Statin Therapy based on CPG

1. STATIN THERAPY
STATIN THERAPY

2. Primary
Prevention
0
1
Secondar
y
Preventio
n
0
2
Adverse
Effects
0
3
Non-Statin
Therapy
0
4
TABLE OF CONTENTS

3. HMG-CoA
Reductase
Inhibitors LDL-C Plasma
levels
Hepatic LDL receptor activity
Circulating LDL clearance
STATINS

4. Primary
Prevention
01
In specific populations with disease
entities

5. Screening and
Treatment
Algorithm for
the
Management of
Dyslipidemia

6. ≥ 2 risk
factors
≥45 years
with LDL
≥130 mg/dL
02
01
Prevention in: Individuals with
no ASCVD Male sex
Postmenopausal
Smoker
HPN
Obesity (>25kg/m2)
Family history of CHD
LVH
Proteinuria

7. Screening and
Treatment
Algorithm for
the
Management of
Dyslipidemia

8. Diabetic only
With > 1 risk factor
(based on Risk Factor Counting
method)
Recurrent CV
(stroke, unstable angina, MI)
LDL Levels
Prevention in: Individuals with
Diabetes Mellitus
< 100mg/dL
< 70mg/dL
< 55mg/dL

9. Screening and
Treatment
Algorithm for
the
Management of
Dyslipidemia

10. Without target organ damage
With target organ damage
LDL Levels
Prevention in: Individuals with FH
< 70mg/dL
< 55mg/dL

11. Screening and
Treatment
Algorithm for
the
Management of
Dyslipidemia

13. Secondary
Prevention
02
Dyslipidemia Management on Acute Coronary
Syndrome

14. Among individuals with acute
coronary syndrome (ACS),
should statins be given?

15. • For individuals with ACS, early high-
intensity statin that is maximally-tolerated
is RECOMMENDED and should not be
discontinued.
• Statins should be given to ACS patients
immediately

16. Statin Treatment Intensity

17. Cholesterol target for different
patient groups

18. Adverse Effects
03

19. Among individuals taking statin
therapy, what is the
risk of developing adverse
effects?

20. a. Statin-associated Muscle Symptoms
b. New-onset Diabetes
c. Dementia / cognitive dysfunction / intracerebral
hemorrhage

21. • Treatment with statins is associated
with a low risk of developing statin-
associated muscle symptoms (SAMS),
but the benefits of cardiovascular risk
reduction outweigh the risk

22. Algorithm for Statin Induced
Myopathy

23. • Treatment with statins is associated
with an increased risk of new-onset
diabetes mellitus, but the benefits of
statin treatment for cardiovascular
risk reduction outweigh the risk.

24. • Treatment with statins is not
associated with the development of
dementia and cognitive dysfunction
• Treatment with statins is not
associated with an increased risk of
intracerebral hemorrhage

25. Non-Statin
Therapy
04
Brief Details on the use of Ezetimibe,
Fenofibrates, and Omega Fatty Acids

26. Among individuals with ASCVD,
should ezetimibe be given on top
of statin therapy?

27. Ezetimibe
A cholesterol absorption inhibitor that
targets uptake at the jejunal enterocyte
brush border
Inhibits intestinal cholesterol
absorption by selectively blocking the
NPC1L1 protein in the jejunal brush
border, integral to the uptake of
intestinal lumen micelles into the
enterocyte

28. • For individuals with documented
ACS, and target LDL-C has not been
reached despite maximally tolerated
high-intensity statin therapy,
ezetimibe may be added on top of
statin therapy to get to goal LDL-C.

29. Among individuals with
ASCVD, should fibrates be given
on top of statin therapy once
LDL-C goal is achieved?

30. • Among individuals not at goal LDL-
C, routinely adding fibrates on top of
statin therapy is NOT
RECOMMENDED for primary or
secondary prevention of
cardiovascular disease.

31. However, adding fibrates to statins may
be considered among MEN with
controlled diabetes, low HDL-C (200
mg/dl) for prevention of CV disease.

32. Fibrates
Good efficacy in
lowering fasting
TG levels
≤20% reduction
of the LDL-C
level
50% reduction of
the TG level
increase of the
HDL-C level of
≤20%

33. Among individuals with ASCVD,
should omega fatty acids be
given on top of statin therapy
once LDL-C goal is achieved

34. • Among individuals with ASCVD,
omega fatty acids (EPA+DHA) given
on top of statin therapy is NOT
RECOMMENDED.
• Among individuals with ASCVD on
statin therapy at goal LDL-C, but
with persistently high triglyceride
levels of 150-499 mg/dl, omega fatty
acids (pure EPA) MAY be given

35. Monitoring of
Lipids and
Enzymes
05

36. How often should
lipids be tested?

37. • Before starting lipid-
lowering drug
treatment, at least
two measurements
should be made, with
an interval of 1–12
weeks, with the
exception of
conditions where
prompt drug treatment
is suggested, such as
ACS and very high-
risk patients.
• After starting
treatment: 8 (±4)
weeks.
• After adjustment of
treatment: 8 (±4)
weeks until the goal is
achieved.
How often should lipids be
tested?

38. How often should lipids be tested
once a patient has achieved the
target or optimal lipid level?
Annually

39. How often should
liver enzymes (ALT)
be routinely
measured in patients
on lipid-lowering
drugs?

40. • Before treatment
• Once, 8–12 weeks
after starting a drug
treatment or after
dose increase.
• Routine control of
ALT thereafter is not
recommended during
statin treatment,
unless symptoms
suggesting liver
disease evolve.
• During treatment with
fibrates, control of
ALT is still
recommended.
How often should lipids be
tested?

41. What if liver enzymes
become elevated in a
person taking lipid-
lowering drugs?

42. Elevated ALT
ALT ≥3×
ULN
ALT <3× ULN
≥3×
<3×
• Continue therapy.
• Recheck liver enzymes in 4–6 weeks.
• Stop lipid-lowering therapy or reduce dose and
recheck liver enzymes within 4–6 weeks.
• Cautious reintroduction of therapy may be
considered after ALT has returned to normal.
• If ALT remains elevated check for the other

43. How often should CK be
measured in patients taking
lipid-lowering drugs?

44. Pre-treatment
• Before starting
therapy
• If baseline CK is
>4× ULN, do not
start drug therapy;
recheck
Monitoring
• Routine
monitoring of CK
is not necessary
• Check CK if
patient develops
myalgia
How often should CK be
measured in patients taking
lipid-lowering drugs?

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