Abstract

It is not well known which lesions are progressed or regressed in patients with angina pectoris who use statins. We assessed the impact of plaque components on plaque progression in patients with angina pectoris who used rosuvastatin 10 mg/day using virtual histology plus intravascular ultrasound. Sixty-six patients who underwent baseline and 9-month follow-up virtual histology plus intravascular ultrasound for nonintervened intermediate coronary stenosis were grouped according to plaque progression (increase of plaque plus media area, n = 22) or plaque regression (decrease of plaque plus media area, n = 44) at baseline minimum lumen area (MLA) site at follow-up and compared the various parameters including baseline plaque components between the 2 groups. Follow-up low-density lipoprotein cholesterol was not significantly different between the progression and regression groups (85 ± 30 vs 82 ± 24 mg/dl, p = 0.6). Baseline percent necrotic core (NC) area was significantly larger (26.1 ± 10.9% vs 17.6 ± 10.8%, p = 0.004) and baseline percent fibrofatty area was significantly smaller (8.1 ± 6.2% vs 14.2 ± 12.1%, p = 0.008) at the MLA site in the progression group compared to the regression group. Thin-cap fibroatheroma was observed more frequently in the progression group compared to the regression group (32% vs 9%, p = 0.020). Change of plaque plus media area from baseline to follow-up at the MLA site correlated with baseline percent NC area (r = 0.375, p = 0.002), baseline percent fibrofatty area (r = -0.388, p = 0.001), and baseline percent fibrotic area (r = -0.242, p = 0.050). Baseline percent NC area at the MLA site was an independent predictor of plaque progression at follow-up (odds ratio 1.265, 95% confidence interval 1.069 to 1.497, p = 0.006). In conclusion, NC is associated with plaque progression in patients when low-density lipoprotein cholesterol level is around 80 mg/dl at 9-month follow-up in patients with angina pectoris on rosuvastatin 10 mg/day.

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