Abstract

Abstract Background Perivascular fat attenuation index (FAI) assessed by coronary computed tomography (CCTA) has been demonstrated to represent a reliable marker of coronary inflammation. Several studies have explored the potential anti-inflammatory effects of statins in reducing the risk of plaque rupture and subsequent cardiovascular events. However, the effect of statin therapy on FAI has not been clearly demonstrated so far. Purpose Our objective was to investigate the changes in perivascular FAI at the level of coronary lesions, as measured by coronary computed tomography (CCTA), following long-term high-dose statin therapy. Methods This study includes 23 patients who presented with typical chest pain, had a low to intermediate likelihood of coronary artery disease, and underwent a CCTA examination which revealed the existence of at least one coronary atheromatous plaque. Statin therapy was initiated in all patients according to guidelines. The CCTA was repeated after a time interval ranging from 1.5 to 3 years. Lesion-specific perivascular FAI, together with different plaque characteristics, were measured at both baseline and follow-up using a new AI-powered medical device called CaRi-Heart®. Results The mean age of the participants was 61.72 ± 8.86 at the time of the first scan, and 65.21% (n = 15) of them were male. At baseline, the CT density of the adipose tissue (ranging from -190 to -30 HU), was not significantly different between the two groups. A significant decrease in serum lipids following statin therapy was recorded during follow-up: from 193.4 ± 47.09 to 145.2 ± 34.7, p = 0.04 for total cholesterol, and from 101.77 ± 25.20 to 86.41 ± 21.09, p = 0.02 for LDL cholesterol. The FAI-score consistently decreased from baseline to follow-up, especially in the left anterior descending artery: from 15.87 ± 9.32 vs. 12.40 ± 7.55, p = 0.04, while there was no significant decrease in coronary inflammation at the level of left circumflex artery (13.98 ± 6.16 vs. 13.10 ± 6.59, p = ns), or right coronary artery (20.53 ± 13.74 vs. 19.96 ± 16.24, p = ns). Similarly, the FAI-Score Centile values were lower during the second scan, specifically for LAD (0.51 ± 0.28 vs. 0.69 ± 0.29, p = 0.04), while there were no significant differences of FAI score centile in the LCX (0.72 ± 0.28 vs. 0.74 ± 0.26, p = ns) and RCA (0.71 ± 0.32 vs. 0.78 ± 0.21, p = ns). Conclusion CaRi-Heart® mapping technology revealed a significant decrease of coronary inflammation, as expressed by the FAI-score, as a result of high-dose statin treatment especially at the level of the LAD. This indicates a potential role of local factors related to coronary circulation in the complex process of plaque inflammation. The perivascular FAI-score and FAI-score centile may serve as promising imaging biomarkers for monitoring the anti-inflammatory response to statin treatments.Color-coded FAI MappingPVAT-FAI Score of Coronary Inflammation

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