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Management
of
Dyslipidemia
CONTENTS
• Introduction to lipoproteins and dyslipidemia
• Non pharmacological management
• Pharmacological management
• Scenario
Lipoproteins
• Atherogenic
• Non
atherogenic
• Lp(a) ?
Composition
Lipidprofiling
• Lipoprotein measurement – ApoB
• Lipid profile
• Fasting or not ?
Total Cholesterol 120-200
Triglycerides 10-150
HDL Cholesterol 40-60
LDL Cholesterol <130
VLDL Cholesterol Upto 30
DYSLIPIDEMIA
• Dyslipidemias are
generally characterized
clinically by increased
plasma levels of
cholesterol, TGs, or
both, variably
accompanied by
reduced levels of HDL
cholesterol
Dyslipidemia
Familial/Genetic
Secondary
•High dose statin therapy is initiated or
continued as early as possible
•Goal 50% reduction of LDL-C, to <55 mg/dL
•Initial Ezetimibe then PCSK9 inhibitors
•Loading with high dose statins before PCI.
•Intensive statin therapy after TIA & Stroke
PRIMARY
PREVENTION
Risk
calculators
Raised LDL
DIABETES
• IA--- > 40 to 75 years age with diabetes– moderate intensity
Statins
• II A---- assess ascvd risk and If multiple RFs – higher intensity
Statins to reduce ldl by 50 %
• II A ---- > 75 years-old, if on statins- continue
• II B --- Adults with diabetes with ascvd risk >20% -add
ezetimibe.
• II B----- >75 years old with DM, not on statins – start based
on risk- benefit ratio
Old age
•For given TC higher risk in elderly.
•Multiple co-morbities, Medications
•Different pharmacokinetics and dynamics
•Statins to be started at low doses and
titrate.
Children
• Family history of early CVD & hypercholesterolemia –
screening from 2 years
• With obesity and Metabolic syndrome- testing
• Lifestyle changes and caloric restrictions.
• >190 or >160 mg/dL with FH after failure of above
• Reverse cascade of screening.
WOMEN
•Statins are preferred.
•OCPs ? >160mg/dL
•Oestrogen Replacing therapy ?
•Pregnancy and lactation: BAS and lipid apheresis
CKD
• Increased risk of both
atherosclerotic vascular
disease and structural
heart disease
• Specifically rise of TG,
Lp(a)
CKD contd
Inflammatory conditions
• Rheumatoid arthritis (RA), glomerulosclerosis, or pulmonary
fibrosis
• CVD has been cited as the top cause of death in people with RA
• HIV - Immune dysregulation, Systemic inflammation, Antiretroviral
therapy & Dyslipidemia
• Role of hs-CRP, CAC, intimal thickness.
• Assess Risk score and start based on score
• Start on low doses and check for drug interactions.
Raised TG
• TGs are associated but not causal for ASCVD
• Drugs used are statins, fibrates, niacin, ω-3 Fatty Acids
• Treatment to be started If > 200 mg/dL
• Lifestyle and dietary modifications
• 885-1000:Lipid apheresis and insulin infusion till 500
Dyslipidemia as a cause ofPancreatitis
Lipoprotein (a)
• Screen if Premature ASCVD, Familial
• Limited evidence in reducing ascvd on lowering levels
• Drugs – PCSK9 inhibitors, Niacin
• Statins increase
Thankyou

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Hyperlipidmeia Advaces Management.pptx

  • 2. CONTENTS • Introduction to lipoproteins and dyslipidemia • Non pharmacological management • Pharmacological management • Scenario
  • 5. Lipidprofiling • Lipoprotein measurement – ApoB • Lipid profile • Fasting or not ? Total Cholesterol 120-200 Triglycerides 10-150 HDL Cholesterol 40-60 LDL Cholesterol <130 VLDL Cholesterol Upto 30
  • 6. DYSLIPIDEMIA • Dyslipidemias are generally characterized clinically by increased plasma levels of cholesterol, TGs, or both, variably accompanied by reduced levels of HDL cholesterol Dyslipidemia Familial/Genetic Secondary
  • 7.
  • 8. •High dose statin therapy is initiated or continued as early as possible •Goal 50% reduction of LDL-C, to <55 mg/dL •Initial Ezetimibe then PCSK9 inhibitors •Loading with high dose statins before PCI. •Intensive statin therapy after TIA & Stroke
  • 11.
  • 13. DIABETES • IA--- > 40 to 75 years age with diabetes– moderate intensity Statins • II A---- assess ascvd risk and If multiple RFs – higher intensity Statins to reduce ldl by 50 % • II A ---- > 75 years-old, if on statins- continue • II B --- Adults with diabetes with ascvd risk >20% -add ezetimibe. • II B----- >75 years old with DM, not on statins – start based on risk- benefit ratio
  • 14. Old age •For given TC higher risk in elderly. •Multiple co-morbities, Medications •Different pharmacokinetics and dynamics •Statins to be started at low doses and titrate.
  • 15. Children • Family history of early CVD & hypercholesterolemia – screening from 2 years • With obesity and Metabolic syndrome- testing • Lifestyle changes and caloric restrictions. • >190 or >160 mg/dL with FH after failure of above • Reverse cascade of screening.
  • 16. WOMEN •Statins are preferred. •OCPs ? >160mg/dL •Oestrogen Replacing therapy ? •Pregnancy and lactation: BAS and lipid apheresis
  • 17. CKD • Increased risk of both atherosclerotic vascular disease and structural heart disease • Specifically rise of TG, Lp(a)
  • 19. Inflammatory conditions • Rheumatoid arthritis (RA), glomerulosclerosis, or pulmonary fibrosis • CVD has been cited as the top cause of death in people with RA • HIV - Immune dysregulation, Systemic inflammation, Antiretroviral therapy & Dyslipidemia • Role of hs-CRP, CAC, intimal thickness. • Assess Risk score and start based on score • Start on low doses and check for drug interactions.
  • 20. Raised TG • TGs are associated but not causal for ASCVD • Drugs used are statins, fibrates, niacin, ω-3 Fatty Acids • Treatment to be started If > 200 mg/dL • Lifestyle and dietary modifications • 885-1000:Lipid apheresis and insulin infusion till 500
  • 21.
  • 22. Dyslipidemia as a cause ofPancreatitis
  • 23. Lipoprotein (a) • Screen if Premature ASCVD, Familial • Limited evidence in reducing ascvd on lowering levels • Drugs – PCSK9 inhibitors, Niacin • Statins increase