Statin, like aspirin, should be given as early as possible in patients with acute coronary syndrome.

It is estimated that about 1 million patients are hospitalized for acute coronary events each years in the United States. An acceptable theory is that the acute coronary syndrome is caused by rupture of the atherosclerotic plaque with superimposed thrombus, which is a complex process and involving a number of different stages. Previous studies indicated that inflammation is one of the most important features of vulnerable plaque, and occurs in most vulnerable plaque, comprised of monocytes, macrophages, and lymphocytes in both the cap and in the adventitia. This is supported by evidence that reduction in serum inflammatory marker levels, such as C-reactive protein, significantly decreased coronary events in patients with acute coronary syndrome. A large number of investigations have demonstrated that administration of statin could modify C-reactive protein concentrations with a concurrent fall in cardiovascular events. Our recent data indicated that reduction of inflammatory markers could be achieved within 24 h following a single dose of statin administration after admission in patients with coronary artery disease. Based on the available evidence and in light of the new understanding that statins have pleiotropic effects, especially as a potent anti-inflammatory agent, the statins, like aspirin, should be clinically given as early as possible in patients with acute coronary syndrome.