statin
A statin turns down the body's own cholesterol factory. The liver makes most of the cholesterol in your blood, and a statin throttles the key machine on that production line. With less cholesterol being built, the liver pulls more out of the bloodstream, so harmful LDL cholesterol levels fall and arteries are less likely to fur up.
Statins competitively inhibit HMG-CoA reductase, the rate-limiting enzyme in the liver's cholesterol synthesis pathway. The drop in intracellular cholesterol prompts liver cells to make more LDL receptors, which clear more LDL cholesterol from the blood. Examples include atorvastatin, simvastatin, rosuvastatin and pravastatin. Beyond lowering LDL, statins stabilize artery wall plaques and reduce inflammation, and large trials show they cut heart attacks and strokes in those at risk.
Statins are generally well tolerated, but they can cause muscle aches, and rarely a serious muscle breakdown called rhabdomyolysis, especially at high doses or when blood levels rise from interacting drugs that inhibit their metabolism (for example via CYP3A4). They can modestly raise liver enzymes and slightly increase the risk of new diabetes. Because cholesterol synthesis peaks at night, shorter-acting statins like simvastatin are taken in the evening.
After a heart attack, a patient is started on high-intensity atorvastatin to drive LDL cholesterol low and reduce the chance of a second event, regardless of the starting cholesterol level.
After cardiovascular events, statins are given for risk reduction, not just to a cholesterol number.
Grapefruit juice inhibits CYP3A4 and can raise levels of some statins enough to increase muscle toxicity, a classic food-drug interaction.