Statins & Pharmacotherapy of Dyslipidemia
HMG-CoA reductase inhibitors as the cornerstone, the validated LDL-lowering add-on ladder, and the shift to cardiovascular-outcome modification
Past RGUHS + DNB + MPMSU + MUHS + VNSGU · 27
RGUHSMay '25
RGUHSMay '25
MPMSUOct '25
MPMSUMay '25
MUHSWinter '24
MPMSU2022
DNBDec '22
VNSGUApr '22
RGUHSNov '21
RGUHSJul '21
DNBJun '21
MUHSSummer '21
MUHSSummer '21
MPMSUJul '20
RGUHSNov '18
RGUHSMay '18
MPMSU2018
MPMSU2018
MUHSSummer '18
MUHSSummer '17 Suppl
DNBDec '15
MUHSSummer '14
DNBDec '12
RGUHSMay '11
MPMSU2011
MPMSU2009
RGUHSSep '06
Introduction
- Dyslipidaemia — A disorder of lipoprotein metabolism — overproduction or deficiency — encompassing hypercholesterolaemia, hypertriglyceridaemia and low HDL-cholesterol; it is the major modifiable driver of atherosclerotic cardiovascular disease (ASCVD), the leading cause of death worldwide.
- Two clinical sequelae — Atherosclerosis (from raised apo B-100-containing lipoproteins → MI, stroke, PVD) and acute pancreatitis (from severe hypertriglyceridaemia, typically TG > 700–1000 mg/dL when LPL clearance saturates).
- Therapeutic goal — Hypolipidaemic drugs aim to reduce fatal and non-fatal ASCVD events — not merely to normalise a lipid number; statins (HMG-CoA reductase inhibitors) are the cornerstone of every guideline.
- Key lever — The liver expresses ~75% of LDL receptors and clears ~75% of plasma LDL — so hepatic LDL-receptor expression is the modulatable lever, and the most effective diet change and the most effective drug class (statins) both work by up-regulating it.
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Statins Dyslipidemia
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