Clinical evidence has emphasized the importance of coronary plaques’ characteristics, rather than lumen stenosis, for the outcome of cardiovascular events. Coronary computed tomographic angiography (CCTA) has a well-established role as a non-invasive tool for assessing plaques. The aim of this study was to compare clinical characteristics and CCTA-derived information of stable patients with non-severe plaques in predicting major adverse cardiac events (MACEs) during follow-up. We retrospectively selected 371 patients (64% male) who underwent CCTA in our center from March 2016 to January 2021 with Coronary Artery Disease—Reporting and Data System (CAD-RADS) 0 to 3. Of those, 198 patients (53% male) had CAD-RADS 0 to 1. Among them, 183 (49%) had normal pericoronary fat attenuation index (pFAI), while 15 (60% male) had pFAI ≥ 70.1 Hounsfield unit (HU). The remaining 173 patients (76% male) had CAD-RADS 2 to 3 and were divided into patients with at least one low attenuation plaque (LAP) and patients without LAPs (n-LAP). Compared to n-LAP, patients with LAPs had higher pFAI (p = 0.005) and had more plaques than patients with n-LAP. Presence of LAPs was significantly higher in elderly (p p p = 0.0001, hyperlipemia p = 0.0003, smoking p = 0.0003, diabetes p = p = 0.0007). Among patients with CAD-RADS 0 to 1, the ones with pFAI ≥ 70.1 HU were more often hyperlipidemic (p = 0.05) and smokers (p = 0.007). Follow-up (25,4 months, range: 17.6–39.2 months) demonstrated that LAP and pFAI ≥ 70.1 significantly and independently (p = 0.04) predisposed to outcomes (overall mortality and interventional procedures). There is an added value of CCTA-derived features in stratifying cardiovascular risk in low- to intermediate-risk patients with non-severe, non-calcified coronary plaques. This is of utmost clinical relevance as it is possible to identify a subset of patients with increased risk who need strengthening in therapeutic management and closer follow-up even in the absence of severe CAD. Further studies are needed to evaluate the effect of medical treatments on pericoronary inflammation and plaque composition.
