Long-term high-dose statin therapy significantly increased calcified plaque portions (p<0.0001), decreased non-calcified plaque volume (p=0.0209), and reduced PCAT attenuation in the LAD (p=0.0142).
Observational (n=52)
Does high-dose statin treatment reduce pericoronary inflammation and improve plaque distribution in patients with chest pain and documented atheromatous plaque?
Long-term high-dose statin therapy significantly reduces pericoronary inflammation and promotes plaque stabilization by decreasing non-calcified plaque volume and increasing calcification.
Computed tomography angiography (CTA) has validated the use of pericoronary adipose tissue (PCAT) attenuation as a credible indicator of coronary inflammation, playing a crucial role in coronary artery disease (CAD). This study aimed to evaluate the long-term effects of high-dose statins on PCAT attenuation at coronary lesion sites and changes in plaque distribution. Our prospective observational study included 52 patients (mean age 60.43) with chest pain, a low-to-intermediate likelihood of CAD, who had documented atheromatous plaque through CTA, performed approximately 1 year and 3 years after inclusion. We utilized the advanced features of the CaRi-Heart® and syngo.via Frontier® systems to assess coronary plaques and changes in PCAT attenuation. The investigation of changes in plaque morphology revealed significant alterations. Notably, in mixed plaques, calcified portions increased (p < 0.0001), while non-calcified plaque volume (NCPV) decreased (p = 0.0209). PCAT attenuation generally decreased after one year and remained low, indicating reduced inflammation in the following arteries: left anterior descending artery (LAD) (p = 0.0142), left circumflex artery (LCX) (p = 0.0513), and right coronary artery (RCA) (p = 0.1249). The CaRi-Heart® risk also decreased significantly (p = 0.0041). Linear regression analysis demonstrated a correlation between increased PCAT attenuation and higher volumes of NCPV (p < 0.0001, r = 0.3032) and lipid-rich plaque volume (p < 0.0001, r = 0.3281). Our study provides evidence that high-dose statin therapy significantly reduces CAD risk factors, inflammation, and plaque vulnerability, as evidenced by the notable decrease in PCAT attenuation, a critical indicator of plaque progression.
Matyas et al. (Tue,) conducted a observational in Chest pain with low-to-intermediate likelihood of CAD and documented atheromatous plaque (n=52). High-dose statins was evaluated on PCAT attenuation at coronary lesion sites and changes in plaque distribution. Long-term high-dose statin therapy significantly increased calcified plaque portions (p<0.0001), decreased non-calcified plaque volume (p=0.0209), and reduced PCAT attenuation in the LAD (p=0.0142).