Purpose: The rationale of this study was to identify patients with fast progression of coronary plaque volume PV and characterize changes in PV and plaque components over time.Method: Total PV (TPV... Show morePurpose: The rationale of this study was to identify patients with fast progression of coronary plaque volume PV and characterize changes in PV and plaque components over time.Method: Total PV (TPV) was measured in 350 patients undergoing serial coronary computed tomography angiography (median scan interval 3.6 years) using semi-automated software. Plaque morphology was assessed based on attenuation values and stratified into calcified, fibrous, fibrous-fatty and low-attenuation PV for volumetric measurements. Every plaque was additionally classified as either calcified, partially calcified or non-calcified.Results: In total, 812 and 955 plaques were detected in the first and second scan. Mean TPV increase was 20 % on a per-patient base (51.3 mm(3) [interquartile range (IQR): 14.4, 126.7] vs. 61.6 mm(3) [IQR: 16.7, 170.0]). TPV increase was driven by calcified PV (first scan: 7.6 mm(3) [IQR: 0.2, 33.6] vs. second scan: 16.6 mm(3) [IQR: 1.8, 62.1], p < 0.01). Forty-two patients showed fast progression of TPV, defined as > 1.3 mm(3) increase of TPV per month. Male sex (odds ratio 3.1, p = 0.02) and typical angina (odds ratio 3.95, p = 0.03) were identified as risk factors for fast TPV progression, while high-density lipoprotein cholesterol had a protective effect (odds ratio per 10 mg/dl increase of HDL cholesterol: 0.72, p < 0.01). Progression to > 50 % stenosis at follow-up was observed in 34 of 327 (10.4 %) calcified plaques, in 13 of 401 (3.2 %) partially calcified plaques and 2 of 221 (0.9 %) non-calcified plaques (p < 0.01).Conclusion: Fast plaque progression was observed in male patients and patients with typical angina. High HDL cholesterol showed a protective effect. Show less
