Clinical trials have demonstrated that β-blockers substantially reduce recurrent myocardial infarction, sudden cardiac death, and total mortality rates in patients with myocardial infarction (1–5, 16). A suggested mechanism for the long-term beneficial effects of β-blockers is their possible antiatherosclerotic effect. Many animal models have provided evidence that β-blockers can slow the development of atherosclerosis (17–21). However, the antiatherosclerotic effects of β-blockers have not been demonstrated in the human coronary artery. Our study suggests that β-blockers have considerable coronary antiatherosclerotic effects. According to the linear effects models, atheroma volume statistically significantly decreased by 2.4 mm3/y in patients who received β-blocker treatment, corresponding to a regression of atheroma volume of approximately 1.3% per year. A nonsignificant decrease of 0.4 mm3/y occurred in patients who did not receive β-blockers. No direct data exist about the amount of differential change in atheroma volume that is associated with better clinical outcomes. However, indirect evidence from the REVERSAL (7) and PROVE-IT (Pravastatin or Atorvastatin Evaluation and Infection Therapy) (22) studies, which used the same treatment regimens (atorvastatin, 80 mg/d, vs. pravastatin, 40 mg/d), suggests that the annual difference in change in atheroma volume of approximately 3.5 mm3 favoring atorvastatin, 80 mg, found in REVERSAL should be clinically important. This is because atorvastatin, 80 mg, in the PROVE-IT study was associated with a statistically significant 16% reduction in the clinical end point (23). In our analysis, the effect size of β-blockers (difference of 2.0 mm3/y) was smaller than that of intensive lipid-lowering therapy compared with moderate lipid-lowering therapy in REVERSAL.