BACKGROUND AND OBJECTIVES: Identification of coronary sites susceptible to progression or nonprogression might provide additional information to select medical or surgical treatment and furthermore for appropriate timing for percutaneous transluminal coronary angioplasty or coronary artery bypass graft. METHODS: We reviewed serial coronary arteriograms of 50 patients with coronary artery disease retrospectively. Patients were managed with standard treatment including anti-hypertensives, antiplatelets, lipid-lowering agents and other risk factor management by attending physician's decision. Patients who received percutaneous transluminal angioplasty, coronary artery bypass graft or thrombolysis were excluded. Cononary arteriographies were undertaken with average 33 months interval. Criteria for the progression and regression were the changes of the luminal diameter narrowing of the arterial segment by 20% or more reduction or increase, respectively. Results: Patients show progressive change, regressive change or no significant interval change in 50%, 12% and 30% of total 50 patients, respectively. Male gender, angiographic interval were the significant predictor of progressive change. In terms of coronary segment, stable segments are most frequent 52.2% (72/138) and progression in 40.2% (74/184), regression in 27.5% (38/138). Initial coronary lesions with low grade stenosis (less than 50%) have a tendency to progress than that of high grade stenosis (70% or more) Percentage diameter stenosis of new lesion are not related linearly with the interval between two sequential angiographies. CONCLUSION: Number of patients with progressive coronary arteriogram are more frequent than the patients with regressive change or no interval change. Progression and regression are frequent finding of serial coronary arteriography in usual clinical practice. Progression and regression are found frequently in the same patient at different coronary branches (16 patients). It suggested that the local factors may play an important role in the pathogenesis of coronary artery disease as well as systemic risk factors.