Abstract 10740: Effects of Renin-Angiotensin-Aldosterone-System Inhibitors on Coronary Atherosclerotic Plaques: Results From the Paradigm Registry

Introduction: Coronary CT Angiogram (CCTA) has become a powerful tool in the diagnosis and risk stratification of coronary artery disease (CAD), but can also provide unique insight into the effects of pharmacotherapy on the progression of atherosclerosis. Although Renin-Angiotensin-Aldosterone-System (RAAS) inhibitors are indicated in patients with stable CAD, their impact on the progression of coronary atherosclerosis is unclear. Methods: We performed a prospective, multinational study consisting of a registry of patients without history of CAD who underwent serial CCTAs at an interscan interval of >2 years. Patients taking RAAS inhibitors were propensity matched to RAAS inhibitor naïve patients based on clinical and CCTA characteristics at the baseline. Atherosclerotic plaques in CCTAs were quantitatively analyzed for percent atheroma volume (PAV) according to plaque composition (necrotic core, fibro-fatty plaque, fibrous plaque, and calcium) using predefined Hounsfield unit thresholds. Results: Of 1,248 patients from the registry, 299 RAAS inhibitor taking patients were matched to 299 RAAS inhibitor naïve patients. Over a median interval of 3.9 years, there was no significant difference in annual progression of total PAV between RAAS inhibitor naive vs taking patients (0.75 vs 0.79 %/year, p = 0.66), nor was there any difference in the progression of necrotic core (-0.02 vs 0.002 %/year, p = 0.09), fibrofatty plaque (-0.03 vs.0.05 %/year, p = 0.67), fibrous plaque (0.29 vs 0.25 %/year, p =0.91), or calcified plaque (0.51 vs. 0.51 %/year, p = 0.37). Conclusions: Within this cohort of patients, the use of RAAS inhibitors over a period of nearly 4 years did not have a measurable impact on progression of total atherosclerotic plaque or any plaque subtypes assessed by CCTA. These results suggest that the benefit of RAAS inhibition is independent of an effect on coronary plaque progression.