Interní Med. 2012; 14(11): 406-411
The most frequent mechanism of the development of acute coronary syndrome (ACS) is fissuring or rupture of a coronary atherosclerotic
plaque, leading to intra-luminal thrombus formation with subsequent coronary artery obstruction. It remains questionable
whether cholesterol lowering may directly influence these pathogenic pathways; there is, however, a class among lipid-lowering
drugs, with clear evidence of its favorable effects in ACS patients – statins. In addition to their lipid-lowering effect, statins also suppress
inflammation, improve endothelial dysfunction, inhibit oxidative stress, or increase myocardial tolerance to acute ischemia.
Most importantly, statins have been repeatedly shown to improve outcomes not only in stable forms of ischemic heart disease, but
also in patients with ACS. The hardest evidence in ACS patients has been shown for “intensive statin therapy” represented mostly by
atorvastatin 80 mg (alternatively by rosuvastatin 20–40 mg). In comparison with placebo or standard statin, intensive statin therapy
reduces even all-cause mortality in ACS patients. Based on available data, intensive statin therapy should be started in all ACS patients.
At the present time, however, administration of statins is the only lipid-lowering treatment in ACS with proven efficacy and
safety. Currently, several clinical trials are under way that were designed to test the effects of other hypolipidemics, administered
on top of statin therapy after ACS, such as cholesteryl ester transfer protein (CETP) inhibitors or PCSK9 inhibitors, that reduce LDL
receptor degradation.
Published: December 1, 2012 Show citation