UNLABELLED: Computed tomography angiography (CTA) enables characterization of non-calcified coronary atherosclerotic lesions (NCALs) and assessment of plaque vulnerability. We investigated whether the characteristics of NCALs detected by 64-slice CTA were influenced by preceding statin therapy and serum lipid profiles. METHODS: Among 493 consecutive patients who underwent coronary CTA, we enrolled 114 patients with NCALs. We divided the patients into three groups according to preceding statin therapy: intensive statins (IS, n=24), moderate statins (MS, n = 26), and no statin (NS, n = 64). The vulnerability of each NCAL was evaluated by density (low-density plaque defined as CT density ≤ 38 HU), positive remodeling (remodeling index > 1.05), and the presence of adjacent spotty calcification. RESULTS: Percentages of patients in the IS, MS, and NS groups with low-density NCALs were 46%, 58%, and 80%, respectively (p = 0.009) and positive remodeling NCALs were 54%, 58%, and 75%, respectively (p = 0.10). We also found an inverse correlation between serum LDL-C level and the minimum plaque CT density. According to the regression equation, a CT density of 38 HU corresponded with LDL-C of 100 mg/dl. The number of low-density plaques was positively correlated with low-density to high-density lipoprotein cholesterol ratio (LDL-C/HDL-C). An LDL-C/HDL-C > 2.5 independently predicted multiple low-density plaques (OR 2.39 [95%CI: 1.28-4.86], p < 0.001). CONCLUSIONS: Our CTA findings demonstrate that low-density NCALs occur less frequently in patients with intensive statin pre-treatment. A high LDL-C/HDL-C ratio is also associated with larger numbers of low-density NCALs.
UNLABELLED: Computed tomography angiography (CTA) enables characterization of non-calcified coronary atherosclerotic lesions (NCALs) and assessment of plaque vulnerability. We investigated whether the characteristics of NCALs detected by 64-slice CTA were influenced by preceding statin therapy and serum lipid profiles. METHODS: Among 493 consecutive patients who underwent coronary CTA, we enrolled 114 patients with NCALs. We divided the patients into three groups according to preceding statin therapy: intensive statins (IS, n=24), moderate statins (MS, n = 26), and no statin (NS, n = 64). The vulnerability of each NCAL was evaluated by density (low-density plaque defined as CT density ≤ 38 HU), positive remodeling (remodeling index > 1.05), and the presence of adjacent spottycalcification. RESULTS: Percentages of patients in the IS, MS, and NS groups with low-density NCALs were 46%, 58%, and 80%, respectively (p = 0.009) and positive remodeling NCALs were 54%, 58%, and 75%, respectively (p = 0.10). We also found an inverse correlation between serum LDL-C level and the minimum plaque CT density. According to the regression equation, a CT density of 38 HU corresponded with LDL-C of 100 mg/dl. The number of low-density plaques was positively correlated with low-density to high-density lipoprotein cholesterol ratio (LDL-C/HDL-C). An LDL-C/HDL-C > 2.5 independently predicted multiple low-density plaques (OR 2.39 [95%CI: 1.28-4.86], p < 0.001). CONCLUSIONS: Our CTA findings demonstrate that low-density NCALs occur less frequently in patients with intensive statin pre-treatment. A high LDL-C/HDL-C ratio is also associated with larger numbers of low-density NCALs.
Authors: Ryo Nakazato; Heidi Gransar; Daniel S Berman; Victor Y Cheng; Fay Y Lin; Stephan Achenbach; Mouaz Al-Mallah; Matthew J Budoff; Filippo Cademartiri; Tracy Q Callister; Hyuk-Jae Chang; Ricardo C Cury; Kavitha Chinnaiyan; Benjamin J W Chow; Augustin Delago; Martin Hadamitzky; Joerg Hausleiter; Philipp Kaufmann; Erica Maffei; Gilbert Raff; Leslee J Shaw; Todd C Villines; Allison Dunning; Gudrun Feuchtner; Yong-Jin Kim; Jonathon Leipsic; James K Min Journal: Atherosclerosis Date: 2012-08-24 Impact factor: 5.162