To the Editor: Angiogenesis and atherogenesis share a number of pathways suggesting that interrelated tradeoffs might be inherent to therapies designed to enhance collateral formation and cardiac repair (1). This “Janus-like” effect on atherosclerosis progression was observed in several experimental models exposed to therapy with bone marrow stem cells (BMSCs)(1–4). A recent clinical study reported high rates of in-stent restenosis after BMSC mobilization (5). In our study (6), CD133 enriched BMSC exerted beneficial effects on cardiac recovery in patients with reperfused myocardial infarction, but the restenosis rates were also higher as expected after intracoronary BMSC therapy (7–11). Hence, we investigated the effects of intracoronary CD133 enriched BMSC on in-stent neointimal proliferation and distal atherosclerosis progression in patients with recent myocardial infarction treated with angioplasty using bare-metal stents. Thirty-eight patients with acute myocardial infarction due to occlusion of the proximal left anterior descending coronary artery (LAD) were studied. The cell group consisted of 21 patients receiving intracoronary injection of CD133 enriched BMSC and follow-up catheterization with quantitative coronary angiography (QCA) and coronary functional assessment with the pressurederived fractional flow reserve (FFR)(12, 13). The control group consisted of 17 patients matched for ejection fraction, infarction size, and location with control catheterization between 4 and 8 months after the infarction. Segmental QCA analysis was performed for the stented segment and non-stented portion of the mid LAD and distal LAD. Data are shown as mean SEM. Paired t test and unpaired t test were used as appropriate. There were no differences in clinical and demographic characteristics between groups (not shown). Baseline angiographic and functional characteristics are shown in Table 1. At follow-up, no significant changes were noted in luminal diameters of the contralateral artery (CLA) of either group (from 2.66 0.09 mm to 2.65 0.10 mm in the cell group, and from 2.71 0.14 mm to

2.78 0.17 mm in the control group, both p NS). In contrast, higher loss index of the stented segment in the cell group (0.42 0.07 vs. 0.22 0.06, p 0.05) was paralleled by a greater leftward shift in the cumulative distribution of the minimal luminal diameter (MLD) as compared with the control group (Fig. 1 A). In non-stented segments, cumulative luminal loss of the reference diameter (RD) and MLD at the mid and distal segment of the infarct-related artery (IRA) were higher in the cell group