <250mg/day.
• Replace source of saturated Fat and cholesterol with lean
meat,low fat dairy products and low glycemic index
carbohydrates.
• Reduce energy dense food e.g fat and soft drinks whilst
increasing activity and exercise.
• Increase consumption of cardioprotective and nutrient dense
food such as vegetables, unrefined carbohydates such as
vegetabes ,un refined carbohydrates,fish, pulses, nuts,
legumes, fruit etc .
• Adjust alcohol consumption ,reduce intake if excessive or if
associated with hypertension , hypertriglyceridemia or central
obesity .
• Add supplementary food containing nutrients, such as
omega-3 fatty acids , dietry fibers, plants sterols

29. • statin should be used that reduces LDL-C to 100 mg/dL
AND achieves at least a 30% lowering of LDL-C.
• triglycerides 200 mg/dL should be treated with statins to
lower non– HDL-C to 130 mg/dL.
• triglycerides 500 mg/dL should be started on fibrate
therapy in addition to statin

30. HIGH RISK PATIENTS
• intensification of LDL-C–lowering drug therapy with
a bile acid sequestrant
• to treat very high-risk patients with statin therapy to
lower LDL-C to 70 mg/dL
• very high risk* and who have triglycerides 200
mg/dL, a non–HDL-C goal of 100 mg/dL is
reasonable
• ezetimibe -for patients who do not tolerate or
achieve target LDL-C with statins, bile acid
sequestrants,‡ and/or niacin.
• For all patients, it may be reasonable to
recommend omega-3 fatty acids from fish or fish oil
capsules (1 g/d) for cardiovascular disease risk
reduction

31. PRIMARY PREVENTION WITH LIPID-LOWERING
THERAPY
• The clinical approach to primary prevention is
founded on the public health approach that calls
for lifestyle changes, including:
1) reduced intakes of saturated fat and
cholesterol,
2) increased physical activity, and
3) weight control
• trials show that Lipid-lowering drugs reduce risk for
major coronary events and coronary death even in
the short term.

32. SECONDARY PREVENTION WITH LIPID-
LOWERING THERAPY
• Lipid-lowering therapy reduces total mortality,
coronary mortality, major coronary events,
coronary artery procedures, and stroke in persons
with established CHD
• lipid measures should be taken on admission or
within 24 hours.
• Adjustment of therapy may be needed after 12
weeks.