Aim To elucidate the relationship between autophagy of peripheral blood monocyte （PBM） and the vulnerability of atherosclerotic plaques. Methods Forty patients with stable angina pectoris （SAP）, 40 patients with acute coronary syndrome （ACS） compromised the study groups. All patients underwent coronary angiography （CAG） and intravascular ultrasound （IVUS） examinations. The expression levels of autophagy related protein Beclin-1, microtubule-associated protein 1 light chain 3 （MAP1-LC3） and Atg5-Atg12 complex in PBM were detected by Western blot. MAP1-LC3 （autophagy-specific protein） in the PMB was also examined by laser scanning confocal microscope. Results Sixty two plaques were detected by IVUS in the SAP patients, which included 30 fibrous ones, while 71 plaques were evidenced in the ACS group, which encompassed 40 lipid ones. The expression levels of Beclin-1, MAP1-LC3 and Atg5-Atg12 complex in PBM in ACS patients were significantly lower than those in SAP patients （P<0.01）. Conclusion The patients in SAP group had more stable fibrous plaques than those in the ACS group （P<0.01）, while the ACS patients had more vulnerable soft lipid ones than those in the SAP group （P<0.01）. The autophagy of PBM in patients with coronary heart disease （CHD） decreases with the increasing vulnerability of atherosclerotic plaques. Enhancing the autophagy of PBM may be a potential therapeutic target of stabilizing atherosclerotic plaques, which will reduce the acute coronary events and lower the mortality of patients with CHD.