Statins

HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors. The reductase catalyses the conversion of HMG-CoA to mevalonic acid
Simvastatin + pravastatin + atorvastatin decrease hepatic CHO synthesis
LDL ↓20-55%
HDL ↑ 5-15 %
TG ↓ 10-35 %
All statins produce peak LDL CH lowering after 1-2 weeks of therapy
Statins are effective in both primary & secondary dyslipidemias
Statins are given at bed time to obtain maximum effect.
Not necessary for atorvastatin & rosuvastatin which have long plasma half life
All statins except rosuvastatins are metabolized by CYP3A4
Pleiotropic actions:
improved endothelial function
reduced vascular inflammation and platelet aggregability
antithrombotic action
stabilisation of atherosclerotic plaques
increased neovascularisation of ischaemic tissue
enhanced fibrinolysis
immune suppression
osteoclast apoptosis and increased synthetic activity in
osteoblasts
Pharmacokinetics
well absorbed when given orally
extracted by the liver (target tissue), undergo extensive presystemic biotransformation

Simvastatin is an inactive pro-drug
C l i n i c a l u s e s
Secondary prevention of myocardial infarction and stroke in patients who have symptomatic atherosclerotic disease (angina, transient ischemic attacks) following acute myocardial infarction or stroke
Primary prevention of arterial disease in patients who are at high risk because of elevated serum CHO concentration, especially it there are other risk factors for atherosclerosis
Atorvastatin lowers serum CHO in patients with homozygous familiar hypercholesterolemia
A d v e r s e e f f e c t s:
mild gastrointestinal disturbances

increased plasma activities in liver enzymes

severe myositis (rhabdomyolysis), muscle tenderness & rise in Creatine phosphate kinase (CPK) levels, myopathy
and angio-oedema (rare), myopathy is more common when enzyme inhibitors are used simultaneously