Describes dyslipidemia, classification, pathophysiology, risk factors and its treatment

1. Dr Avvaru Deepthi
KLE college of pharmacy

2. Dyslipidemias are disorders of lipoprotein metabolism, including lipoprotein
overproduction or deficiency. These disorders may be manifested by elevation of the
serum total cholesterol, LDL and triglyceride concentrations and a decrease in HDL
cholesterol concentration.
Various lipoproteins:

3. • Transport dietary lipids from intestine
to liver (exogenous)
• Transport lipids from liver to peripheral
tissues (endogenous)
• Cholesterol is a waxy substance
produced and released by cells in the
liver.
• The body uses cholesterol to form cell
membranes, aid in digestion, convert
Vitamin D in the skin and
develop hormones.
• Lipoproteins form a package for the
cholesterol:
• Low density lipoproteins (LDL)
• High density lipoproteins (HDL)

4. Fredrickson classification of
dyslipidemia

5. PATHOPHYSIOLOGY

7. Screening
• Lipid profile
• HDL
• Triglyceride
• Calculated LDL-C
• Fredrickson classification , particle size, c-
reactive protein
• Ankle brachial index less than 0.9
• Apo lipoprotein B more than 130mg/dl
• Framingham risk score

9. Lipid association of India
• Indian expert consensus document on management of
dyslipidemia in Indians.
• Compared with the western populations, Indians tend to
have higher triglyceride levels and lower HDL-C but the
total cholestrol and LDL-C levels are generally lower.
• Indians have high prevalence of diabetes, obesity and
metabolic syndrome, all of which are characterised by high
TG levels, low HDL-C and higher prevalence of small
dense LDL particles, which is also known as atherogenic
dyslipidemia.
• Among various lipid markers, the ratio of apolipoprotein B
to apolipoprotein A-1 appears to be the best indicator of
ASCVD risk.

10. Risk category

12. Treatment goals and statin initation thresholds
according to ASCVD risk categories
Pharmacological treatment
•HMG –CoA reductase inhibitors : atorvastatin , rosuvastatin
•Bile acid sequestrants : cholestryamine, colesevelam
•Fibrates : fenofibrate, gemfibrozil
•Nicotinic acid : niacin
•Cholestrol absorption inhibitors : ezetimibe
•PCSK-9 inhibitors : alirocumab

13. International guidelines: AHA

14. International guidelines: AHA

15. COVID-19
• There is scarcity of evidence regarding the efficacy and
risk of different strategies in patients with COVID-19
disease.
• COVID-19 disease may trigger destabilisation of
chronic CVD.
• Aspirin dosage given for the secondary prevention of
atherothrombosis has no anti-inflammatory potential
and there should not be interrupted in COVID-19
patients without any other relevant reasons.
• Anti- viral therapy, it is of major importance to correct
modifiable predisposing factors.

16. SARS-COV-2 infection causes
dyslipidemia

17. Advances in the management of
dyslipidemia
• PCSK9-I
• PCSK9 inhibition by Monoclonal antibodies
• Evolocumab or Alirocumab are second line treatments for hyperlipidaemia.
• Human monoclonal antibodies; PCSK9 inhibitors can be given (140 mg injection every 2 weeks )
• when LDL is persistently above the thresholds despite maximal tolerated lipid-lowering therapy.
• Binding of LDL with PCSK9 leads to degradation of the LDL receptor, and then less LDL is removed
from the circulation.
• Inhibiting PCSK9 from being degraded therefore promotes removal of LDL cholesterol from
circulation
• After subcutaneous administration of alirocumab, maximal suppression of free PCSK9 occurs within 4
to 8 hours.
• Inclisiran
• Ethyl ester of eicosapentaenoic acid

18. • THANK YOU