Dyslipidemia AHA/ ACC 2013 guidline

1. DYSLIPEDEMIA
Dr Fahad albedaiwi
Resident family medicine

2. OBJECTIVES
• Introduction
• Epidemiology
• Classifications
• Diagnosis
• Screening
• Managment

3. Introduction
Dyslipidemia is a metabolic disorders characterized
by elevation of plasma cholesterol, triglycerides
(TGs), or both, or a low high-density lipoprotein
level that contributes to the development of
atherosclerosis.
Causes may be primary or secondary.
Diagnosis is by measuring plasma levels of total
cholesterol, TGs, and individual lipoproteins.
Treatment involves dietary changes, exercise, and
lipid-lowering drugs.

4. Epidemiology
• As demonstrated in the current study, the
prevalence of dyslipidemia among adults in
the KSA ranges from 20% to 44%,

5. CLINICAL CLASSIFICATION OF
DYSLIPIDEMIAS
• according to the Fredrickson phenotype
(This system does not take into account specific lipoprotein abnormalities)

6. Etiology
• Primary (genetic) causes and secondary
(lifestyle and other)
• 1ry{
•Familial hypercholesterolemia
•Familial defective apo B-100
•PCSK9 gain of function mutations
•Polygenic hypercholesterolemia
•LPL deficiency
•Apo C-II deficiency
•Familial hypertriglyceridemia
•Familial combined hyperlipidemia
•Familial dysbetalipoproteinemia
•Primary hypoalphalipoproteinemia
(familial or nonfamilial)
•Familial apo A/apo C-III
deficiency/mutations
•Familial apo A/apo C-III
deficiency/mutations
•Familial LCAT deficiency
•Tangier disease
•Familial HDL deficiency
•Hepatic lipase deficiency
•Cholesteryl ester storage
disease and Wolman disease
•Sitosterolemia
•Cerebrotendinous
xanthomatosis

7. • 2ry:
 A sedentary lifestyle
 Diabetes mellitus
 Alcohol overuse
 Chronic kidney disease
 Primary biliary cirrhosis
 cholestatic liver diseases
Hypothyroidism
Cigarette smoking
Obesity
Drugs: thiazides, β-blockers, retinoids,
highly active antiretroviral
agents, cyclosporine, tacrolimus, estrogen and
progestins, and glucocorticoids

8. Diagnosis
• History
• Physical examination.
• Lipid profile.

9. Symptoms and Signs
• usually causes no symptoms
• paresthesias, dypsnea, and confusion
• symptomatic vascular disease: CAD, stroke &
peripheral vascular disease
• acute pancreatitis
• arcus corneae and tendinous xanthomas
• planar or tuberous xanthomas.
• a creamy white appearance (lipemia retinalis).

11. • Serum lipid profile (measured total
cholesterol, TG, and HDL cholesterol and
calculated LDL cholesterol and VLDL)

12. screening
• Whom to test ?
based on overall cardiovascular (CV) risk .
influenced by age, sex, and other risk factors for CV
disease including hypertension, smoking, and
family history of premature coronary heart
disease (CHD)

13. 2012

14. management

15. Statin Benefit groups
• The evidence:
– The Expert Panel found extensive and consistent
evidence supporting the use of statins for the
prevention of ASCVD in many higher risk primary and
all secondary prevention individuals.
– In the RCTs reviewed, initiation of moderateintensity
therapy (lowering LDL–C by approximately 30% to
<50%), or high-intensity statin therapy (lowering LDL–
C by approximately ≥50%), is a critical factor in
reducing ASCVD events.
– Statin therapy reduces ASCVD events across the
spectrum of baseline LDL–C levels >70 mg/dL.

16. Statin Benefit groups (Contd.)
• The groups:
1. Individuals with clinical ASCVD.
2. Individuals with primary elevations of LDL–C
>190 mg/dL.
3. Individuals with diabetes aged 40 to 75 years
with LDL–C 70 to189 mg/dL and without clinical
ASCVD.
4. Individuals 40-75 with or without clinical ASCVD
or diabetes with LDL–C 70 to189 mg/dL and
estimated 10-year ASCVD risk >7.5%.

17. Clinical ASCVD
• Clinical ASCVD is defined by the inclusion
criteria for the secondary prevention statin
RCTs:
1. acute coronary syndromes
2. history of MI
3. stable or unstable angina
4. coronary or other arterial revascularization,
5. stroke, TIA, or peripheral arterial disease
presumed to be of atherosclerotic origin).

19. Other risk factors to consider
• Primary LDL–C ≥160 mg/dL or other evidence of
genetic hyperlipidemias
• family history of premature ASCVD with onset
<55 years of age in a first degree male relative or
<65 years of age in a first degree female relative
• Highsensitivity C-reactive protein >2 mg/L
• CAC score ≥300 Agatston score or ≥75 percentile
for age, sex
• Ethnicity
• ankle-brachial index <0.9

20. Characteristics predisposing
individuals to statin adverse effects
• Multiple or serious comorbidities, including
impaired renal or hepatic function.
• History of previous statin intolerance or
muscle disorders.
• Unexplained ALT elevations >3 times ULN.
• Patient characteristics or concomitant use of
drugs affecting statin metabolism.
• >75 years of age.

21. • Additional characteristics that may modify the
decision to use higher statin intensities may
include, but are not limited to:
– History of hemorrhagic stroke.
– Asian ancestry.

23. Why are we giving statins to
everyone?!
• The findings support the use of statins to
prevent both nonfatal and fatal ASCVD events.
• This can reduce the burden of disability from
nonfatal stroke (for which women are at
higher risk than men) and nonfatal CHD
events.
• Primary and secondary prevention of ASCVD
with statins can reduce rising healthcare costs.

24. Why are we giving statins to
everyone?!
• high level of evidence was found that statins reduce
total mortality in individuals with a history of prior
ASCVD events (e.g., secondary prevention settings).
• In individuals with no prior history of ASCVD events
(e.g., primary prevention setting), there is moderate
evidence that statins reduce total mortality in
individuals at increased ASCVD risk.
• It should be noted, 2 meta-analyses published after the
completion of the Expert Panel’s systematic review
provide strong evidence that statins reduce total
mortality in primary prevention.

25. Statin therapy: Moderate and high

26. Initiating treatment in a patient with ASCVD

27. Initiating
treatment in
a patient
with no
ASCVD

28. Monitoring Statin
Therapy

29. Statin intolerance
• It is reasonable to evaluate and treat muscle symptoms,
including pain, tenderness, stiffness, cramping, weakness,
or fatigue, in statin-treated patients according to the
following management algorithm:
– To avoid unnecessary discontinuation of statins, obtain a history
of prior or current muscle symptoms to establish a baseline
before initiating statin therapy.
– If unexplained severe muscle symptoms or fatigue develop
during statin therapy, promptly discontinue the statin and
address the possibility of rhabdomyolysis by evaluating CK,
creatinine, and a urinalysis for myoglobinuria.

30. Statin intolerance (contd.)
• If mild to moderate muscle symptoms develop during
statin therapy:
– Discontinue the statin until the symptoms can be
evaluated.
– Evaluate the patient for other conditions that might
increase the risk for muscle symptoms (e.g.,
hypothyroidism, reduced renal or hepatic function,
rheumatologic disorders such as polymyalgia rheumatica,
steroid myopathy, vitamin D deficiency, or primary muscle
diseases.)
– If muscle symptoms resolve, and if no contraindication
exists, give the patient the original or a lower dose of the
same statin to establish a causal relationship between the
muscle symptoms and statin therapy.

31. Statin intolerance (contd.)
• If a causal relationship exists, discontinue the original
statin. Once muscle symptoms resolve, use a low dose of a
different statin.
• Once a low dose of a statin is tolerated, gradually increase
the dose as tolerated.
• If, after 2 months without statin treatment, muscle
symptoms or elevated CK levels do not resolve completely,
consider other causes of muscle symptoms listed above.
• If persistent muscle symptoms are determined to arise
from a condition unrelated to statin therapy, or if the
predisposing condition has been treated, resume statin
therapy at the original dose.

32. Non statins (Niacin)

33. Non statins (Bile Acid sequestrants)

34. Non statins (Chol. Abs. inhibitors)

35. Non statins (Fibrates)

36. Non statins (Fibrates)

37. Non statins (Omega 3 fatty acid)
EPA, eicosapentaenoic acid ; DHA, docosahexanoic acid

38. Hypertriglyceridemia
• The most clinically relevant complication of
hypertriglyceridemia is acute pancreatitis, yet
only 10% of cases are a direct consequence of
triglyceride levels.
• Because documentation for a specific
threshold in triglyceride-induced pancreatitis
is lacking, levels associated with increased risk
are arbitrarily defined as triglyceride levels
1000 mg/dL

39. • Although borderline-high and high triglyceride
levels (150 to 500 mg/dL) are not associated
with pancreatitis, they are correlated with
atherogenic RLPs and apo CIII– enriched
particles.
• The elevations in triglyceride levels serve as a
biomarker for visceral adiposity, IR, DM, and
nonalcoholic hepatic steatosis (fatty liver).
RLP = Remenant LipoProtiens, IR = Insulin resistance

40. Effect of nutrition on TG

41. Effect of drugs on TG

42. Take home messages
• The treatment of hyperlipidemia is dependent on
the risk it poses on the patient concerning
ASVCD.
• Statins are beneficial in both primary and
secondary prevention of ASCVD.
• There is not enough evidence to support that
hypertriglyceridemia directly poses risk as far as
ASCVD.
• Hypertriglyceridemia is a marker for other
disease that are directly linked to ASCVD such as
visceral adiposity, IR and DM.

43. Case 1
50 year old white female
•Total cholesterol 180
•HDL: 50
•SBP: 130
•taking anti-hTN meds
•+diabetic
•+smoker
•Calculated 10 yr ASCVD: 9.8%

45. • high intensity statin

46. Case 2
48 year old white female
• Total cholesterol 180
• HDL: 55
• SBP: 130
• Not taking anti-hTN meds
• +diabetic
• Non-smoker
• Calculated 10 yr risk ASCVD : 1.8%

48. • Moderate intensity statin

49. References