[Progress in diagnosis and treatment of acute coronary syndrome]

Acute coronary syndrome is caused by disruption of a coronary atherosclerotic plaque. It is recognized that the risk of plaque disruption depends more on plaque composition than on plaque size. Therefore, it is important to establish imaging techniques and clinical markers for the identification of vulnerable plaques. Intravascular ultrasound and angioscope may reveal important features of vulnerable plaques. In the near future, optical coherence tomography and intravascular thermography may further improve the characterization of plaques. Systemic markers of inflammation, such as CRP and SAA, may reflect the intensity of inflammation in the atherosclerotic lesion. Clinical observations indicate that plaques may be stabilized by lipid-lowering drugs, anti-oxidants, estrogen and Chlamydia-killing antibiotics. After plaque rupture, new generation antiplatelet and anticoagulant drugs, such as GPIIb/IIIa antagonists and low-molecular heparin, can limit the mural thrombi formation more effectively.