1.
Welcome!
Mastering cholesterol to optimise CVD
prevention – Targeting lipids: A primary
and secondary care perspective
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2.
Introducing
Lipids:
A Primary Care
Approach
Dr Sue Kemsley
GP
Primary Care Lipid Lead for Innovation Agency (AHSN NWC)
Primary Care Co-Lead for C&M Strategic Cardiac Network
GPwSI Cardiology

3.
LDL-C causes
atherosclerosis; a disease
process directly causing
ASCVD & CVD events
CVD
EVENTS
LDL-C

4.
ABC of CVD
Prevention
Atrial Fibrillation
Blood Pressure
Cholesterol

5.
Optimising statins predicted to save over £700m in 5 years

6.
NHS CVD
Prevention
Recovery
• 25% of all UK deaths
• Largest cause of
premature deaths in
deprived areas
• NHS Long Term Plan:
Single biggest area
where NHS can save
lives in next 10 years
ASCVD

7.
NHS CVD
Prevention
Recovery
For every 1 mmol/L reduction in LDL-C, there is a reduction in annual
CVD risk of 28%.
National ambitions for
cholesterol state by 2029:
75% of 40–74-year-olds will
have a CVD risk assessment &
cholesterol reading recorded
on a primary care data system
in the last five years
45% of 40–74-year-olds with
=> 20% 10-year risk of
developing CVD in primary
care are treated with statins
And by 2024:
25% of people with Familial
Hypercholesterolaemia (FH)
are diagnosed and treated
optimally according to NICE FH
guidance

8.
Why should primary care focus on lipids now?
PCN DES & IIF Targets 2022: CVD risk & FH detection
New guidance & clinical targets: NHS Lipid Pathway and
Statin Intolerance Pathway
Multidrug approach to lipids: Statins, Ezetimibe, Bempedoic acid,
Inclisiran, PCSK9i and Vazkepa

9.
Why are we
not managing
lipids better?
• Lipid disorders not perceived as causing a disease process
• Lipids often thought difficult to treat so why bother?
• Bad press for lipid medications
• Statin "side effects”, statin reluctance and nocebo effect
• Often poor compliance
• Confusion over guidance and treatment targets
• Often tagged on to a consultations in primary care with
multiple issues making a difficult conversation unmanageable
• Clinician and patient inertia

10.
Aims
Who should have a cholesterol test and when
Discuss the range of treatment options
The NHS Lipid Pathway as a lipid therapy decision
aid
The statin intolerance pathway to address side effects
How to work at scale to optimise lipid therapies

11.
Primary Prevention
<=84yrs & QRISK=>10%
T2DM & QRISK=>10%
T1DM (plus risk factor*)
CKD eGFR<60 and/or albuminuria
All age >84 (consider frailty etc)
Secondary Prevention
All ASCVD
(MI/angina/revascularisation
TIA/stoke/PAD)
When to think lipid intervention in primary care?
Familial Hyperlipidaemia

12.
Chronic Long Term Condition Reviews
• All ASVCD
• Coronary artery disease: Angina, MI, CABG, stent
• Cerebrovascular disease: stroke, TIA
• Peripheral arterial disease including AAA
• Genetic or suspected diagnosis of FH
• Hypertension
• AF
• Diabetes
• CKD
• All 84+ years! (but tailor this to the individual)
• CVD risk >10%
• Other chronic diseases e.g. COPD, inflammatory disease, severe psoriasis
When to think lipid therapies? Who is high risk?

13.
40-74 Years NHS Health Check
• Currently only around 45% of eligible patients have an NHS health check
• Only eligible if fit and well
• Not eligible if,
• ASVCD
• HTN
• AF
• Heart failure
• Diagnosis of FH
• Diagnosis of CVD risk >10% & already on lipid therapy
• Treat if QRISK>10%
When to consider lipid disorders in primary care?
Finding high risk undiagnosed patients

14.
Familial
Hypercholesterolaemia
• Think identification
• Refer for genetic and cascade testing
• Do not use QRISK
• 50% reduction in non-HDL-C

15.
PCN DES & GP data
searches
• Age <=29 total
cholesterol >7.5
• Age >=30 total
cholesterol >9.0
• UCLP Lipids search
18-39 Years
• Single lipid
profile to
consider FH
• Point of care
test
Childhood
• 12 month
heel-prick test
• Genetic
testing if high
• Family
cascade
testing if baby
has positive
results
• Lifestyle
advice for ALL
families
Finding familial hypercholesterolaemia in primary care

16.
Suspected heterozygous FH diagnosis
Fasting lipid profile
Criteria levels more accurate for people <30 years
Criteria levels increase as people get older
• Adult <30 years: Fasting TC >7.5 and/or LDL-C >4.9 and/or non-HDL-C >5.9
• Child <16 years: Fasting TC >6.7 and/or LDL-C >4.0
• Anyone with TC>9.0mmol/L and/or LDL-C >6.5mmol/L and/or non-HDL-C >7.5mmol/L or fasting
triglycerides > 10mmol/L
Especially if; personal and/or family history of confirmed CHD (<60 years) and with no secondary
causes
Refer to diagnose FH if severe Hyperlipidemia, and especially if;
Use FH risk calculator

17.
Suspected homozygous FH diagnosis
Adult under 30 years: LDL-C >13
Child under16 years: LDL-C >11

18.
CM.FHS@nhs.net / 0151 254 3248
• Pilot service April 22-Sept 23 with aim to become a fully commissioned long term
service.
• Service aim: Identify individuals across C&M who are at risk of FH. The 1:250 incidence
equates to 10,000 people.
• Specialist nurse-led with paediatric and adult training. Lipidologist clinical lead.
• Remote consultations provide counselling, support and genetic testing to confirm and
discuss FH diagnosis and provide detailed patient information to support effective
treatment with lipid therapies.
• Cascade genetic testing for family members.
• All referrals welcome via referral form available in EMIS (includes Welsh Lipid Score)
• FH team are supporting education in the region through a series of webinars, drop-in
meetings (MS Teams) and tailored educational sessions

19.
Treatment Options

20.
Lipid Therapies
Statins
• 40-50% LDL-C
reduction
• LFT baseline,
each
titration, 12
months and
then not
again if
normal
• Need to
manage
“intolerance”
Ezetimibe
• Add on to
statin with
additional
24% LDL-C
reduction, or
monotherapy
• No
monitoring
• Well
tolerated
Bempedoic
acid
• Add on to
Ezetimibe
monotherapy
with
additional
28% LDL-C
reduction
• Only need to
monitor
renal/liver
function if
severe
impairment
Inclisiran
• ASCVD after
max statin ±
Ezetemibe
• Additional
50% LDL-C
reduction
• Twice yearly
injection
• Can be
administered
in primary
care
PCSK9i
• ASCVD
and/or FH
• 25-75% LDL-C
reduction
• 2 weekly self
injector
• Secondary
care only
Vazkepa
• Add on
therapy to
reduce
triglycerides
• Included in
updated NHS
Lipid Pathway
Dec 2022

21.
NHS Lipid
Pathway

22.
Statin
Intensity

23.
Ezetimibe,
Bempedoic Acid,
Inclisiran &
PCSK9i
Secondary
Prevention Only
(*FH)

24.
Eligibility
criteria for
injectables
If non-HDL-C >2.5 check fasting lipid profile
to check LDL-C to determine eligibility.
(Could consider use of equation to calculate
LDL-C equivalent.)
Inclisiran may be used if fasting LDL-C
(or equivalent) =>2.6
PCSK9i
Without CVD High risk Very high
risk
Not FH Not indicated LDL-C >4.0 LDL-C >3.5
FH LDL-C >5.0 LDL-C>3.5

25.
Statin Reluctance Nocebo effect

26.
Summary of when to check a blood test for lipid profile
• Any age to assess risk of FH if no previous assessment,
• Assess CVD risk for primary prevention in patients 40-74 years 5 yearly
(NHS health check)
• Check treatment to target (non-HDL-C <= 2.5) for ALL on lipid therapies
annually (Except FH>50% reduction from baseline)
• Reassess CVD risk when treating new diagnosis of diabetes or
hypothyroidism or significant lifestyle interventions
Random lipids if,
• Significantly raised triglycerides
• Patient with ASCVD being considered for Inclisiran
• Patient with FH being considered for PCSK9i
Fasting lipids if,

27.
Optimising Lipids at Scale

28.
Using Digital Tools: UCLP Framework
Secondary Prevention Stratification
Primary Prevention Stratification

29.
UCLP secondary prevention lipid search run across all practices in PCN
PCN care co-ordinator ensures up to date blood tests and offers lipid
review to patients in order from UCLP groups 1, 2, and 3 in a Clinical
Pharmacist/ANP clinic
Prescriber-led clinic optimises oral lipid therapy according to the NHS
lipid pathway and statin intolerance pathway with lifestyle
counselling
Patients identified as eligible for Inclisiran if not to target following
optimisation of oral therapies
Inclisiran clinic with care co-ordinator recall system for 3-month
and 6-month injections
Initial weekly
MDT for
advice and
support
FH
suspects
referred
to lipid
clinic
PCN approach to optimising lipid therapies

30.
Summary: Lipid disorders in primary care
Case finding and MECC for lipid disorders including FH
Multi drug approach
Manage statin intolerance
Treat to target
Consider pathways to optimise at scale

31.
Maximise
prevention
by optimising
all CVD risks
CVD risk
Lifestyle
Atrial
Fibrillation
Blood
pressure
Cholesterol
Diabetes
CKD
Inflammatory
Disease
Heart failure
Ethnicity
Family
history
Age & sex

32.
Thank you

33.
Introducing lipids:
A secondary care approach
DR GAVIN GALASKO
CONSULTANT INTERVENTIONAL CARDIOLOGIST
CLINICAL LEAD FOR THE BLACKPOOL LIPID CLINIC
DIRECTOR OF RESEARCH, DEVELOPMENT AND INNOVATION
BLACKPOOL TEACHING HOSPITALS NHS FOUNDATION TRUST
IA AND CARDIAC NETWORK LIPID LEAD FOR L&SC

34.
Who should secondary care treat
with lipid lowering therapy and how?
 Lipid lowering guidelines
 NICE clinical guideline 181 [Lipid Modification for 1o and 2o prevention],
July 2014 (currently being updated)
 NICE approved NHS/Accelerated Access Collaborative Guideline (lipid
pathway), Dec 2022
 AHSN Lipid Optimisation Pathway following acute cardiovascular event,
Nov 2022
 NICE clinical guideline 71 [Familial Hypercholesterolaemia], Aug 2008

35.
NHS/AAC Lipid pathway p1

36.
NHS/AAC Lipid pathway p2

37.
AHSN Lipid optimisation pathway
following acute cardiovascular event

38.
Primary prevention

39.
Assessment and diagnosis
 For primary prevention of CVD in primary care, a systematic strategy
should be used to identify people likely to be at high risk of CVD
(≥10%,10 yr risk)
 Use QRISK2/3 risk assessment tool to assess CVD risk for primary
prevention in people 40-84 years of age
 Consider FH (familial hypercholesterolaemia) if chol >7.5mM
(especially if family history of premature CVD)
 Do not use risk assessment tool in people with eGFR < 60
ml/min/1.73m2 and/or albuminuria
 Do not use risk score in patients with proven CHD, ischaemic stroke,
type 1 DM, PVD, familial ↑ lipidaemia
 Treat secondary causes of dyslipidaemia first
 E.g. nephrotic syn/DM/↑EtoH/dTFTs/medications eg steroids/biliary
obstruction/pregnancy

40.
Key assessments/advice
 Smoking status
 Alcohol consumption
 Blood pressure
 BMI or other measure of obesity
 U&Es and eGFR, LFTs
 Total Chol, non-HDL chol, HDL and triglycerides
 HbA1c
 TSH
 Recommend healthy lifestyle changes

41.
Statins
 After managing modifiable RFs, if still appropriate and after informed
discussion start Atorvastatin 20mg od
 Measure full non-fasting lipid profile after 3 months
 Target: >40% reduction in non-HDL cholesterol
 If not achieved discuss adherence, diet, lifestyle
 If at higher risk consider increasing dose up to 80mg
 If still not achieved consider adding Ezetimibe 10mg od
 Annual review to ensure ongoing adherence

42.
Diabetes
 Use QRISK2 risk assessment tool to assess CVD in people with type 2
diabetes
 Offer Atorvastatin 20mg for those with ≥10% 10-year risk of developing
CVD
 Offer Atorvastatin 20mg for primary prevention of CVD for adults
with type 1 DM who:
 Are >40 or
 Have had type I DM for >10 years or
 Have established nephropathy or
 Have other CVD risk factors
 Consider Atorvastatin 20 mg for all adults with type 1 diabetes

43.
Renal Failure
 Offer Atorvastatin 20mg for 1o and 2o prevention of CVD
 Increase dose if a >40% ↓ in non-HDL chol is not achieved (total chol –
HDL-chol)
 Discuss use of higher doses with renal specialist if eGFR is
<30ml/min/1.73m2

44.
Secondary prevention

45.
Statins
 Offer statin therapy to patients with acute or established CVD (CHD, PVD,
ischaemic CVA). Take lipid sample within 24o of admission
 Address all modifiable risk factors – smoking, diet, BP, DM, obesity etc
 Initiate treatment with Atorvastatin 80mg od
 Use a lower dose if:
 Potential drug interactions
 High risk of adverse events
 Patient preference
 Reassess lipid profile after 3 months high-intensity statin and see if target
reached (non-HDL chol ↓ >40%)
 If target not reached;
 Discuss adherence and timing of dose
 Optimise adherence to diet and lifestyle measures
 Consider increasing dose if started on <80mg Atorvastatin
 Consider role of other NICE-approved agents;
 Ezetimibe/Bempedoic acid/Inclisiran/PCSK9 inhibitors/Icosapent ethyl

46.
Pre-statin advice
 Before offering statin, ask about persistent generalised muscle pains.
If yes, measure CK
 If CK > 5xULN do not start statin
 If CK 1-5x ULN start at a lower dose
 Advise that if they develop muscle symptoms (pain, tenderness or
weakness) seek medical advice and measure CK levels
 Statins are contraindicated in pregnancy (potential teratogenic risk)
so stop them if pregnancy possible

47.
Statins follow up
 Measure total, HDL and non-HDL chol in all people who have been
started on high intensity statin treatment at 3 months (non-fasting)
 Provide annual medication reviews
 Discuss medicine adherence, lifestyle modification and address CVD risk
factors
 Consider annual non-fasting blood test for non-HDL cholesterol
 Do not measure CK levels routinely
 Do measure CK levels if muscle symptoms occur (pain, tenderness,
weakness)

48.
Monitoring patients on statins
 Baseline liver enzymes should be measured before starting statin.
LFTs should then be measured within 3 months and at 12 months,
but not again unless clinically indicated
 People with ↑transaminases but <3xULN should not be excluded
from statin use
 If an unexplained peripheral neuropathy develops then stop statin
and seek specialist advice

49.
Statin therapy alternatives
NICE CG 181: Lipid modification July 2014
 For primary or secondary prevention of CVD, or in CKD or Type 1 DM,
do not offer:
 Nicotinic acid (Niacin)
 Anion exchange resins
 Omega-3 fatty acid compounds
 Do not routinely offer fibrates (sometimes used in specialist lipid
clinics)
 People with primary hypercholesterolaemia should be considered for
Ezetimibe in line with NICE TA 132+385 guidance
 (acts synergistically with statins: ↓ intestinal cholesterol absorption vs
statins ↓ chol production)
 10-20% reduction in LDL-C

50.
Treatment option
0
-5
-10
-15
-20
-25
-30
Baseline
%
LDL-C
reduction
from
baseline
In a randomised, multicentre, double-blind, parallel-
group study that measured % change from baseline
in LDL-C after 6 weeks’ treatment.
(n=579)
Up titrating to 80 mg
of atorvastatin
Atorvastatin 40 mg plus
10 mg of ezetimibe
% LDL-C reduction
from baseline
11%
27%
1. Leiter LA et al. Am J Cardiol 2008; 102(11): 1495–1501.
P<0.001
Ezetimibe
Adding 10mg to Atorvastatin 40mg superior to ↑ Atorv. to 80mg

51.
Bempedoic acid
 NICE TA 694 approved, April ‘21, 180mg od
 Adenosine triphosphate citrate lyase (ACL) inhibitor which inhibits
cholesterol synthesis in the liver, thereby lowering LDL-C
 Always recommended with Ezetimibe and only if:
 Statins contraindicated or not tolerated
 Ezetimibe monotherapy does not hit target
 Agreed company pricing structure adhered to (confidential)
 c15% reduction in LDL-C
 SEs: ↑LFTs, ↑uric acid/gout, joint pains

52.
Inclisiran
 NICE TA 733 approved, Oct ’21
 284 mg Inclisiran in 1.5ml solution, subcutaneous dose
 Give after 3 months then 6 monthly (2x/yr)
 Small interfering RNA (siRNA) that ↑LDLRs via interference of PCSK-
9 production
 Secondary prevention only (CHD, ischaemic stroke, PVD) and LDL-C
≥2.6mM
 Must be on maximum tolerated statin ± Ezetemibe
 Lowers LDL-C by approx. 50%
 Can be prescribed in primary and secondary care

53.
PCSK9 inhibitors
 Monoclonal antibodies that inactivate proprotein convertase subtilisin-
kexin type 9 (PCSK9)
 Alirocumab (Praluent) and Evolocumab (Repatha)
 Increase LDL-receptors on the surface of hepatocytes 
↑uptake/degradation of LDL by liver
 Given by fortnightly subcutaneous injections (75-150 or 140mg)
  Dramatic ↓LDL and ↓Non-HDL chol levels (50-60% reductions)
 Act synergistically with statins
 Statins reduce cholesterol synthesis + ↑ hepatocyte LDL-receptor levels
 but increase PCSK9 levels (which act to reduce LDL-receptor levels)
 Main role in FH, but role in non-FH 2o prevention
 MMGs red coding (hospital prescription only)

54.
NICE PCSK9 inhibitor guidance
NICE TA 393 + TA 394, 2016

55.
Icosapent ethyl (Vazkepa)
 NICE TA 805 approved, July ’22
 Stable ethyl ester of omega-3 fatty acid
 Mechanism of action not fully understood
 998mg capsules, 2xbd
 Secondary prevention (CHD, ischaemic stroke, PVD) or DM and at
least one other risk factor
 Must be on statin therapy
 Must have: LDL-C 1.04-2.6mM + TG≥1.7mM
 ↓TG c20%, ↓non-HDL-C c10-15%
 SEs: ↑bleeding time, AF, constipation, MSk pains
 Can be prescribed in primary + secondary care

56.
Familial Hypercholesterolaemia
Nice Guidelines (CG71), 2008 (last updated Nov 2017)

57.
Very common - frequency ~1/300-500 > 120,000 in UK
Often underdiagnosed < 15,000 cases known in 2008 (12.5%)
Very High CHD event rates untreated
0
20000
40000
60000
80000
100000
120000
140000
2000 2004 2008 2012 2016 2020
Number
FH
known
Survey UK Lipid Clinics
Missing >85%
of predicted
Marks, et al 2004
HEARTUK 2008
Neil, et al BMJ 2000
How common is FH?
Age
(years)
♂
% CHD
♀
% CHD
<30 5 0
30-39 22 2
40-49 48 7
50-59 80 51
60-69 100 75
Slack, Lancet.1969;1380-2
Natural History

58.
Diagnosing FH (NICE CG 71)
 Consider FH in adults with total cholesterol >7.5mM, especially if there
is a family history of premature CHD
 Exclude secondary causes of hyperlipidaemia
 Use the Simon Broome Criteria for diagnosis (can also use Dutch Lipid
Clinic Network Score)
 Absence of clinical signs (e.g. tendon xanthomata) does not exclude
the diagnosis
 Take two fasting LDL-C measurements to confirm diagnosis

59.
Simon Broome Diagnostic Criteria
Definite FH:
 TC > 6.7 mmol/l or LDL-C >4.0 mmol/l (child <16y)
or TC > 7.5 mmol/l or LDL-C >4.9 mmol/l (adult)
plus one of:
 tendon xanthomas in patient, or in 10 relative (parent, sibling,
child), or in 20 relative (grandparent, uncle, aunt), or
 DNA-based evidence of an LDL receptor mutation, familial
defective apo B-100, or a PCSK9 mutation.
Possible FH is defined as the above lipid cut-offs plus one of:
 family history of myocardial infarction: below age of 50 years in
20 relative or below age 60 years in 10 relative, or
 family history of raised TC >7.5 mmol/l in adult 10 or 20 relative
or > 6.7 mmol/l in child or sibling <16y

60.
Xanthomata
Xanthelasma Tendon Xanthomata
Palmar Xanthomata Tendon Xanthomata
Tuberous Xanthomata
Eruptive Xanthomata

61.
FH Management
 Start Statin ± Ezetimibe
 Onward referral to lipid clinic:
 For confirmation of diagnosis ± cascade testing
 For consideration of PCSK9i therapy
 Known FH who fail to achieve a reduction of LDL-C from baseline
of >50% despite maximum tolerated dose of statin + ezetimibe
 Young people with FH should be referred to paediatric FH
specialist. Therapy to be considered from age 10
 Any adult with FH at very high risk of a coronary event
 Established coronary disease
 A family history of premature coronary disease
 Two or more other cardiovascular risk factors

62.
Blackpool Lipid Clinic
(established October 2018)

63.
The team
 Marie Wilcock - Advanced Nurse Practitioner
 Dr Gavin Galasko – Consultant Cardiologist
 Dr Tawfiq Choudhury – Consultant Cardiologist
 Noel Topping – Cardiac Pharmacist
 Clinical Biochemist due to start shortly
 2018/19 – 1 monthly clinic
 2022 – 4-5 clinics per week plus weekly MDT

64.
Referral criteria
1. Possible Familial Hypercholesterolaemia (FH):
Pre-treatment total chol >7.5mM and either a family history of myocardial
infarction at age < 50-60 years or a family history of FH (Simon Broome)
2. Unexplained severe hyperlipidaemia without a family history
Total chol > 9mM, or fasting LDL chol >6.5mM, or non-HDL chol > 7.5mM, or
fasting triglycerides > 10mM (once other causes excluded e.g. EtOH/TFT)
3. Secondary prevention:
In patients with established CVD (ischaemic stroke/TIA, PVD, ACS, coronary
revascularisation) refer if total chol >6mM or fasting LDL chol >4mM despite
best-tolerated lipid-lowering therapy, or if statin intolerant
Suggested Investigations Prior to Referral:
FBC, Biochemical profile, ALT/AST, TSH and fasting lipid profile

65.
Demographics to date
Year Mean age
(years)
Average max
chol (when
known)
Range of
chol levels
Proportion
with max
≥7.5mM
2019 54.9 8.9mM 5.5 - 14mM 87%
2020 57.0 9.0mM 5.6 - 19.5mM 87%
2021 54.2 9.1mM 5.5 - 14mM 89%
2022 54.5 8.7mM 3.1 – 20mM 81%

66.
Genetic Testing for FH 2021/22
 Testing of referred patients for FH
 Criteria used:
 Simon Broome criteria for possible FH
 Dutch lipid score for probable FH (score ≥6)
 Welsh score
 26 patients found to have FH on genetic testing
 16/110 new FH cases found (15% pick up) (proband
testing)
 10/27 cases found (37% pick up) in relatives of patients
with FH (cascade testing)

67.
Lipid management quiz

68.
Case study one
 45 year old ♂ type II diabetic with hypertension
 Total chol 6.5mM, LDL 3.2mM, HDL 1.0mM
 Calculated 10 year QRISK 2 CVD risk of .....
 What initial lipid therapy would you recommend?
1. None - dietary advice only
2. Atorvastatin 20mg od
3. Atorvastatin 80mg od
4. Alternative statin – which one
5. Statin + Ezetimibe
6. Something else
17 %

69.
Case study two
 55 year old ♂ with BP, T2DM, old MI, PVD
 Total chol 5.0mM, LDL 2.8mM, HDL 1.0mM, on Simvastatin 40mg
 Would you recommend any change in lipid therapy?
1. None - dietary advice only
2. Change to Atorvastatin 20mg od
3. Change to Atorvastatin 80mg od
4. Change to another statin and/or medication
5. Something else

70.
Case study three
 62 year old ♀ smoker, BP, angina
 Baseline LDL-C: 4.24 mM
 On Simvastatin 40mg od but experiencing muscle pains too severe
to continue treatment
 What alternative lipid lowering therapy might you advise?
1. Anion exchange resin eg cholestyramine
2. Nicotinic acid (Niacin)
3. Fibrate e.g. fenofibrate
4. Omega-3 fatty acid preparation
5. Alternative statin / lower dose statin
6. Ezetimibe monotherapy
7. Measure CK levels

71.
Case study four
 47 year old ♂ smoker
 Discharged on Atorvastatin 80mg after recent NSTEMI, treated with
PCI and stent
 Father died of a heart attack at 51
 Total chol 6.1mM, LDL-C 4.24 mM on Rx
 What might you advise?
1. Addition of Omega-3 fatty acids
2. Addition of Ezetimibe 10mg od
3. Alternative statin – if so which?
4. Something else – if so what?
5. Check he is actually taking his atorvastatin
6. Refer to local lipid clinic (for assessment of possible FH and for
consideration of PCSK9i)

72.
Case study five
 55 year old ♂ with BP, previous MI, CKD
 Baseline Total chol 7.6mM, HDL 0.9mM, LDL-C: 5.5mM prior to statins
(non HDL-chol ..........)
 Initiated on Atorvastatin 40mg but was titrated down to 20mg od due
to severe muscle pain
 Currently LDL-C 3.9mM, Total chol 5.7mM, HDL 1.0mM (non HDL–chol
4.7mM -30% reduction on treatment)
 Would you recommend any change in lipid therapy?
1. No change
2. Up titrate to Atorvastatin 40mg again
3. Change to Rosuvastatin 20mg od
4. Add Ezetimibe 10mg od to Atorvastatin
5. Consider FH + referral to lipid clinic if family history of IHD
6. Consider Inclisiran if LDL-C >2.6mM after adding ezetimibe
6.7mM

73.
Learning points
 Primary prevention: Atorvastatin 20mg
 Secondary prevention: Atorvastatin 80mg
 Think FH if chol > 7.5mM + FHx IHD <50/60 yrs
 Aim for 40% reduction in non-HDL Chol (so pre-treatment lvls key)
 Consider Ezetimibe if statin intolerant / lipid targets not achieved
 Consider referral to lipid clinic if ?FH
 Consider referral to lipid clinic in secondary prevention if fasting LDL
persistently >4mM despite statin therapy or if statin intolerant

74.
Any questions?