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Smoking and obesity predict high-risk plaque by coronary CTA in low coronary artery calcium score (CACS)

Published:April 23, 2021DOI:https://doi.org/10.1016/j.jcct.2021.04.003

      Abstract

      Background

      The AHA recommends statins in patients with CACS>100 AU. However in patients with low CACS (1–99 AU), no clear statement is provided, leaving the clinician in a grey-zone. High-risk plaque (HRP) criteria by coronary CTA are novel imaging biomarkers indicating a higher a-priori cardiovascular (CV) risk, which could help for decision-making. Therefore the objective of our study was to identify which CV-risk factors predict HRP in patients with low CACS 1–99.

      Methods

      1003 symptomatic patients with low-to-intermediate risk, a clinical indication for coronary computed tomography angiography (CCTA) and who had a coronary artery calcium score (CACS) between 1 and 99 AU, were enrolled. CCTA analysis included: stenosis severity and HRP-criteria: low-attenuation plaque (LAP <30HU, <60HU and <90HU) napkin-ring-sign, spotty calcification and positive remodeling. Multivariate regression models were created for predicting HRP-criteria by the major 5 cardiovascular risk factors (CVRF) (smoking, arterial hypertension, positive family history, dyslipidemia, diabetes) and obesity (BMI>25 ​kg/m2).

      Results

      304 (33.5%) were smokers. 20.4% of smokers had HRP compared with only 14.9% of non-smokers (p ​= ​0.045). Male gender was associated with HRP (p ​< ​0.001).
      Smoking but not the other 5 CVRF had the most associations with HRP-criteria (LAP<60HU/≥2 criteria:OR 1.59; 95%CI:1.07–2.35), LAP<90HU (OR 1.57; 95%CI:1.01–2.43), Napkin-Ring-Sign (OR 1.78; 95%CI:1.02–3.1) and positive remodelling (OR 1.54; 95%CI:1.09–2.19). Smoking predicted fibrofatty LAP<90HU in males only. Obesity predicted LAP<60HU in both females and males.

      Conclusions

      In patients with low CACS 1-99AU, male gender, smoking and obesity, but not the other CVRF predict HRP. These patients would rather benefit from intensification of primary CV-prevention measures such as statins.

      Keywords

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